The Practice of Clinical Echocardiography

The Practice of Clinical Echocardiography III

Second Edition Catherine M. Otto MD Professor of Medicine Acting Director, Division of Cardiology Director, Training Programs in Cardiovascular Disease Associate Director, Echocardiography Laboratory University of Washington Seattle, Washington

W.B. SAUNDERS COMPANY An Imprint of Elsevier Science Philadelphia•London•New York•St. Louis•Sydney•Toronto

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W.B. SAUNDERS COMPANY An Imprint of Elsevier Science The Curtis Center Independence Square West Philadelphia, Pennsylvania 19106 Library of Congress Cataloging-in-Publication Data The practice of clinical echocardiography / [edited by] Catherine M. Otto.—2nd ed. p. cm. Includes bibliographical references and index. ISBN 0-7216-9204-4 1. Echocardiography. I. Otto, Catherine M. [DNLM: 1. Echocardiography. WG 141.5.E2 P8942 2002] RC683.5.U5 C57 2002 616.1'207543-dc21 2001049709 Acquisitions Editor: Richard Zorab Production Editor: Robin E. Davis Production Manager: Mary Stermel Illustration Specialist: Rita Martello Book Designers: Catherine Bradish and Lynn Foulk THE PRACTICE OF CLINICAL ECHOCARDIOGRAPHY, Second Edition ISBN 0-7216-9204-4

Copyright © 2002, 1997 by W.B. Saunders Company. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher. Printed in the United States of America. Last digit is the print number: 9 8 7 6 5 4 3 2 1

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Contributors

Gerard P. Aurigemma MD Professor of Medicine and Radiology, University of Massachusetts Medical School; Director, Noninvasive Cardiology, University of Massachusetts Medical Center, Worcester, Massachusetts Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Thomas J. Benedetti MD Professor of Obstetrics and Gynecology, University of Washington School of Medicine, Seattle, Washington The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy Ann F. Bolger MD Associate Clinical Professor of Medicine, Division of Cardiology, University of California, San Francisco, School of Medicine; Director of Echocardiography, San Francisco General Hospital, San Francisco, California Aortic Dissection and Trauma: Value and Limitations of

Echocardiography Hans G. Bosch MSc Senior Staff Member, Division of Image Processing, Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands Two-Dimensional Echocardiographic Digital Image Processing and Approaches to Endocardial Edge Detection Ian G. Burwash MD Professor of Medicine, University of Ottawa; Active Attending Staff, University of Ottawa Heart Institute, Ottawa, Ontario, Canada Indications, Procedure, Image Planes, and Doppler Flows Benjamin F. Byrd III MD Associate Professor of Medicine, Division of Cardiology, Vanderbilt University School of Medicine; Director, Echocardiography Laboratory, Vanderbilt University Medical Center, Nashville, Tennessee Maintaining Quality in the Echocardiography Laboratory Kwan-Leung Chan MD Professor of Medicine, University of Ottawa; Active Attending Staff, University of Ottawa Heart Institute, Ottawa, Ontario, Canada Indications, Procedure, Image Planes, and Doppler Flows Edmond W. Chen MD Fellow, Division of Cardiology, University of California, San Francisco, School of Medicine, San Francisco, California Echocardiographic Evaluation of the Patient with a Systemic

Embolic Event John S. Child MD Professor, University of California, Los Angeles, School of Medicine; Co-Chief, Division of Cardiology, Director, Ahmanson/UCLA Adult Congenital Heart Disease Center, UCLA Medical Center, Los Angeles, California Echocardiographic Evaluation of the Adult with Postoperative Congenital Heart Disease Joseph A. Diamond MD Assistant Professor of Medicine, Mount Sinai School of Medicine; Assistant Attending, The Mount Sinai Medical Center, New York, New York Hypertension: Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy Pamela S. Douglas MD Tuchman Professor of Medicine; Head, Cardiovascular Medicine Section, University of Wisconsin Medical School, Madison, Wisconsin Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Thomas R. Easterling MD Associate Professor of Obstetrics and Gynecology, University of Washington School of Medicine, Seattle, Washington The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy Peter J. Fitzgerald MD, PhD Associate Professor of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford, California Intravascular Ultrasound: Histologic Correlation and Clinical

Applications Kirsten E. Fleischman MD, MPH Assistant Professor in Residence, University of California, San Francisco, School of Medicine; Attending Physician, University of California, San Francisco, Medical Center, San Francisco, California The Role of Echocardiographic Evaluation in Patients Presenting with Acute Chest Pain to the Emergency Room: Diagnosis, Triage, Treatment Decisions, Outcome Elyse Foster MD Professor of Clinical Medicine, University of California, San Francisco, School of Medicine; Director, Adult Echocardiography Laboratory, Moffitt-Long Hospital, San Francisco, California Echocardiography in the Coronary Care Unit: Management of Acute Myicardial Infarction, Detection of Complications, and Prognostic Implications

William H. Gaasch MD Professor of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts; Director, Cardiovascular Research, Lahey Clinic, Burlington, Massachusetts Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Edward F. Gibbons MD Assistant Clinical Professor of Medicine, University of Washington School of Medicine; Director of Echocardiography, Director of Inpatient Cardiology Services, Virginia Mason Medical Center, Seattle, Washington

Education and Training of Physicians and Sonographers John S. Gottdiener MD Professor of Medicine, State University of New York at Stony Brook, School of Medicine; Director, Noninvasive Cardiac Imaging, St. Francis Hospital, Roslyn, New York Hypertension: Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy Brian P. Griffin MD Director, Cardiovascular Disease Training Program, The Cleveland Clinic Foundation, Cleveland, Ohio Echocardiography in Patient Selection, Operative Planning and Intraoperative Evaluation of Mitral Valve Repair Sheila K. Heinle MD Clinical Assistant Professor of Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas Quantitation of Valvular Regurgitation: Beyond Color Flow Mapping Mary Etta E. King MD Associate Professor of Pediatrics, Harvard Medical School; Director, Pediatric Echocardiography, Massachusetts General Hospital, Boston, Massachusetts Echocardiographic Evaluation of the Adult with Unoperated Congenital Heart Disease Tim Kinnaird MB Fellow in Cardiovascular Medicine, London Chest Hospital, London, United Kingdom Pericardial Disease

Katsuhiro Kitamura MD Research Fellow in Medicine, Stanford University Medical Center, Stanford, California Intravascular Ultrasound: Histologic Correlation and Clinical Applications Allan L. Klein MD Professor of Medicine, Ohio State University College of Medicine; Director, Cardiovascular Imaging Research, The Cleveland Clinic Foundation, Cleveland, Ohio Restrictive Cardiomyopathy: Diagnosis and Prognostic Implications Carol Kraft RDCS Lead Cardiac Sonographer, Virginia Mason Medical Center, Seattle, Washington Education and Training of Physicians and Sonographers Carolyn K. Landolfo MD Assistant Professor of Medicine, Duke University School of Medicine; Director, Adult Echocardiography, Duke University Medical Center, Durham, North Carolina The Role of Echocardiography in the Timing of Surgical Intervention for Chronic Mitral and Aortic Regurgitation Jannet F. Lewis MD Professor of Medicine, George Washington University Medical Center; Director of Echocardiography, George Washington University Hospital, Washington, D.C. Doppler and Two-Dimensional Echocardiographic Evaluation in Acute and Long-term Management of the Heart Failure Patient David T. Linker MD

Associate Professor of Medicine, Division of Cardiology; Adjunct Associate Professor of Bioengineering; University of Washington School of Medicine, Seattle, Washington Principles of Intravascular Ultrasound Warren J. Manning MD Associate Professor of Medicine and Radiology, Harvard Medical School; Section Chief, Non-invasive Cardiac Imaging, Beth Israel Deaconess Medical Center, Boston, Massachusetts The Role of Echocardiography in Atrial Fibrillation and Flutter Pamela A. Marcovitz MD Director, Clinical Cardiology Fellowship Program; Director, Echocardiographic Research, William Beaumont Hospital, Royal Oak, Michigan Exercise Echocardiography: Stress Testing in the Initial Diagnosis of Coronary Artery Disease and in Patients with Prior Revascularization or Myocardial Infarction Roy W. Martin PhD Research Professor, Department of Anesthesiology and Center for Bioengineering, Applied Physics Laboratory, University of Washington School of Medicine, Seattle, Washington Interaction of Ultrasound with Tissue, Approaches to Tissue Characterization, and Measurement Accuracy Thomas H. Marwick MD, PhD Professor of Medicine, Head of Section, University of Queensland Department of Medicine; Director of Echocardiography, Princess Alexandra Hospital, Brisbane, Queensland, Australia Stress Echocardiography with Nonexercise Techniques: Principles, Protocals, Interpretation, and Clinical Applications David J. Meier MD

Cardiology Fellow, University of Michigan Health System, Ann Arbor, Michigan The Role of Echocardiography in the Timing of Surgical Intervention of Chronic Mitral and Aortic Regurgitation

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Bradley I. Munt MD Clinical Instructor, The University of British Columbia Department of Medicine; Cardiologist, Providence Healthcare and St. Paul's Hospital, Vancouver, British Columbia, Canada Pericardial Disease Danielle Noll MD Department of Cardiology, Echocardiography, Medizinische Klinik, Klinikum Innentadt, Munich, Germany Myocardial Contrast Echocardiography: Methods, Analysis, and Applications Catherine M. Otto MD Professor of Medicine; Acting Director, Division of Cardiology; Director, Training Programs in Cardiovascular Disease; Associate Director, Echocardiography Laboratory, University of Washington School of Medicine, Seattle, Washington Aortic Stenosis: Echocardiographic Evaluation of Disease Severity, Disease Progression, and the Role of Echocardiography in Clinical Decision Making; The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy; Echocardiographic Findings in Acute and Chronic Pulmonary Disease Donald C. Oxorn MD

Associate Professor of Anesthesiology, Adjunct Associate Professor of Medicine, University of Washington School of Medicine, Seattle, Washington Monitoring Ventricular Function in the Operating Room: Impact on Clinical Outcome Abraham C. Parail MD Fellow in Cardiology, University of Wisconsin Medical School, Milwaukee, Wisconsin Aging Changes Seen on Echocardiography Robert A. Phillips MD, PhD Associate Professor of Medicine, Mount Sinai School of Medicine; Director, Department of Medicine, Lenox Hill Hospital, New York, New York Hypertension: Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy Thomas R. Porter MD Associate Professor, University of Nebraska College of Medicine, Diagnostic Cardiac Ultrasound and Noninvasive Diagnostics, University of Nebraska Medical Center, Omaha, Nebraska Myocardial Contrast Echocardiography: Methods, Analysis, and Applications Harry Rakowski MD Professor of Medicine, Division of Cardiology, University of Toronto; Staff Cardiologist, Toronto General Hospital, Toronto, Ontario, Canada Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy Rita F. Redberg MD

Associate Professor of Medicine, Division of Cardiology, University of California, San Francisco, School of Medicine, San Francisco, California Echocardiographic Evaluation of the Patient with a Systemic Embolic Event Johan H. C. Reiber PhD Professor of Medical Imaging, Director, Division of Image Processing, Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands Two-Dimensional Echocardiographi Digital Image Processing and Approaches to Endocardial Edge Detection Cheryl L. Reid MD Associate Professor of Medicine, University of California, Irvine College of Medicine; Director, Non-invasive Cardiology, University of California, Irvine, Medical Center, Orange, California Echocardiography in the Patient Undergoing Catheter Balloon Mitral Commissurotomy: Patient Selection, Hemodynamic Results, Complications, and Long-term Outcome Carlos A. Roldan MD Associate Professor of Medicine, University of New Mexico School of Medicine; Staff Cardiologist, Director, Echocardiography Laboratory, Veterans Affairs Medical Center; Staff Cardiologist, University of New Mexico Health Sciences Center, Albuquerque, New Mexico Echocardiographic Findings in Systemic Diseases Characterized by Immune-Mediated Injury Elizabeth W. Ryan MD

Research Fellow in Cardiology, Division of Cardiology, University of California, San Francisco, School of Medicine, San Francisco, California Aortic Dissection and Trauma: Value and Limitations of Echocardiography Kiran B. Sagar MD Professor of Cardiology and Medicine, University of Wisconsin Medical School, Milwaukee, Wisconsin Aging Changes Seen on Echocardiography Nelson B. Schiller MD Professor of Medicine, Radiology, and Anesthesia, University of California, San Francisco, School of Medicine; Director of Echocardiography, San Francisco Veterans Affairs Medical Center; Attending Physician, Cardiology, Echocardiography, and Adult Congenital Heart Disease, Moffitt-Long Hospital, San Francisco, California Clinical Decision Making in Endocarditis Ingela Schnittger MD Professor of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California The Role of Echocardiography in the Evaluation of Patients After Heart Transplantation Douglas S. Segar MD Clinical Associate Professor of Medicine, Indiana University School of Medicine, Indiana Heart Institute, Indianapolis, Indiana The Digital Echocardiography Laboratory

VIII

David M. Shavelle MD

Interventional Cardiology Fellow, Good Samaritan Hospital, Los Angeles, California Aortic Stenosis: Echocardiographic Evaluation of Disease Severity, Disease Progression, and the Role of Echocardiography in Clinical Decision Making Florence H. Sheehan MD Research Professor of Medicine, Division of Cardiology, University of Washington School of Medicine, Seattle, Washington Quantitative Evaluation of Regional Left Ventricular Systolic Function; Three-Dimensional Echocardiography: Approaches and Applications Bruce K. Shively MD Associate Professor of Cardiology, Oregon Health and Science University; Co-Director, Echocardiography Laboratory, Oregon Health and Science University Hospital, Portland, Oregon Echocardiographic Findings in Systemic Diseases Characterized by Immune-Mediated Injury Mikel D. Smith MD Professor of Internal Medicine/Cardiology, University of Kentucky College of Medicine; Director, Adult Echocardiography Laboratory, Gill Cardiovascular Institute, Albert B. Chandler Medical Center, Lexington, Kentucky Left Ventricular Diastolic Function: Clinical Utility of Doppler Echocardiography A. Rebecca Snider MD Consultant, Pediatric Cardiology, Monmouth Junction, New Jersey General Echocardiographic Approach to the Adult with Suspected Congenital Heart Disease Mark R. Starling MD Professor of Internal Medicine,

Director of Cardiology Training Program, Associate Chief of Cardiology, University of Michigan Medical School; Chief, Cardiology Section, VA Ann Arbor Healthcare System, Ann Arbor, Michigan The Role of Echocardiography in the Timing of Surgical Intervention for Chronic Mitral and Aortic Regurgitation William J. Stewart MD Associate Professor of Medicine, Department of Cardiology, Staff Cardiologist, The Cleveland Clinic Foundation, Cleveland, Ohio Echocardiography in Patient Selection, Operative Planning, and Intraoperative Evaluation of Mitral Valve Repair Marcus F. Stoddard MD Professor of Medicine, University of Louisville School of Medicine; Director, Noninvasive Cardiology, University of Louisville Hospital, Louisville, Kentucky Echocardiography in the Evaluation of Cardiac Disease Due to Endocinopathies, Renal Disease, Obesity, and Nutritional Deficiencies Maran Thamilarasan MD Assistant Staff Cardiologist, The Cleveland Clinic Foundation, Cleveland, Ohio Restrictive Cardiomyopathy: Diagnosis and Prognostic Implications Christopher R. Thompson MD, CM Clinical Associate Professor of Medicine (Cardiology), Director, Echocardiography Laboratory, St. Paul's Hospital, Vancouver, British Columbia, Canada Pericardial Disease Aneesh V. Tolat MD

Clinical Fellow in Medicine, Harvard Medical School; Clinical Fellow in Cardiovascular Diseases, Beth Israel Deaconess Medical Center, Boston, Massachusetts The Role of Echocardiography in Atrial Fibrillation and Flutter Brandon R. Travis PhD School of Chemical Engineering, Georgia Institute of Technology, Atlanta, Georgia Fluid Dynamics of Prosthetic Valves Zian H. Tseng MD Cardiology Fellow, University of California, San Francisco, School of Medicine, San Francisco, California Echocardiography in the Coronary Care Unit: Management of Acute Myocardial Infarction, Detection of Complications, and Prognostic Implications Hannah A. Valantine MD Professor of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California The Role of Echocardiography in the Evaluation of Patients After Heart Transplantation Samuel Wang MD Assistant Professor of Clinical Internal Medicine, University of California, Davis, School of Medicine; Attending Physician, University of California, Davis, Medical Center, Sacramento, California The Role of Echocardiographic Evaluation in Patients Presenting with Acute Chest Pain to the Emergency Room: Diagnosis, Triage, Treatment Decisions, Outcome E. Douglas Wigle MD Professor of Medicine, University of Toronto; Staff Cardiologist,

Toronto General Hospital, Toronto, Ontario, Canada Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy Selwyn P. Wong MD Cardiologist, Middlemore Hospital, Auckland, New Zealand Echocardiographic Findings in Acute and Chronic Pulmonary Disease Anna Woo MD Assistant Professor of Medicine, Division of Cardiology, University of Toronto; Staff Cardiologist, Toronto General Hospital, Toronto, Ontario, Canada Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy

Feng Xie MD Research Assistant Professor, Cardiology, University of Nebraska Medical Center, Omaha, Nebraska Myocardial Contrast Echocardiography: Methods, Analysis, and Applications Paul G. Yock MD Professor of Medicine, Stanford University School of Medicine, Stanford, California Intravascular Ultrasound: Histologic Correlation and Clinical Applications Ajit P. Yoganathan PhD Regents Professor of Biomedical Engineering, The Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia

Fluid Dynamics of Prosthetic Valves Miguel Zabalgoitia MD Professor of Medicine; Director, Echocardiography Laboratory, University of Texas Health Science Center, San Antonio, Texas Echocardiographic Recognition and Quantitation of Prosthetic Valve Dysfunction William A. Zoghbi MD Professor of Medicine, Director of Echocardiography Research, Baylor College of Medicine; Associate Director, Echocardiography Laboratory, The Methodist Hospital, Houston, Texas Echocardiographic Recognition of Unusual Complications After Surgery on the Great Vessels and Cardiac Valves

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Preface Echocardiography increasingly has become a key component in the routine evaluation of patients with suspected or known cardiovascular disease. As this technique has evolved and matured, the role of the echocardiographer has shifted from simply providing a description of images to providing an integrated assessment of echocardiographic data in conjunction with the other clinical data from each patient. In effect, echocardiography has become a specialized type of cardiology consultation. The information now requested by the referring physician includes not only the qualitative and quantitative interpretation of the echocardiographic images and Doppler flow data but also a discussion of how this information might affect clinical decision making. Specific examples include decisions regarding medical or surgical therapy (e.g., treatment of endocarditis, surgery for aortic dissection), optimal timing of intervention in patients with chronic cardiac diseases (e.g., valvular regurgitation, mitral stenosis), prognostic implications (e.g., heart disease in pregnancy, heart failure patients), and the possible need for and frequency of periodic diagnostic evaluation (e.g., congenital heart disease, the postoperative patient). This book reflects our role as clinicians with specialized expertise in echocardiography and is of value to cardiology fellows pursuing advanced training in echocardiography, cardiologists in clinical practice, researchers using echocardiographic techniques, and other individuals using echocardiographic approaches in the clinical setting (including anesthesiologists, radiologists, emergency medicine physicians, and obstetricians), as well as to cardiac sonographers, cardiovascular technologists, and nursing professionals.

Each chapter provides an advanced level of discussion, written by an expert in the field, building upon the basic material in the Textbook of Clinical Echocardiography (C. M. Otto, 2nd Edition, WB Saunders, Philadelphia, 2000). The emphasis is on optimal data acquisition, results of recent studies, quantitative approaches to data analysis, potential technical limitations, and areas of active research, in addition to a detailed discussion of the impact of echocardiographic data on patient management. Tables, line drawings, echocardiographic images, and Doppler tracings are used to summarize and illustrate key points. In this Second Edition, the text has been revised to reflect recent advances, illustrations and tables have been updated, and new references have been added to each chapter. The book is organized into sections based on major diagnostic categories. In this new edition, an introductory section on transesophageal echocardiography has been added. Chapters include basic principles of transesophageal imaging, monitoring of ventricular function in the operating room, and a discussion of echocardiographic evaluation of aortic dissection and trauma. Other detailed information on the role of transesophageal echocardiography is integrated into subsequent chapters, which are organized by disease categories. The next section focuses on the left ventricle, with chapters spanning the spectrum from emerging new techniques (e.g., myocardial contrast echocardiography, automated edge detection, tissue characterization, three-dimensional echocardiography) to critical appraisals of quantitative techniques (e.g., left ventricular geometry and systolic function, evaluation of regional function, and assessment of diastolic function). The section on ischemic heart disease includes chapters on the role of echocardiography in the emergency room and coronary care unit, stress echocardiography (exercise and nonexercise), and the basic principles, instrumentation, and clinical applications of intravascular ultrasound in patients with coronary artery disease. The critical role that echocardiography now plays in management of patients with valvular heart disease is evident in a section of chapters on technical aspects of echocardiographic evaluation, optimal timing of surgery and periodic evaluation of patients with valvular regurgitation, management of patients undergoing balloon mitral commissurotomy, clinical decision making in patients with endocarditis, evaluation of disease severity, progression in valvular aortic stenosis, and evaluation of prosthetic valves. The following clinically oriented sections bring together data from both the

echocardiographic and general cardiology literature to discuss the role of echocardiography in patients with cardiomyopathies (heart failure, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and the posttransplant patient) and pericardial disease, pregnant patients with cardiac disease, and a wide range of other vascular and systemic diseases that lead to cardiac dysfunction (hypertension, aortic dissection, pulmonary disease, systemic immune-mediated diseases, renal disease, aging, systemic embolic events, and cardiac arrhythmias). In recognition of the increasing number of adult patients presenting with congenital heart disease, either as a new diagnosis or following prior surgical procedures, three chapters are devoted to this topic. In addition, a new section has been added on the echocardiography laboratory to address issues that increasingly affect our clinical practice, including education and training of echocardiographers, quality improvement in the echocardiography laboratory, and the transition to a digital laboratory. It is hoped that this book will provide the needed background to support and supplement clinical experience and expertise. Of course, competency in the acquisition and interpretation of echocardiographic and Doppler data depends on appropriate clinical education and training as detailed in accreditation requirements for both physicians and technologists, and as recommended by professional societies including the American Society of Echocardiography, the American College of Cardiology, and the American Heart Association. I strongly support these educational requirements and training recommendations; XII

readers of this book are urged to review the relevant documents. In addition, there continue to be advances both in the the technical aspects of image and flow data acquisition and in our understanding of the clinical implications of specific echocardiographic findings. This book represents our knowledge base at one point in time; readers should consult the current literature for the most up-to-date information. Although an extensive list of carefully selected references is provided with each chapter, the echocardiographic literature is so robust that it is impractical to include all relevant references; the reader can use an online medical literature search if an all-inclusive listing is desired. Catherine M. Otto MD

Acknowledgments

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Sincere thanks are due to the many individuals who made this book possible. Primary recognition goes to the chapter contributors who provided scholarly, thoughtful, and insightful discussions and who integrated the clinical and echocardiographic information into a format that benefits our readers. The support staff at each of our institutions deserves our appreciation for manuscript preparation and providing effective communication, with special thanks to Sharon Kemp and Bev Bubela. The many research subjects who contributed to the data on which our current understanding is based certainly are worthy of our appreciation. The cardiac sonographers at the University of Washington Medical Center (Rachel Elizalde, RDCS; Michelle C. Fujioka, RDMS; Carolyn J. Gardner, RDCS; Caryn D'Jang, RDCS; Scott Simicich, RDCS; David Stolte, RDCS; Rebecca G. Schwaegler, RDMS; Erin Trent, RDCS; and Todd R. Zwink, RDMS) merit acknowledgment. In addition, gratitude is due to Richard Zorab and the production team at W.B. Saunders. Finally, I thank my family for their constant encouragement and support.

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NOTICE Medicine is an ever-changing field. Standard safety precautions must be followed, but as new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the method and duration of administration, and contraindications. It is the responsibility of the treating physician, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual patient. Neither the Publisher nor the editor assumes any liability for any injury and/or damage to persons or property arising from this publication. THE PUBLISHER

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Section 1 - Transesophageal Echocardiography

Chapter 1 - Indications, Procedure, Image Planes, and Doppler Flows Ian G. Burwash MD Kwan-Leung Chan MD

Transesophageal echocardiography (TEE) has become a valuable diagnostic imaging modality for the dynamic assessment of cardiac anatomy and function. Since the initial description of esophageal echocardiography in 1976,[1] the potential role and utility of TEE in the evaluation of diseases of the heart and great vessels have expanded to involve all aspects of cardiac disease. The close proximity of the esophagus to the heart and great vessels provided the echocardiographer with an easily accessible window with the potential for excellent visualization of cardiac structures, avoiding the intervening lung and chest wall tissues that limit transthoracic imaging. The potential of TEE to provide a valuable imaging tool became widely recognized in the 1980s with advancements in TEE probe technology, including the availability of single-plane phased array transducers and the addition of color flow and continuous wave Doppler imaging technology. TEE does not supplant transthoracic echocardiography

(TTE), however; it is a complementary imaging modality with its own strengths and weaknesses. The 2

introduction of biplane TEE transducers in the late 1980s and multiplane transducers in the 1990s has resulted in a further expansion of potential diagnostic applications. Perhaps the best evidence of TEE's diagnostic utility and value in patient management is the widespread use of this technology. TEE is found in the inpatient and outpatient ambulatory setting, in the operating room, in the intensive care unit, and in the emergency department. Currently, TEE accounts for approximately 5% to 10% of all echocardiography studies performed. The indications and utility of TEE will likely expand in the future with new technologic advancements such as three-dimensional echocardiography.

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Performance of Transesophageal Echocardiography Transesophageal echocardiography is a semi-invasive procedure that should be performed only by a properly trained physician who understands the indications for and potential complications of the procedure. Both technical and cognitive skills are required for the competent performance and interpretation of TEE studies (Table 1-1) , and guidelines on training have been published.[2] The physician should be assisted by an experienced sonographer whose tasks are to ensure that optimal images are obtained by adjusting the controls of the echocardiographic system and to ensure safety by monitoring the responses of the patient during the procedure. Although family members or friends are usually not allowed in the room when the procedure is being performed, there are situations in which their presence can be helpful. The presence of a parent can have a calming effect when one is dealing with an apprehensive teenager. A friend or a relative who speaks the same language can relieve much of the anxiety when dealing with an anxious patient who is not fluent in English. Transesophageal echocardiography should be performed in a spacious room that can comfortably accommodate a stretcher. The room should be equipped with an oxygen outlet and suction facilities. A pulse oximeter should be available, to be used mainly in cyanotic patients and patients with severe lung disease. The TEE probe should be carefully examined prior to each use. In addition to visual inspection, it is important to palpate the probe, particularly the flexion portion, to ensure that there is no unusual wear and tear of the probe.[3] Stretching of the steering cables may result in increased flexibility and mobility of the probe tip with buckling of the probe tip within the esophagus.[4] This phenomenon is associated with a poor TEE image and resistance to probe withdrawal. The probe should be advanced into the stomach and straightened by retroflexion of the extreme antiflexed probe tip. We have also detected perforation of the TEE probe sheath by a ruptured steering cable and recommend inspection of the casing for any protruding wires prior to probe insertion.[3] The flexion controls

need to be tested on a regular basis. Anterior flexion should exceed 90 degrees, and right and left flexion should approach 90 degrees. TABLE 1-1 -- Cognitive and Technical Skills Required for the Performance of Transesophageal Echocardiography (TEE) Cognitive Skills Knowledge of appropriate indications, contraindications, and risks of TEE Understanding of differential diagnostic considerations in each clinical case Knowledge of physical principles of echocardiographic image formation and blood flow velocity measurement Familiarity with the operation of the ultrasonographic instrument, including the function of all controls affecting the quality of the data displayed Knowledge of normal cardiovascular anatomy, as visualized tomographically Knowledge of alterations in cardiovascular anatomy resulting from acquired and congenital heart diseases Knowledge of normal cardiovascular hemodynamics and fluid dynamics Knowledge of alterations in cardiovascular hemodynamics and blood flow resulting from acquired and congenital heart diseases Understanding of component techniques for general echocardiography and TEE, including when to use these methods to investigate specific clinical questions Ability to distinguish adequate from inadequate echocardiographic data and to distinguish an adequate from an inadequate TEE examination Knowledge of other cardiovascular diagnostic methods for correlation with TEE findings Ability to communicate examination results to patient, other health care professionals, and medical record Technical Skills Proficiency in performing a complete standard echocardiographic examination, using all echocardiographic modalities relevant to the case Proficiency in safely passing the TEE transducer into the esophagus and

stomach and in adjusting probe position to obtain the necessary tomographic images and Doppler data Proficiency in correctly operating the ultrasonographic instrument, including all controls affecting the quality of the data displayed Proficiency in recognizing abnormalities of cardiac structure and function as detected from the transesophageal and transgastric windows, in distinguishing normal from abnormal findings, and in recognizing artifacts Proficiency in performing qualitative and quantitative analysis of the echocardiographic data From Pearlman AS, Gardin JM, Martin RP, et al: J Am Soc Echocardiogr 1992;5:187–194. Preparation of Patient Patients should be contacted at least 12 hours before the procedure and instructed to fast for at least 4 hours before the procedure. They are informed that they should be accompanied, because they will not be able to drive or return to work for several hours owing to the lingering effect of sedation. On the day of the study, the procedure is explained in greater detail, and informed consent is obtained. Patients are told to expect mild abdominal discomfort and gagging following the insertion of the probe and are reassured that these responses are transient. A 20-gauge intravenous cannula is then inserted for administration of medications and contrast agents, if necessary. Lidocaine hydrochloride spray is routinely used for topical anesthesia, which should cover the posterior pharynx and the tongue. We usually use diazepam 2 to 10 mg intravenously 3

for sedation.[5] Midazolam at 0.05 mg/kg, with a total dose between 1 and 5 mg, can also be used. Sedation is used in about 85% of our patients and should be more sparingly used in elderly patients, because they tend to be more stoic and the effect of sedation is more likely prolonged. On the other hand, sedation is essential in young anxious patients and when the study is expected to be protracted. We aim for light sedation so that at the end of the procedure the patients are awake and can leave with an escort. Heavy sedation is needed in situations in which blunting the hemodynamic responses to the procedure is desirable. One obvious example is a patient undergoing TEE for suspected aortic

dissection.[6] It has not been our practice to use anticholinergic agents such as glycopyrrolate to decrease salivation. In the rare circ*mstances in which there is excessive salivation, it is usually adequate to simply instruct the patient to let the saliva dribble onto the towel placed under the chin, or the saliva can be removed by intermittent suction. Bacteremia is not a significant risk in TEE, and we do not use antibiotic prophylaxis to prevent endocarditis even in patients with prosthetic heart valves.[7] [8] Esophageal Intubation We perform the TEE study with the patient in the left decubitus position. The physician, the sonographer, and the echocardiographic system are all positioned on the left-hand side of the patient.[5] Artificial teeth or dentures are routinely removed. The flexion controls should be unlocked to allow for maximum flexibility of the probe when it is being inserted. The patient's head should be in a flexed position. The tip of the probe is kept relatively straight and gently advanced to the back of the throat. It should be maintained in a central position, because deviation to either side increases the likelihood that it may become lodged in the piriform fossa. The operator can facilitate this process by inserting one or two fingers into the patient's oropharynx to direct the path of the probe. Gentle pressure is exerted and the patient is instructed to swallow. The swallowing mechanism helps guide the probe into the esophagus. In older patients, cervical spondylosis with prominent protrusion into the posterior pharynx can create difficulty with passage of the probe.[5] Manually depressing the back of the tongue provides more room, allowing the TEE probe to assume a less acute angle and facilitating the intubation of the esophagus. If significant resistance is encountered when the probe is advanced, it is prudent to withdraw the probe and then initiate a new attempt. Esophageal intubation is more difficult with the multiplane probe than with the smaller monoplane and biplane probes.[9] [10] The latter can be used, if available, when esophageal intubation cannot be achieved with a multiplane probe. In experienced hands, the rate of failure of esophageal intubation should be less than 2%.[5] [9] [11]

A bite guard should always be used, except in edentulous patients. Our practice is to put it between the patient's teeth after the TEE probe has been successfully passed into the esophagus. Patients with a very sensitive pharynx may close their mouths involuntarily during esophageal intubation. In these patients, it is safer to insert the bite guard before the insertion of

the TEE probe. The patient should be instructed to keep the guard between the teeth throughout the procedure, and regular checks should be made to ensure that it is in the proper position to prevent damage to the probe or injury to the patient. Even when the probe is inserted without difficulties, it is not uncommon for the patient to develop nausea with or without mild retrosternal or abdominal discomfort. We find it useful to pause for 10 to 15 seconds to allow these symptoms to subside before proceeding with echocardiographic imaging. Our practice is to start with images acquired from the esophagus before advancing the probe into the stomach for the gastric views. The gastroesophageal sphincter is usually reached when the probe is advanced 40 cm from the teeth. Gentle pressure is all that is required to advance the probe through the gastroesophageal sphincter. The patient may again experience nausea and mild discomfort, and it may be advisable to pause momentarily for these symptoms to subside. Imaging of the proximal descending thoracic aorta and aortic arch is generally reserved for the end of the study, because the probe needs to be positioned in the upper esophagus and the patient is generally more aware of the probe at this position and tends to have more discomfort and gagging. Inadvertent passage of the probe into the trachea can occur, particularly in deeply sedated patients. The development of stridor and incessant cough should alert the operator of this possibility. Furthermore, it would be difficult to advance the probe beyond 30 cm from the teeth and the image quality is usually poor.[5] In patients on mechanical ventilation, esophageal intubation is more difficult. We usually introduce the probe with the patient lying supine, because the airway is protected and aspiration is unlikely. The probe is positioned behind the endotracheal tube and gently advanced. It is helpful to have the patient's mandible pulled forward when the probe is being advanced. If there is undue resistance at about 25 to 30 cm from the teeth, slight deflation of the cuff of the endotracheal tube can be considered to ease the passage of the probe. We do not usually remove the gastric tube, which can be used as a guide to help in the proper positioning and passage of the TEE probe. In a minority of intubated patients, successful esophageal intubation may be achieved only with direct laryngoscopy. Image Format There is no general agreement on how the imaging planes should be

displayed. Our preference is to orient the images such that the right-sided structures are on the left side of the screen and the left-sided on the right. The apex of the imaging plane with the electronic artifact is at the top of the screen. Thus, in the longitudinal views, superior structures are to the right of the screen and the inferior to the left.[12]

TABLE 1-2 -- Standard Imaging Planes with Multiplane Transesophageal Echocardiography (TEE) at the University of Ottawa Heart Institute

Imaging View Basal

Fourchamber

Standard Imaging Plane Aortic valve

Angle of Imaging Array (degrees) 0–60

Atrial septum

90–120

Pulmonary bifurcation

0–30

Left ventricle

0–180

Mitral valve

0–180

Left ventricular outflow tract

120–160

Transgastric Left ventricle Mitral valve

0–150 0–150

Main Cardiac Structures Aortic valve, coronary arteries, left atrial appendage, pulmonary veins Fossa ovalis, superior vena cava, inferior vena cava Pulmonic valve, main and right pulmonary arteries, proximal left pulmonary artery Left ventricle (regional and global function), right ventricle, tricuspid valve Anterior and posterior mitral leaflets, papillary muscles, chords Aortic valve, ascending aorta, left and right ventricular outflow tracts, pulmonic valve, main pulmonary artery Left ventricle, right ventricle, tricuspid valve Anterior and posterior mitral leaflets, papillary muscles,

Aortic

Coronary sinus Descending thoracic aorta Aortic arch

chords Coronary sinus, tricuspid valve

Entire descending thoracic aorta

Aortic arch, arch vessels, left pulmonary artery

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Standard Imaging Planes Advances in TEE transducer technology have culminated in the development of the multiplane probe capable of two-dimensional and color flow imaging in multiple planes. The imaging plane can be steered electronically from 0 to 180 degrees by means of a pressure-sensitive switch, providing views unattainable by monoplane and biplane probes. The following discussion focuses only on standard imaging views routinely performed at the University of Ottawa Heart Institute using multiplane TEE (Table 1-2) . These views are considered "standard" because they have important clinical relevance and can be obtained in most patients with specific imaging planes. Four basic maneuvers are used to obtain specific tomographic views with TEE.[13] The first relates to the positioning of the probe by advancement or withdrawal of the probe. Although this is a simple maneuver, it is the most crucial, and the imaging views can be conveniently categorized according to the location of the TEE probe within the esophagus or stomach (Fig. 11) . The second maneuver involves rotation of the probe from side to side. This is particularly useful when using longitudinal imaging planes, which provide a better demonstration of the continuity between vertically aligned structures such as the superior vena cava and the arch vessels.[12] [13] Steering the imaging plane using the pressure-sensitive switch is the third maneuver to obtain different tomographic views. The ability to image cardiac structures from 0 to 180 degrees not only enhances understanding of cardiac anatomy but also provides a ready means for three-dimensional reconstruction. [14] [15] The fourth maneuver involves manipulation of the anterior-posterior and right-left flexion control knobs. The availability of a steerable imaging plane has drastically reduced the need to use the flexion knobs, but there are situations in which these knobs play a crucial role in obtaining proper tomographic views.[10] [13] The versatility of multiplane TEE provides an almost infinite number of

imaging planes. In our experience, it is useful to categorize them into four groups: basal, four-chamber, transgastric, and aortic views (see Fig. 1-1) . Table 1-2 summarizes the standard imaging planes and the cardiac structures evaluated in these four groups of views. Basal Views The basal group of views is obtained with the TEE probe located in the midesophagus. The base of the heart, Figure 1-1 Diagram showing the transesophageal echocardiography transducer locations for the four standard imaging views: basal (A), fourchamber (B), transgastric (C), and aortic (D).

particularly the aortic valve, is well seen. The relationship of the two great arteries can be very well defined and followed cephalad to at least the level of the pulmonary bifurcation. Beyond this level, the interposing trachea make imaging impossible. Three tomographic planes are found to be particularly useful and are routinely performed at our laboratory. Aortic Valve

A short-axis view of the aortic valve can be obtained with the probe at about 30 to 35 cm from the teeth. The left coronary cusp often appears to have nodular thickening if the aortic valve is cut obliquely, which is often the case at 0 degrees.[12] Steering the imaging plane to 30 to 60 degrees should eliminate this artifact by providing an optimal short-axis view of the aortic valve (Fig. 1-2) . [13] A slight pull-back of the transducer should allow visualization of both the left and right coronary arteries. The left coronary artery can be followed to its bifurcation into the left anterior descending and circumflex arteries (Fig. 1-3) . The right coronary artery is more difficult to display, and usually only the proximal 2 to 3 cm is seen (Fig. 14) . Other structures well seen in this view are the left atrial appendage and the left pulmonary veins. The partition between these structures can be quite bulbous and should not be confused with an abnormal intracardiac mass (see Fig. 1-4) .[16] Rotating the probe to the right should reveal the right pulmonary veins.

We like the horizontal plane in imaging the four pulmonary veins. The left and right pulmonary veins are imaged separately. It is difficult to image the upper and lower pulmonary veins, left or right, in the same view because the veins are not located in the same plane with the lower pulmonary veins posterior and inferior to the upper pulmonary veins.[17] When one pulmonary vein is identified, a slight translational movement of the probe should bring out the other, because the orifices of the upper and Figure 1-2 The aortic valve was imaged with the imaging plane at about 60 degrees, showing the three cusps in systole. LA, left atrium; RA, right atrium; RV, right ventricle.

Figure 1-3 The left coronary artery (arrows) was imaged at 0 degrees. Ao, aorta; LA, left atrium.

lower pulmonary veins are in close proximity. The lower pulmonary veins run horizontal to the imaging plane, whereas the upper veins are more anterior and at an obtuse angle, making them more suitable for Doppler assessment. The right and left atrial appendages wrap around the great arteries anteriorly. The left atrial appendage is more prominent and can consist of multiple lobes.[18] A comprehensive interrogation using multiple imaging planes should be performed to exclude left atrial appendage thrombus in the appropriate clinical setting. The right atrial appendage is smaller and triangular in shape (Fig. 1-5) . The endocardial surfaces of both appendages are corrugated and should not be confused with small thrombi.[16] A long-axis view of the aorta can be achieved with the imaging plane at about 120 degrees. A more rightward imaging plane, such as 150 degrees, may be Figure 1-4 The proximal right coronary artery (small arrows) and the bulbous partition between the left atrial appendage and the left upper pulmonary vein (large arrow) are demonstrated. Ao, aorta; LA, left atrium.

Figure 1-5 The atrial septum was preferentially imaged using the longitudinal plane to demonstrate its relation with the superior vena cava (SVC). LA, left atrium; RA, right atrium; RAA, right atrial appendage.

needed if the ascending aorta is dilated and tortuous. This view allows the visualization of a longer length of the ascending aorta and thus significantly reduces the blind spot caused by the interposing trachea. Atrial Septum

We prefer to image the atrial septum using the longitudinal plane at 90 to 120 degrees. The fossa ovalis, which is the thinnest part of the atrial septum, and the continuity of the superior vena cava with the right atrium are very well demonstrated in this view (see Fig. 1-5) . This view is particularly valuable in demonstrating the sinus venosus atrial septal defect, which is usually located just inferior to the entrance of the superior vena cava.[19] [20] The foramen ovale, if present, is located at the superior aspect of the fossa ovalis and is readily seen in this view. It is important to advance the probe to the level of the inferior vena cava so as not to neglect the inferior aspect of the atrial septum.[21] Careful sweep of the atrial septum with left-right rotation is needed to visualize the entire atrial septum. Continuous rotation from right to left will sequentially demonstrate the left ventricular outflow tract and the right ventricular outflow tract. Rotating the probe to the right shows the right upper pulmonary vein and provides parallel alignment for Doppler assessment. Pulmonary Bifurcation

The pulmonary bifurcation view is achieved by withdrawal of the probe with the imaging plane at 0 degrees. The pulmonic valve and main pulmonary artery are best seen slightly superior to the aortic valve (Fig. 16) . The pulmonic valve is thinner than the aortic valve and is usually difficult to image in a true cross section. Further slight withdrawal allows imaging the pulmonary bifurcation. The entire length of the right pulmonary artery but only the very proximal portion of the left pulmonary artery can be seen. The right pulmonary artery can usually be followed to its first bifurcation by rotation of the probe rightward, but this maneuver is better performed with the longitudinal plane at 90 degrees. Gradual rotation from left to right provides good visualization in cross section of the entire right pulmonary artery and its first bifurcation. This is an important view in

the detection of proximal pulmonary emboli.[22] [23] Four-Chamber Views Four-chamber views are obtained with the transducer within the middle to lower esophagus. It is difficult to image the left ventricle in its true long axis. Excessive anterior flexion should be avoided to prevent foreshortening of the ventricles. Indeed, to optimize visualization of the left ventricle, it is advisable to withdraw the probe slightly and at the same time attempt gentle retroflexion while maintaining adequate contact between the imaging surface and the esophagus. In the setting of a dilated and unfolded aorta, rotating the imaging plane to about 20 to 30 degrees may be necessary to obtain the four-chamber view without the aorta obscuring the tricuspid valve and part of the right ventricle. Left Ventricle

The inferior septum and anterolateral wall are usually seen in the fourchamber view (Fig. 1-7) . The left ventricular apex is difficult to visualize, particularly in patients with a dilated left ventricle. In addition to retroflexion, rightward flexion can often be helpful to minimize foreshortening of the left ventricle. Far-field imaging can be improved by decreasing the transmission frequency. A continuous sweep from 0 to 180 degrees should be performed to examine the different left ventricular segments Figure 1-6 The bifurcation of the main pulmonary artery (MPA) into the right (RPA) and left (LPA) pulmonary arteries was imaged using the transverse plane. Ao, aorta.

Figure 1-7 The four-chamber view showing the left ventricle (LV) and mitral valve. LA, left atrium; RA, right atrium; RV, right ventricle.

so as to have a comprehensive assessment of left ventricular global and regional function (Fig. 1-8) .

Mitral Valve

The mitral valve is well seen using the four-chamber view, but the depth of the imaging plane should be reduced to enhance the resolution of the image ( see Fig. 1-7 and Fig. 1-8 ). To identify the individual scallops of the anterior and posterior mitral leaflets, a careful sweep from 0 to 180 degrees should be made. The technique of visualizing specific scallops of the mitral leaflets have been published,[24] but patient-to-patient variation should be kept in mind. The presence of a good long-axis view of the aortic valve and proximal ascending aorta, usually at Figure 1-8 The left ventricle and mitral valve can be comprehensively assessed by a continuous sweep of the imaging plane, which was about 100 degrees in this example. LA, left atrium; LV, left ventricle.

120 degrees, is a good indication that the middle scallops of both the anterior and the posterior mitral leaflets are imaged and provides the internal reference for the analysis of the other imaging planes. Both papillary muscles can be imaged but usually not in the same plane. The subvalvular chords are seldom completely imaged because they are frequently obscured by the mitral leaflets. The morphologic information obtained from this view should be corroborated by the short-axis view of the mitral valve obtained from the transgastric view, which also allows a better assessment of the subvalvular structures, including the papillary muscles and chords. Four-chamber views are ideal for the assessment of mitral regurgitation in relation to the number of regurgitant jets, the direction of the regurgitant jets, and the severity of regurgitation. [25] [26] Left Ventricular Outflow Tract

We like to image the left ventricular outflow tract at 120 to 160 degrees, because the outflow tract has a horizontal alignment in this plane that may allow optimal imaging even in the setting of a prosthetic aortic valve (Fig. 1-9) . The opening and closing of the aortic valve as well as the presence or absence of aortic regurgitation can be well visualized. The proximal ascending aorta is present in this view. A slight withdrawal of the probe will allow more of the ascending aorta to be visualized (Fig. 1-10) . A slight rotation to the left will show the right ventricular outflow tract with the thin pulmonic valve. Both the motion of the pulmonic valve and the presence or absence of pulmonic regurgitation can be adequately assessed

using this view. Transgastric Views There is slight resistance during the passage of the TEE probe through the gastroesophageal junction, and the Figure 1-9 The left ventricular outflow tract was well seen with the imaging plane at about 120 degrees. Ao, aorta; LA, left atrium; LV, left ventricle; RVOT, right ventricular outflow tract.

Figure 1-10 Slight withdrawal of the probe relative to the probe position used to acquire the image shown in Figure 1-9 showed the right pulmonary artery (RPA) in short axis and more of the ascending aorta (Ao). LA, left atrium.

appearance of the liver is a clear indication that the probe is in the stomach. Anterior flexion, often with leftward rotation and flexion, is required to achieve good contact between the imaging surface and the gastric wall. Extreme anterior flexion with further advancement of the probe can sometimes produce images similar to the five-chamber views obtained from the subxiphoid surface approach. Left Ventricle

Multiple cross sections of the left ventricle can usually be obtained using the transgastric approach ( Fig. 1-11 and Fig. 1-12 ). These are the views commonly used in the intraoperative assessment of left ventricular function.[24] Optimization of the short-axis views of the left ventricle Figure 1-11 Transgastric short-axis view of the left ventricle (LV) at the papillary muscle level.

Figure 1-12 Transgastric long-axis view of the left ventricle (LV) with

visualization of the apex.

can be achieved with leftward rotation accompanied by leftward flexion. To visualize the left ventricular apex, gentle advancement of the probe is required together with slight retroflexion. In our experience, the short-axis view of the left ventricular apex can be obtained in about 60% of cases. Another way to visualize the left ventricular apex is to use the longitudinal plane at about 90 degrees (see Fig. 1-12) . Careful lateral rotation can be used to obtain comprehensive regional assessment of the left ventricle. Leftward rotation of this imaging plane can yield a good alignment with the left ventricular outflow tract and aortic valve to allow accurate measurement of the transaortic pressure gradients in the setting of aortic stenosis (Fig. 1-13) . [27] The right ventricle can be seen with rightward rotation of the probe. Both short- and long-axis views of the tricuspid valve are achievable, although Figure 1-13 Transgastric transesophageal echocardiography approach to assess the severity of aortic stenosis using continuous wave Doppler echocardiography.

the tricuspid valve and its papillary muscles are better assessed with the long-axis plane. Mitral Valve

The mitral valve can be best assessed using the horizontal imaging plane with the transducer brought up to near the gastroesophageal junction (Fig. 1-14) . Anterior flexion and leftward flexion are usually required to optimize this view. Adjusting the imaging plane to about 20 degrees will help to bring out the lateral commissure. This view provides unambiguous assessment of the individual scallops of both the anterior and posterior mitral leaflets and thus should be attempted in all patients with myxomatous mitral valve degeneration. In our experience, this view is achievable in about 70% of patients. Both the papillary muscle and chords can be demonstrated, and the continuity between these structures and the mitral leaflets is best seen in the long-axis plane. Coronary Sinus

The coronary sinus comes into view when the probe is withdrawn to be near the gastroesophageal junction and the flexion knobs are in relatively neutral positions (Fig. 1-15) . This view can also be achieved by retroflexion with the probe in the lower esophagus. The coronary sinus is seen as a vascular structure located posterior to the left ventricle at the atrioventricular groove draining into the right atrium. The tricuspid valve can be visualized to the right and anterior. A dilated coronary sinus should raise the possibility of the presence of a persistent left superior vena cava, which is the most common cause. Leftward rotation while following the coronary sinus may sometimes demonstrate this anomalous vein. In the esophageal views, the left superior vena cava is usually sandwiched between the left atrial appendage and the left upper pulmonary vein.[28] Figure 1-14 The mitral valve was demonstrated in the short axis showing the anterior (arrows) and posterior (arrowheads) mitral leaflets.

Figure 1-15 The coronary sinus (CS) was demonstrated with the probe at the gastroesophageal junction. LV, left ventricle; RV, right ventricle.

Aortic Views The thoracic aorta is well assessed by TEE because of its close proximity to the esophagus. Descending Thoracic Aorta

The best way to assess the descending thoracic aorta is to use the horizontal imaging plane with the transducer rotated leftward and posterior, followed by slow withdrawal from the level of the diaphragm to the aortic arch (Fig. 1-16) .[16] Because of the relationship between the Figure 1-16 The descending aorta was imaged in the short axis to allow good visualization of entire circumference.

Figure 1-17 The aortic arch (AA) was imaged using the longitudinal plane, showing the origin of the left subclavian artery (LSA).

esophagus and the aorta, slight rotational adjustment is required to visualize the entire circumference of the aortic wall as the probe is slowly withdrawn.[29] If the aorta is dilated or tortuous, proper short-axis views of the descending aorta will require adjustment of the imaging plane by 0 to 90 degrees. Aortic Arch

The longitudinal imaging plane at 90 degrees is preferred in imaging the aortic arch because it allows visualization of the entire circumference of the aorta (Fig. 1-17) .[29] Anterior rotation of the longitudinal plane should visualize the entire aortic arch, but the proximal aortic arch may not be visualized when the aortic arch is unfolded. The transducer will need to be withdrawn slightly to image the arch vessels, which course superiorly. In one third of patients, all three arch vessels can be imaged, but in the other two thirds of patients, only the two distal arch vessels can be imaged. It is rare not to be able to image at least one arch vessel. As a rule, the brachiocephalic artery, which is anterior and more rightward, is the most difficult to image because of the interposing trachea. The transverse plane in a more superior location may sometimes show the three arch vessels in their short axis. Advancing the probe by 1 to 2 cm so that the imaging plane is just inferior to the aortic arch can frequently image the proximal left pulmonary artery. It is sometimes possible to follow it to the first bifurcation. This view should be sought in the assessment of patients suspected of having pulmonary embolism.

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Doppler Examination Transesophageal echocardiography can be used to assess the flow patterns across the four cardiac valves, but it does not provide additional information to TTE. Furthermore, good alignment with the transvalvular flows may not be feasible because of the anatomic confines of the esophagus. On the other hand, intracardiac flows such as pulmonary vein flow and left atrial appendage flow are best evaluated by TEE and provide important insight into intracardiac hemodynamics. Pulmonary Vein Flow The pulmonary veins are imaged from the midesophagus level. Pulmonary vein flow can be assessed by placing the pulsed Doppler = sample=20 volume 0.5 to 1.0 cm into the pulmonary veins. The anterior to posterior = direction of the left and right upper pulmonary veins allows the Doppler = ultrasound beam to be aligned parallel to blood flow. This often cannot = be=20 achieved when interrogating the left and right lower pulmonary = veins. The normal pulmonary venous flow pattern can be = divided=20 into three phases: (1) antegrade systolic flow, (2) antegrade diastolic = flow,=20 and (3) retrograde atrial contraction flow reversal (F= ig.=20 1-18) . Two phases of antegrade systolic flow can usually be = appreciated on=20 transesophageal study. Systolic flow is dependent on apical displacement = of the=20 annulus, which is predominantly determined by left ventricular function, = atrial=20 relaxation, and atrial compliance.[3= 0]=20 [3= 1]=20 Left atrial pressure also affects antegrade systolic flow, with = increases in=20 left atrial pressure reducing systolic flow.[3= 0]=20 [3= 1]=20 Mitral regurgitation increases left atrial pressure during systole and = may=20 result in systolic flow reversal in one or all pulmonary=20 veins.[3= 0]=20 [3= 1] =20 Diastolic antegrade flow occurs as the mitral valve opens and left = atrial=20 pressure falls. The diastolic flow profile is dependent on left atrial = pressure,=20 left ventricular relaxation, and ventricular compliance. = [3= 0] =20 [3= 1]=20 Atrial contraction flow reversal is dependent on atrial contractility, = atrial=20 systolic pressure, and left ventricular compliance. The normal pulmonary = venous=20 flow pattern is dependent on heart rate and age.[3= 1]=20 [3= 2]=20 Higher systolic pulmonary venous flow velocities, higher atrial reversal = velocities, and smaller diastolic flow velocities=20

Figure = 1-18 Normal pulmonary venous flow showing two antegrade = flows in=20 ventricular systole and diastole, with a diminutive retrograde flow = caused by=20 atrial contraction. .

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patients younger than 50 years of=20 age.[3= 1]=20 [3= 2]=20 Left Atrial Appendage Flow The left atrial appendage can be imaged from = the=20 midesophagus

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aortic valve short-axis view (30 to 60 degrees) or the = midesophagus=20 two-chamber view (80 to 100 degrees). Left atrial appendage flow should = be=20 recorded by positioning the color flow sector over the left atrial = appendage and=20 placing the pulsed-Doppler sample volume at the site of maximal flow = velocity.=20 This usually occurs in the proximal or middle third of the left atrial=20 appendage. Velocity recordings from the distal third of the left atrial=20 appendage frequently incorporate wall motion artefacts and are usually=20 unsatisfactory. Low-velocity flow may be present, and wall filters = should be set=20 low. The pattern of left atrial appendage flow is = dependent on=20 cardiac rhythm.[3= 3]=20 In patients with sinus rhythm, four left atrial appendage flow waves = have been=20 described (F= ig.=20 1-19) : (1) a large positive wave after the electrocardiographic = P-wave,=20 which represents left atrial appendage contraction and emptying; (2) a = large=20 negative early systolic wave immediately following the QRS complex = representing=20 left atrial appendage filling; (3) alternating positive and negative = waves of=20 decreasing velocity throughout the remainder of systole representing = passive=20 flow in and out of the appendage; and (4) a low-velocity positive = emptying wave=20 in early diastole coinciding with rapid left ventricular filling. In = addition, a=20 low-velocity middiastolic negative filling wave representing appendage = filling=20 from the pulmonary veins may follow the early diastolic atrial appendage = emptying wave. The normal velocities are as follows: left atrial = appendage=20 contraction, 60 =B1 14; left atrial appendage filling, 52 =B1 13; and = early=20 diastolic filling, 20 =B1 11 cm per second.[3= 3]=20 [3= 4] =20 In patients with atrial fibrillation, a regular = atrial=20 contraction wave is absent. However, the left atrial appendage continues = to=20 contract, resulting in irregular oscillating positive and negative = emptying and=20 filling waves with variable velocities. The velocities are usually = larger during=20 ventricular diastole when the mitral valve is open, and=20

Figure = 1-19 Normal left atrial appendage flow pattern in sinus = rhythm,=20 showing prominent atrial emptying and filling = velocities.

smaller during systole when the mitral valve is closed. = Of note,=20 mean left atrial appendage velocities tend to be lower with higher heart = rates=20 because of the smaller proportion of time spent during diastole.

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The = early=20 diastolic appendage emptying wave, which coincides with early rapid left = ventricular filling, may still be visualized in atrial fibrillation. In = patients=20 with atrial flutter, the velocity waves are more regular and tend to be = of=20 greater velocity because of the slower atrial contraction rate.=20 Factors other than cardiac rhythm that may = affect left=20 atrial appendage velocities have recently been reviewed and include age, = heart=20 rate, left atrial contractility, left atrial pressure, left ventricular = systolic=20 and diastolic function, mitral stenosis, and mitral=20 regurgitation.[3= 3]=20 The potential clinical utility of assessing = left atrial=20 appendage velocities relates to the association of left atrial appendage = velocities with left atrial spontaneous echo contrast and left atrial = appendage=20 thrombus.[3= 3]=20 [3= 5]=20 [3= 6]=20 Atrial fibrillation patients with a left atrial appendage contraction = velocity=20 of less than 20 cm per second are more likely to have left atrial = appendage=20 thrombus and have a greater risk of ischemic stroke compared with = patients with=20 left atrial appendage velocities of 20 cm per second or=20 greater.[3= 5]=20 [3= 6]=20 Lower left atrial appendage velocity has also been observed in stroke = patients=20 with normal sinus rhythm.[3= 7]=20 Other potential utilities may relate to an ability of left atrial = appendage=20 velocities to predict the success of maintaining sinus rhythm following=20 cardioversion of atrial fibrillation.[3= 3]=20 [3= 8]=20 Coronary Artery Flow The assessment of coronary artery flow may be = limited by=20 motion of the heart during the cardiac cycle and difficulties aligning = the=20 Doppler ultrasound beam parallel to coronary blood flow. Coronary artery = blood=20 flow and coronary artery blood flow reserve are best measured in the = distal left=20 main coronary artery or proximal left anterior descending artery using = the=20 midesophagus aortic valve short-axis view, in which the pulsed-Doppler=20 ultrasound beam can be aligned parallel to coronary blood flow. The = ultrasound=20 beam can only rarely be aligned parallel to flow in the left circumflex = artery,=20 and the right coronary artery cannot be imaged in up to half of all = patients.=20 The normal Doppler flow signal is characterized by a large diastolic = component=20 and small systolic component moving away from the transducer. In = general, normal=20 diastolic velocities are 60 cm per second or less, and diastolic = velocities=20 greater 100 cm per second

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suggest significant obstruction in the=20 artery.[3= 9]=20 [4= 0]=20 [4= 1]=20 Additionally, coronary artery flow reserve can be assessed by measuring = peak or=20 mean diastolic coronary flow velocities at rest and then following = dipyridamole=20 or adenosine infusion. [4= 0]=20 [4= 2]=20 Transaortic and Transpulmonary Flow Transaortic flow can be assessed by imaging the = left=20 ventricular outflow tract and aortic valve in the transgastric long-axis = view=20 (100 to 135 degrees) or deep transgastric long-axis view (0 degrees), in = which=20 the probe is=20 12

advanced deep into the stomach = adjacent=20 to the left ventricular apex and anteflexed until the imaging plane is = directed=20 superiorly to the base of the heart. In these views, the pulsed-Doppler = or=20 continuous wave Doppler beam can be aligned parallel to blood flow to = measure=20 transaortic velocity. Stroke volume can be derived with the additional=20 measurement of either the midesophagus left ventricular outflow tract = diameter=20 or the short-axis aortic valve orifice area at valve leaflet=20 level.[4= 3]=20 [4= 4]=20 In patients with aortic stenosis or other forms of left ventricular = outflow=20 tract obstruction, the transvalvular pressure gradients can be derived = using the=20 simplified Bernoulli equation and continuous wave Doppler signals = obtained from=20 the transgastric longaxis or deep transgastric long-axis view.=20 [2= 7]=20 Transpulmonary flow has been measured by = combining either=20 pulsed Doppler or continuous wave Doppler velocity measurements of = pulmonary=20 artery flow obtained from mid-esophagus short- axis images of the main = pulmonary=20 artery and measurements of the main pulmonary artery=20 diameter.[4= 5]=20 [4= 6]=20 Transmitral and Transtricuspid Flow In the midesophageal four-chamber view or = long-axis view,=20 the pulsed Doppler ultrasound beam can be aligned parallel to = transmitral flow=20 to accurately measure transmitral filling velocities. The pulsed Doppler = sample=20 volume should be kept small (3 to 5 mm) and positioned at the mitral = valve=20 leaflet tips for the evaluation of diastolic function and filling=20 pressures.[3= 0]=20 In contrast, transmitral stroke volume is measured by placing the sample = volume=20 at the mitral

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valve annulus, so that velocity and annular dimensions are = measured at the same location.[4= 7]=20 [4= 8]=20 Transtricuspid filling can be assessed by = pulsed Doppler=20 measurements obtained in the midesophageal four-chamber view. However, = it is=20 frequently not possible to align the Doppler ultrasound beam parallel to = blood=20 flow. The transtricuspid filling pattern is similar to the transmitral = filling=20 pattern, although lower velocities are present.

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Indications for Transesophageal Echocardiography The potential utility of TEE in the assessment and management of patients with suspected and overt cardiac disease is wide-ranging and encompasses the spectrum of cardiac problems encountered in clinical cardiology. TEE can be performed on patients in the ambulatory setting, intensive care unit, coronary care unit, or operating room. In general, TTE should be employed as the initial diagnostic investigation, as this technique is noninvasive and will entail no risk to the patient. Patient factors such as obesity, emphysema, or chest deformities frequently limit ultrasound penetration, resulting in nondiagnostic TTE studies. Surgical bandages may limit the number of available acoustic windows, and mechanical ventilation and surgical devices, such as traction and intra-aortic balloon pumps, may limit the ability to properly position the patient. Subcutaneous emphysema may result in the complete TABLE 1-3 -- Common Indications for Transesophageal Echocardiography Nondiagnostic transthoracic echocardiogram Assessment of native valve disease Assessment of prosthetic valves Assessment of infective endocarditis Assessment of a suspected cardioembolic event Assessment of cardiac tumors Assessment of atrial septal abnormalities Assessment of aortic dissection, intramural hematomas, and aortic rupture Evaluation of congenital heart disease Detection of anatomic coronary artery disease Stress echocardiography

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Evaluation of pericardial disease Evaluation of critically ill patients Intraoperative monitoring Monitoring during interventional procedures inability of TTE to visualize cardiac structures. TEE should be considered in these patients to obtain the necessary diagnostic information. Despite an adequate TTE study, TEE may be indicated to assess cardiac structures not usually seen by TTE, such as the superior vena cava, pulmonary veins, and the descending thoracic aorta, or to provide improved anatomic details such as the detection of flail mitral valve leaflet scallops and valvular vegetations, which are not consistently detected by TTE. Finally, TEE has important applications in the operating room, which are discussed in Chapter 2 and Chapter 19 . The common clinical indications for TEE are given in Table 1-3 . Native Valve Disease The presence, etiology, and severity of native valve disease can usually be determined by TTE. TEE should be reserved for the clinical situation in which TTE findings are inconclusive or a more precise characterization of the valve lesion will alter the patient management plan. Excellent visualization of the mitral valve anatomy is possible by TEE because of the close proximity of the mitral valve to the TEE transducer and the ability to image with high-frequency transducers. The mitral annulus, leaflets, chordal structures, and papillary muscles can all be visualized and evaluated. The use of a multiplane transducer allows a comprehensive, detailed examination of the valve to determine the location and mechanism of mitral regurgitation (see Chapter 19) . Ruptured chordae tendineae can be visualized, and precise anatomic localization of prolapsing or flail leaflet scallops is possible to predict the potential for successful mitral valve repair.[25] [49] [50] Abnormalities of the papillary muscles, such as a partial or complete rupture, are better visualized by TEE than TTE.[51] The severity of mitral valve regurgitation can be quantified using the methods employed for TTE,[52] but color Doppler velocity regurgitant jet areas tend to be larger in size on TEE than TTE because higher transducer frequencies are used and because of the close proximity of the transducer to

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the regurgitant jet.[53] Pulmonary vein flow can be assessed in nearly all patients and provides 13

a valuable measure of mitral regurgitation severity.[54] [55] Regurgitant vena contracta width, regurgitant volumes, and regurgitant orifice areas using the proximal flow convergence zone can be obtained by TEE.[56] [57] In mitral stenosis, TTE is usually satisfactory in assessing the valve morphology and severity of stenosis (see Chapter 20) . TEE appears equivalent to TTE in assessing valve mobility and leaflet thickening, but subvalvular disease and calcification may be underestimated owing to the shadowing effect of thickening and calcification of the mitral leaflets and annulus in the esophageal views.[58] Transvalvular pressure gradients can be measured by aligning the continuous wave Doppler beam parallel to left ventricular inflow through the mitral valve in the midesophageal views.[59] Effective orifice areas can be derived by the pressure half-time method,[59] the proximal flow convergence method, or orifice planimetry.[60] Orifice planimetry requires a tomographic cut of the distal or most narrow mitral orifice, however, which is technically more difficult to obtain by TEE and frequently not possible. The potential suitability of a patient for percutaneous balloon mitral valvuloplasty usually incorporates a detailed TEE assessment of the left atrial chamber and appendage to identify thrombus, in addition to an evaluation of the mitral valve morphology score and mitral regurgitation severity.[61] Transthoracic echocardiography can adequately visualize most aortic valve abnormalities, and only rarely is TEE required for assessment. However, subvalvular abnormalities such as subaortic membranes frequently require TEE for definitive diagnosis. [62] The assessment of aortic regurgitation severity only rarely necessitates a TEE evaluation (see Chapter 17) . Standard Doppler methods used for TTE may be employed using TEE.[63] One of the best measures, the ratio of color jet area to left ventricular outflow tract area, can be obtained from esophageal short-axis images of the outflow tract immediately inferior to the aortic valve. Jet height to outflow tract height can be obtained from esophageal long-axis images. Holodiastolic flow reversal in the descending aorta is always present with severe aortic regurgitation and can be detected by biplane or multiplane TEE using pulsed Doppler.[64] Aortic regurgitation severity may also be quantified by TEE using proximal flow convergence methods and vena

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contracta width.[65] [66] The severity of aortic stenosis is best quantified using transvalvular pressure gradients or valve areas derived by TTE (see Chapter 22) . Continuous wave Doppler interrogation of the aortic valve is possible by TEE using the transgastric long-axis view (100 to 135 degrees) or deep transgastric long-axis view (0 degrees) in which the probe is advanced deep into the stomach adjacent to the left ventricular apex and anteflexed until the imaging plane is directed superiorly to the base of the heart (see Fig. 113) . Good correlations between TTE and TEE gradients have been reported, despite the limited TEE windows.[27] Anatomic orifice area can be derived by planimetry of the maximum systolic aortic valve orifice visualized from esophageal short-axis images. Proper transducer position should be confirmed by rotating to the longitudinal plane and verifying that the leaflet tips are being imaged. Aortic valve areas derived by orifice planimetry correlate well with valve areas derived by TTE using the continuity equation and Gorlin equation valve areas.[27] , [67] [68] Valve calcification may affect the accuracy of TEEmeasured orifice areas.[69] Importantly, orifice planimetry is often more feasible and accurate using multiplane than biplane TEE.[68] Prosthetic Valves Transesophageal echocardiography is an extremely valuable technique in the assessment of prosthetic valve function, because TTE visualization of the prosthetic valve components and function is often limited by the echogenicity of the prosthetic components (see Chapter 24 and Chapter 25) . Reverberation artifacts, attenuation artifact, and acoustic shadowing obscure visualization of the prosthetic components and limit the visualization of structures beyond the prosthesis. Thickening and calcification of the leaflets, or the presence of a torn or flail bioprosthetic leaflet, are better appreciated on TEE. The structure and motion of the occluding device of a mechanical prosthesis may also be better evaluated. TEE provides increased sensitivity for detecting abnormalities of bioprosthetic and mechanical prostheses when compared to TTE.[70] [71] Small abnormalities of prosthetic valves such as leaflet thickening, flail leaflets, vegetations, thrombi, and filamentous strands can be missed on TTE but appreciated on TEE.[70] [71] [72] [73] [74] [75] [76] [77] TEE can be used to distinguish pannus from thrombus formation[78] and to guide thrombolytic therapy use in patients with the latter condition.[79] TEE is especially valuable in assessing mitral prostheses, as the transducer's posterior

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position provides excellent visualization of vegetations and thrombi, which usually locate on the left atrial aspect of the prosthesis.[70] [73] However, the ventricular aspect of a mitral prosthesis may not be adequately seen, and so TTE should complement the TEE assessment. [80] Transesophageal echocardiography can differentiate between normal variant and pathologic prosthetic valve regurgitation.[71] [72] [73] [74] [75] [81] Prosthetic mitral regurgitation is frequently better evaluated by TEE than TTE,[71] [72] [74] because TEE provides excellent visualization of the left atrial cavity without any intervening prosthetic material. TEE should be performed in patients in whom significant mitral regurgitation is not seen on TTE but is a clinical concern. Importantly, TEE allows characterization of mitral regurgitation jets as paravalvular or transvalvular in origin, which may modify the surgical procedure.[72] [74] [82] Multiplane TEE appears to better delineate paraprosthetic mitral regurgitation as compared with biplane TEE.[82] The incremental benefit of TEE in the assessment of regurgitation severity is less clear for aortic prostheses because the aortic regurgitation jet is usually well seen on TTE, and TEE visualization of prosthetic aortic regurgitation may be compromised by partial obstruction of the aortic regurgitation jet by either a mitral or aortic prosthesis in the esophageal views.[75] All bioprostheses and mechanical prostheses are inherently stenotic. The degree of stenosis is dependent on the prosthesis type and size and the presence of an associated pathologic condition such as leaflet calcification, pannus formation, or valve thrombosis.[83] In general, TTE is sufficient to assess the severity of prosthetic aortic or mitral 14

stenosis, but only TEE has sufficient resolution to distinguish these pathologic conditions.[78] In patients with inadequate TTE findings, TEE can quantify prosthetic mitral stenosis by measuring diastolic pressure gradients, pressure half-time, and effective orifice area using the proximal flow convergence method, as described for native mitral stenosis.[60] [84] Prosthetic aortic stenosis can be assessed by measuring transvalvular pressure gradients, as described for native aortic stenosis. [27] Importantly, flow through certain mechanical aortic prostheses results in localized pressure gradients and significant pressure recovery, which may lead to a discrepancy between Doppler and catheterization pressure gradients and an apparent "overestimation" of Doppler gradients.[85]

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Infective Endocarditis The presence of a vegetation is a hallmark finding of infective endocarditis, and its identification in the clinical setting of suspected endocarditis confirms the diagnosis[86] (see Chapter 21) In native valve endocarditis, the sensitivity of TTE for the detection of vegetations was 28% to 63%, and the sensitivity of TEE was 86% to 98%. [87] [88] [89] [90] [91] The specificity of the TTE and TEE findings for a vegetation appears similar and exceeds 90% when strict echocardiographic criteria are used for diagnosis.[87] [88] [90] Smaller vegetations are more likely to be detected by TEE than TTE.[88] Isolated case reports have suggested that pulmonic valve vegetations may also be better seen by TEE.[92] TEE does not appear to have an increased sensitivity compared with TTE, however, in the detection of tricuspid valve vegetations.[93] Prosthetic valve endocarditis is more difficult to diagnose using either TTE or TEE. The reported sensitivity of TTE for detecting vegetations was 0 to 43%, and the sensitivity of TEE was superior at 33% to 86%.[70] [89] [94] , [95] Thus, TEE should be performed in patients with suspected prosthetic valve endocarditis if the TTE procedure does not identify a vegetation. Although TEE has an improved sensitivity for detecting vegetations compared with TTE, the impact of TEE on diagnosis appears to be greatest in patients with suspected endocarditis with an intermediate clinical probability of endocarditis, especially patients with prosthetic valves.[96] Importantly, the absence of a vegetation on TEE makes the diagnosis of endocarditis unlikely (100 cm per second) with abrupt cessation of flow and, therefore, extremely short deceleration time (120 msec). The A wave component is nearly absent, with a peak velocity of less than 35 cm per second, and resultant peak E/A of 2.2. The Ei /Ai ratio is also increased at 2.4. The dramatic shift of flow to early diastole along with abrupt cessation of the E wave is compatible with the "dip and plateau" pattern seen in right and left ventricular pressure tracings in patients with constrictive pericarditis. The beat-to-beat variation in E wave size is noteworthy and corresponds to changes during respiration frequently seen with constrictive

Figure 6-19 Spectral Doppler transmitral flow in a patient with constrictive pericarditis. The tracing shows high peak E velocity greater than 100 cm/sec and small A component barely visualized because of high heart rate. The beat-to-beat variation in E wave size shows a greater than 50% change during inspiration (arrows). This finding may be helpful in distinguishing constrictive pericarditis from restrictive cardiomyopathy.

physiology, but less often with restrictive cardiomyopathy. Literature Review.

Appleton, Hatle, and Popp have published several studies describing the typical Doppler echocardiographic features of patients with restrictive cardiomyopathy. [20] [107] These series included patients with systemic infiltrative disorders (e.g., amyloidosis and Fabry's disease) and postcardiac transplant patients.[107] Comparison of these patients with normal subjects and with a group with coronary artery disease led to the initial description of the patterns of transmitral flow: impaired relaxation, "normalized," and restrictive.[35] Comparison of flow velocity patterns with invasive hemodynamic data showed correlations between transmitral E wave and left ventricular filling pressure (r = .59), and between IVRT and the rapid filling wave (r = -.72). Klein et al[36] demonstrated similar Doppler findings in a large group of 53 patients with biopsy-proven cardiac amyloidosis. This study found the restrictive pattern to be most associated with advanced stages of the disease. Pulmonary vein flows were also recorded by transthoracic echocardiography in 29 patients and showed that those with advanced disease had markedly decreased peak systolic (S) filling and increased diastolic (D) filling compared with normal subjects.

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Atrial systolic function was believed to remain intact (despite left atrial enlargement), since the Ar wave was prominent in 10 patients. A follow-up study of 63 consecutive patients with biopsy-proven cardiac amyloidosis from the same center has shown a high 1-year mortality rate in patients with the restrictive pattern (51%) compared with those who had a deceleration time greater than 150 msec (8%; P < .001). The combination of shortened deceleration time and increased peak E/peak A ratio greater than 2.1 was the most predictive of a high-risk group, whereas the E/A ratio alone exhibited the single best correlation with survival.[108] Fewer clinical data are available from patients with constrictive pericarditis. A study by Hatle et al[107] compared seven patients with constrictive pericarditis, 12 with restrictive cardiomyopathy, and 20 normal subjects. Both constrictive and restrictive groups demonstrated a shorter transmitral deceleration time during held breathing at end-expiration, compared with control subjects. However, during normal inspiration, the patients with constriction showed marked increases in IVRT (50%) and decreases in peak E wave velocity (mean, -33%; all patients, greater than 25%), and these changes were small in the restrictive and control groups (see Fig. 6-19) . Indeed, no patient in the restrictive group had a greater than 15% change in either variable. The transtricuspid flow velocity changes of an increased peak E wave and a peak A wave with shortened deceleration time were also much larger in the constrictive pericarditis patients. The respiratory variation was not seen in five patients who underwent repeat studies after pericardial stripping. The authors theorized that the dramatic changes in transmitral and transtricuspid flow seen during inspiration likely were due to displacement of the interventricular septum and ventricular interdependence in patients with constriction who have a fixed total cardiac volume. Conversely, patients 131

with restrictive cardiomyopathy have a marked reduction in left ventricular compliance that remains relatively constant regardless of the respiratory phase.[107] Thus, patients with abnormalities in ventricular filling due to restrictive muscle disease or pericardial constriction may be readily identified by the "restrictive" Doppler transmitral filling pattern. These data suggest that careful study of diastolic transmitral and transtricuspid velocity during the

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phases of respiration may also be used to separate these groups. Although these results are promising, larger series are needed to confirm these findings. Pericardial Effusion and Cardiac Tamponade

Abnormalities in left ventricular filling have been described in patients with cardiac tamponade. A preliminary report from Pandian et al[109] first described alterations in flow velocity across all four cardiac valves; these alterations coincided with the phases of respiration. The primary study was carried out in a canine model but also included three patients who had documented tamponade physiology and underwent pericardiocentesis. The authors noted an increase in transtricuspid flow velocities and concomitant decrease in transmitral peak E and A waves (-42%) during inspiration. Appleton et al[110] studied seven patients with tamponade compared with 14 patients who had effusion due to malignancy, cardiac surgery, myocardial infarction, chronic renal failure, or cardiac transplantation. The patients with tamponade and severe hemodynamic alterations had a significant change in transmitral filling indices when the first Doppler beat of expiration was compared with the first beat of inspiration: peak E (−43 ± 9%), peak A (−25 ± 12%), IVRT (85 ± 14 msec), Ei (−52 ± 10%), and Ai (−28 ± 22%). Similar decreases were noted in aortic velocities, whereas transtricuspid and transpulmonic flows increased during inspiration. The variation was eliminated after pericardial drainage. Half of the group of patients without tamponade also showed respiratory variations compared with control subjects, but not of the magnitude seen in patients with tamponade. The authors concluded that the Doppler flow abnormalities seen with effusion are extremely sensitive to changes in pericardial pressure and should be viewed as a continuum.

In an animal model described by Gonzales et al,[111] significant respiratory variation in Doppler parameters was noted to occur at low intrapericardial pressures and preceded the echographic findings traditionally associated with clinical tamponade (i.e., right atrial inversion[112] and right ventricular diastolic collapse[113] ). It was concluded that the Doppler findings are sensitive and persist throughout all stages of tamponade but are not predictive of pericardial pressures or the severity of hemodynamic compromise. Picard et al[114] demonstrated similar findings using aortic and pulmonic flow velocities in animals. Their report did not include mitral or tricuspid Doppler data but acknowledged that the E and A waves tended to

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merge in tamponade because of associated tachycardia, and that the transtricuspid Doppler interrogation was often difficult because of compression of the right heart chambers. These limitations may also prove substantial in patients with severe clinical cardiac tamponade. Myocardial Ischemia

Several studies have demonstrated that acute coronary occlusion results in diastolic dysfunction (see Chapter 12) . Most studies have used Doppler indices recorded before and during angioplasty in patients with angina[15] [115] [116] as the clinical model for evaluating the effects of ischemia on diastolic function. Wind et al[115] reported an increased proportion of left ventricular filling during late diastole and a decreased E/A ratio in 34 patients with normal global systolic function who underwent Doppler echocardiographic examination 1 day before and 1 day after coronary angioplasty for angina. These findings were thought to be consistent with impaired relaxation, as previously reported from radionuclide scans in coronary angioplasty patients.[117] The authors provided indirect evidence that the abnormal diastolic indices were due to a prolongation of IVRT, although this was not directly measured. Labovitz et al[116] investigated 32 patients during coronary angioplasty and found that evidence of diastolic left ventricular dysfunction was the earliest change during coronary occlusion with the balloon, preceding electrocardiographic changes, chest pain, or systolic wall motion abnormalities. Impaired relaxation was the pattern most often exhibited and occurred within 15 seconds of balloon inflation but returned to baseline by 15 seconds after deflation. Masuyama et al[118] also found a reduction in peak E-wave velocities and E/A ratio in serial Doppler echocardiographic studies of patients undergoing percutaneous transluminal coronary angioplasty to be a strong predictor of significant coronary restenosis. The most complete comparison of hemodynamic and Doppler indices of diastolic function in patients with coronary disease has been performed by Stoddard et al.[15] Their study evaluated the relationship of chamber stiffness and relaxation (tau) to the traditional transmitral indices in 35 patients undergoing diagnostic catheterization for chest pain. Subjects without coronary artery disease and with normal relaxation were found to have a direct correlation between increasing chamber stiffness and enhanced early filling velocities. Conversely, the group with coronary

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disease showed a significant indirect correlation between impaired relaxation and decreased peak E velocity. Although their findings differ from those of previous studies in that a variety of patterns of transmitral flow were found, they are consistent with early observations by other investigators.[119] The authors concluded that chamber stiffness has a greater influence than relaxation on the pattern of diastolic filling in patients without coronary disease. In contrast, abnormal relaxation appears to be the predominant factor influencing the Doppler pattern in patients with coronary disease and an abnormal tau value. El-Said et al[120] studied the effects of ischemia on left ventricular filling using Doppler transmitral flow recordings 132

during dobutamine stress echocardiography. Their data showed marked decreases in peak E velocities (-22%) and time to peak E acceleration (28%) in ischemic subjects, whereas 10 control subjects had an increase in both values (+33% and +75%, respectively; P < .0001). There was no overlap in the percentage change from baseline to peak dobutamine stress values between normal subjects and patients who had documented singlevessel coronary disease. The authors also found diastolic abnormalities to be more sensitive than induction of wall motion abnormalities for detecting coronary stenoses. Thus, the transmitral Doppler pattern of impaired relaxation appears to be the type most often seen in association with acute (or induced) myocardial ischemic syndromes. Fewer data exist for patients with chronic coronary artery disease or previous myocardial infarction. Fujii et al[121] showed a reduced E/A ratio and prolonged deceleration time to be common in patients with a history of infarction, regardless of location. Other studies comparing inferior with anterior infarct patients have suggested that transtricuspid Doppler echocardiographic recordings may be more sensitive in demonstrating abnormal filling and high right ventricular end-diastolic pressures.[122] One study also suggests a significant relationship among infarct size, degree of systolic dysfunction, and restrictive transmitral flow patterns.[123] This pattern is seen more often in coronary artery disease patients with a worse functional class and poorer prognosis.[81] [105] However, larger studies specifically designed to assess the clinical applicability of Doppler filling patterns in this population are currently not available.

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Another active area of investigation is the use of Doppler echocardiographic techniques to assess changes in left ventricular relaxation produced by commonly used cardioactive drugs. Myreng and Myhre[124] first reported enhanced relaxation and a shift in left ventricular filling toward early diastole in 20 patients given oral verapamil. The patients studied had documented coronary artery disease and showed baseline transmitral filling patterns that did not differ from those of control subjects. After verapamil administration, an increased peak E velocity and E/A ratio and shortening of IVRT were seen. The authors have reported a similar "normalization" of transmitral flow in coronary disease patients after beta blocker treatment.[125] However, the effects of calcium and beta blockade on diastolic function remain controversial.[126] Caramelli et al[127] concluded that the shift in transmitral flow to early diastole can be attributed to effects on heart rate and an increase in pulmonary wedge pressure in a study of 32 patients with anterior wall infarction who were given intravenous atenolol. Nishimura et al[128] have also shown an increase in peak filling rate and a concomitant rise in left ventricular end-diastolic pressure after intravenous verapamil, with no consistent change in tau in 20 patients with coronary artery disease and preserved left ventricular function. Thus, although the use of Doppler echocardiographic methods for assessing pharmacologic effects on diastolic function remains promising, peak filling rates alone should not be used as a marker for improved relaxation. Pulmonary Hypertension

The role of the pericardium and right ventricular function in left heart filling have been recognized from elegant animal studies by Ross,[129] Sonnenblick,[130] and Glantz and coworkers.[131] [132] Patients with primary pulmonary hypertension have also been found to have abnormal left ventricular filling by Doppler echocardiography. [133] Essentially, these patients have been described as having a redistribution of transmitral flow to late diastole, with low E/A ratio (often 0.3). Destruction can be

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reduced by selecting one image out of every one to several cardiac cycles, triggered to the electrocardiogram. This has been referred to as intermittent imaging. When the intermittent ultrasound impulse is at a high intensity (above 0.9 mechanical index), there is a strong and brief nonlinear echo. This transient scattering process is the third mode of action microbubbles show in an ultrasonographic field in addition to linear and harmonic response to ultrasound waves.[46] [47] Interrupting the high-intensity ultrasound for a short period of time allows for replacement of microbubbles, which then produce contrast enhancement for the following (triggered) frame. When microbubbles are administered as a continuous infusion and the ultrasound pulsing interval is incrementally varied, the reappearance of bubbles in the myocardium permits the calculation of mean microbubble velocity and plateau (or peak) myocardial signal intensity.[48] Multiplying these two variables together, one can better estimate myocardial blood flow. Therefore, with a combination of second harmonic and so-called intermittent imaging, it has become possible to noninvasively examine myocardial perfusion in animals and humans using a wide variety of intravenous higher molecular weight microbubbles.[8] [49] [50] [51] [52] (Harmonic) Power Doppler Power Doppler images are based on the integrated power in the Doppler signal instead of its mean frequency Figure 8-3 Illustration of returning signal intensity (indicated by arrow length). Microbubbles have the greatest harmonic signal intensity, but myocardium also has a harmonic response. Fortunately, the side lobe (SL) artifacts have very little harmonic signal intensity and thus do not reduce the image quality of a harmonic image as they do in fundamental images. (From Porter TR: Harmonic ultrasound imaging during routine and contrast-enhance echocardiography. Cardiac Ultrasound Today 1998;4:121.)

shift, as used in conventional color Doppler.[53] The amplitude of the Doppler signal is related to the concentration of scatterers at a particular location. This amplitude is much greater in the presence of microbubbles when compared with the signal of red blood cells.[54] This Doppler signal is more sensitive but, more importantly, is not subject to aliasing and is independent of the angle of insonation. It is, however, subject to flash artifacts, which occur with movement of the heart. Combining power Doppler with intermittent harmonic imaging (harmonic power Doppler) can

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decrease these flash artifacts at the expense of real-time imaging. Harmonic power Doppler has been successfully employed in animal[55] and human myocardial perfusion studies, showing satisfactory concordance in the comparison between echocardiographic and 99m Tc-sestamibi single photon emission computed tomography (SPECT) stress imaging.[56] [57] Low Mechanical Index Imaging Accelerated Intermittent Imaging

As previously mentioned, microbubbles are destroyed when exposed to ultrasound at high power output. Although 164

interrupting the imaging process by taking triggered images helps keep a sufficient concentration of contrast agent in the myocardial capillaries, the dynamic character of the echocardiographic examination cannot be used with triggered or intermittent imaging. If the mechanical index is set low enough to prevent major bubble destruction, while still allowing the microbubbles to resonate, the image acquisition can be performed continuously (because of the higher frame-rate), and real-time data on both wall motion and perfusion can be obtained. This procedure, termed accelerated intermittent imaging, has proven to be extremely helpful, especially during stress echocardiography in humans.[58] [59] Pulse Inversion Doppler and Power Modulation

Another possibility for achieving real-time visualization of myocardial function and perfusion is the application of the recently developed pulse inversion technique. The intention of this new method is the separation of linear and nonlinear scattering using the radiofrequency domain. Alternately positive and negative pulses of identical amplitude are transmitted into the tissue, the sum signal of which is equal to 0 (Fig. 8-4) . The responses of linear scatterers to that kind of pulses, therefore, will be cancelled. On the other hand, the signal from nonlinear scatterers (which do not react to positive and negative pressures in the same way) will be unequal to 0 and can be registered as a bubble-specific response (see Fig. 84) .[60] Although pulse inversion is subject to motion artifacts, pulse inversion Doppler overcomes this by sending multiple pulses of alternating polarity into the myocardium. This allows one to visualize wall thickening and contrast enhancement simultaneously at very low mechanical indices

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(6 months), echocardiographic infarct size tends to underestimate the volume of necrosis when measured at autopsy.[61] In some cases, the ventricular remodeling process may be responsible for the change in the tendency from early (6 months) underestimation of infarct size.[62] To identify postischemic ventricular dysfunction or "stunned myocardium," investigators have examined the effect of inotropic stimulation on the function of reperfused, noninfarcted myocardium and compared it with the effect on infarcted tissue. Serial 2D echocardiography during dopamine infusion demonstrates an increase in the contractility of the reperfused myocardium, with improvements in systolic wall thickening and fractional area change. This improvement in regional function is associated with an improvement in regional myocardial blood flow.[63] This study and others provided the experimental basis for the clinical use of dobutamine in detecting myocardial viability.[64] [65] [66] [67] [68] [69] Another echocardiographic method under investigation for determining myocardial viability is ultrasonic tissue characterization.[70] [71] [72] Nonischemic myocardium shows cyclic variation in the integrated backscatter, whereas in ischemic myocardium this variation is diminished or lost. MCE using sonicated iodinated contrast media identifies segments with persistent flow deficits despite reperfusion of the epicardial vessel. The areas of no reflow are believed to be due to microvascular damage and correspond to nonviable segments as identified by positron emission tomography and thallium scintigraphy.[73] MCE also can measure the extent of microvascular occlusion,

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254

which occurs after prolonged ischemia and prevents adequate reperfusion. [74]

Infarct Localization Infarcts are localized both with respect to the transmural extent of the infarction (i.e., subendocardial versus transmural) and to the anatomic location as related to the coronary distribution of the infarct related artery. Small nontransmural (i.e., subendocardial) myocardial infarctions may not be detected as an abnormality in contractile function. The transmural extent of infarction and regional systolic function is inversely related to fractional radial shortening in both acute (6 hours after occlusion) and subacute (72 hours after occlusion) infarctions.[60] [75] [76] Fractional shortening continues to deteriorate as the percent of total wall (transmurally) involved increases from 75% to 100%, contradicting the work of others who suggested the subepicardial third of the myocardium contributed little to systolic wall thickening.[77] The circumferential extent of the infarction and, to a lesser extent, its longitudinal extent (i.e., base to apex) correlate with the distribution of the affected coronary artery.[78] [79] The anterior, anterolateral, anteroseptal, and apical (anterior and septal) segments correspond roughly to the left anterior descending artery (LAD) distribution. The lateral wall and lateral apex are in the distribution of the left circumflex. The inferolateral wall is supplied by the posterior descending artery. In 80% of the population, the posterior descending artery arises from the right coronary artery (RCA) and supplies the inferolateral wall as well as the inferior free wall and inferior septum (right dominant). In the other 20% of patients, the posterior descending artery arises from the circumflex artery (left dominant system). The right ventricle is supplied by the RCA via its acute marginal branches. In general, infarctions in the LAD distribution tend to be more apically situated, whereas those in the RCA and the circumflex distribution are more basal in their location. Moreover, the extent of apical involvement and its distribution depends, to a degree, on the relative supply from the left anterior and posterior descending arteries. Of course, the presence of collaterals and previous bypass surgery alters the distribution of ischemia and infarction relative to the involved arterial supply. The most commonly accepted method for analyzing wall motion uses the 16-segment model recommended by the American Society of Echocardiography[38] (Fig. 12-

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1) , with the approximate and most common native coronary arterial distribution in relation to these segments depicted in Figure 12-2 . Experimental Models of Mitral Regurgitation Mitral regurgitation is common in the setting of acute myocardial infarction. Only recently have experimental studies elucidated the mechanism. These studies have demonstrated incomplete coaptation of the mitral valve leaflets owing to alteration of systolic left ventricular geometry Figure 12-1 The 16-segment model for segmental wall motion analysis recommended by the American Society of Echocardiography.[29] A, anterior; AL, anterolateral; AS, anteroseptal; I, inferior; IL, inferolateral; IS, inferoseptal; L, lateral; PSAX, parasternal short axis; S, septal; SAX, short axis.

during ischemia.[80] [81] Infarction of a papillary muscle and the underlying ventricular myocardium results in incomplete leaflet coaptation owing to an increase in the distance from the point of mitral leaflet coaptation to the mitral annulus.[81] [82] Although the extent of the underlying wall motion abnormality may be small and left ventricular function may be globally preserved, papillary muscle ischemia alone is insufficient to cause mitral regurgitation. These studies are supported by the clinical observation that mitral regurgitation occurs in patients with ischemia or infarction of the inferolateral or posteromedial papillary muscle and a small area of underlying myocardium with otherwise well-preserved left ventricular function.[15] Incomplete leaflet coaptation also may occur as a result of severe global left ventricular dysfunction rather than localized papillary muscle dysfunction. [80] The proposed mechanisms contributing to malcoaptation of the leaflets in the setting of global ventricular dysfunction include a prolonged rate of rise of left ventricular pressure (i.e., Figure 12-2 Arterial distribution of blood flow superimposed on a parasternal short-axis view. LAD, left anterior descending; LCx, left circumflex; RCA, right coronary artery.

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decreased dP/dt), with less force exerted on the mitral leaflets; poor systolic approximation of the left ventricular walls; mitral annular dilation; and malalignment of the papillary muscles owing to increased left ventricular end-diastolic volume. More recent data from a canine model using 3D echo-cardiography suggest that functional mitral regurgitation associated with left ventricular systolic dysfunction occurs only in the presence of left ventricular dilation.[83] Hemodynamically significant mitral regurgitation relates strongly to the 3D geometry of the mitral valve attachments at the papillary muscle and annular in the presence of left ventricular dilation (i.e., postpericardiectomy). Likewise, in vitro modeling studies demonstrated an integrated mechanism of regurgitation in which an altered balance between abnormal leaflet tethering and decreased coapting forces results in mitral incompetence.[84] Thus, hemodynamically significant mitral regurgitation is seen both in patients with small inferior myocardial infarctions and posteromedial papillary muscle involvement and in patients with large anterior infarctions, left ventricular dilation, and globally reduced systolic function. Infarct Healing and Remodeling Echocardiographic studies have contributed significantly to the understanding of infarct healing and the ventricular remodeling that takes place in the hours and days following an acute myocardial infarction. The importance of these phenomena are recognized in relation to the beneficial effects of delayed reperfusion and afterload reduction with angiotensin converting enzyme inhibitors that reduce infarct expansion and ventricular dilation. The concept of infarct expansion originated with the observation that the infarcted segment of myocardium thins and stretches with an increase in the circumferential extent of the necrotic zone (Fig. 12-3) (Figure Not Available) . The clinical observation that infarct expansion is associated with higher mortality, both early (in-hospital) and late after myocardial infarction, [85] [86] , [72] led to the postulate that the change in the topography of the infarcted zone increases the hemodynamic burden on the remaining normal walls, Figure 12-3 (Figure Not Available) Concept of infarct expansion. In the initial phase of the infarction (left), there is regional dilation and thinning limited to the infarcted region. Over time, in addition to further expansion of the area of infarct, there may be

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compensatory dilation of the remaining ventricle (right). (Redrawn from Eaton LW, Weiss JL, Bulkley BH, et al: N Engl J Med 1979;300:57–62. Copyright 1979 Massachusetts Medical Society. All rights reserved.)

resulting in ventricular dilation and hypertrophy.[85] [87] [88] Both clinical and experimental data suggest the following: 1. Expansion of the endocardial segment occurs as early as 10 minutes after occlusion.[89] 2. Infarct thinning and expansion are progressive over a period of 7 days. [88]

3. A critical mass of infarction (approximately 20% of total left ventricular mass) was required for expansion.[90] 4. Infarct expansion in the dog is more likely after LAD than after left circumflex occlusion.[89] 5. Infarct expansion led to aneurysm formation.[88] 6. The segment lengths of normal myocardium increase in the presence of infarct expansion, leading to ventricular dilation.[91] 7. Microvascular obstruction in infarcted tissue plays a role in remodeling by reducing local myocardial function, which contributes to the dysfunction of adjacent noninfarcted myocardium.[92] The clinical significance of infarct expansion is further emphasized by the demonstration of the beneficial effects of a patent infarct-related artery. [87] Histologic studies in a rat model of infarction demonstrated that reperfusion too late to salvage myocardium (no reduction in infarct size or transmurality) inhibits infarct expansion[93] and was associated with increased scar thickness.[94] Echocardiographic studies in dogs showed that delayed reperfusion of an infarct (as late as 5 to 6 hours after occlusion) acutely decreases the degree of infarct thinning and ventricular dilation.[95] [96] Although delayed reperfusion may convert a bland infarct into a hemorrhagic infarct and may increase the risk of myocardial rupture slightly, many clinical studies support the concept that an open artery provides substantial benefit, possibly through decreased left ventricular dilation and aneurysm formation and, as a corollary, a decreased incidence of arrhythmias and a lower mortality.[87] [97] The time course of left ventricular remodeling following successful reperfusion in acute myocardial infarction is suggested by a 2D echocardiographic study that showed progressive infarct thinning for up to 1 month and left ventricular dilation for up to 14 days. The degree of remodeling as reflected in left ventricular volume was greatest in the patients with the largest infarcts (peak creatine kinase > 8000 U/L). Despite the progressive remodeling,

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wall motion score improved rapidly by 14 days, and it continued to improve gradually to 1 year. [98] Vasodilator therapy, theoretically through a reduction of left ventricular wall stress, influences post–myocardial infarction remodeling and improves prognosis. The salutary effects of treatment with angiotensin converting enzyme inhibitors, first shown in a rat model by Pfeffer et al,[99] [100] include attenuation of left ventricular dilation, improved left ventricular performance with a downward shift of the pressure-volume curve and higher ejection fraction, and improved long-term survival. These findings were subsequently confirmed in post–myocardial infarction patients with left ventricular dysfunction in the Survival and Ventricular Enlargement (SAVE) trial. Two canine studies using echocardiographic measurements have shown that nitrates and enalapril had similar beneficial effects on the remodeling process.[101] [102] The Carvedilol Heart Attack Pilot Study (CHAPS) demonstrated 256

attenuation of left ventricular remodeling with postinfarction administration of carvedilol. Echocardiography at baseline and after 3 months of treatment showed reduced left ventricular volumes and sphericity (long-axis–to– short-axis ratio).[103]

MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/104.html/top

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Echocardiography in the Diagnosis and Early Risk Stratification of Acute Myocardial Infarction Transferring the experience from the animal laboratory into the CCU, clinical investigators have confirmed the usefulness of echocardiography in diagnosis, localization, prognostic staging, and detecting of complications of myocardial infarction. Diagnostic Role of Echocardiography For an imaging modality to be useful in the diagnosis of myocardial infarction, it must be feasible in the majority of patients. Images of the left ventricle adequate for segmental analysis of wall motion can be obtained in greater than 90% of patients by skilled sonographers.[104] [105] [106] Tissue harmonic imaging and left-sided contrast agents have increased the percentage of patients in whom technically adequate images can be obtained.[107] [108] [109] In one study of segmental and global function in 70 critically ill patients, the number of uninterpretable segments fell from 5.4 with fundamental (standard) imaging to 4.4 with harmonic imaging and finally to 1.1 with a left-sided contrast agent. In addition, the usefulness of the modality is directly related to its sensitivity and specificity and to the prevalence of the disease in the population studied. The accuracy of an echocardiographic diagnosis of a myocardial infarction is dependent on echocardiography's ability to detect wall motion abnormalities in the involved segment. As shown in the animal laboratory, the severity of the wall motion abnormality depends on the transmural extent of the infarction and the circumferential limits depend on the arterial distribution and collateral blood supply. In considering the specificity of wall motion abnormalities for diagnosis of acute myocardial infarction, other causes of segmental dysfunction must be recognized. A false-positive diagnosis can often be avoided if wall

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thickening is examined in addition to endocardial motion. The inward motion of the endocardial surface may be delayed or paradoxical owing to abnormal conduction in the presence of Wolff-Parkinson-White syndrome, [110] a left bundle branch block,[111] or right ventricular pacing. [112] Paradoxical septal motion also is present in right ventricular volume overload and following open heart surgery.[113] [114] In these conditions, the systolic thickening of the septum or other involved segment (e.g., posterolateral wall in Wolff-Parkinson-White syndrome, type A) should be preserved.[115] Nonischemic causes of segmental dysfunction that result in reduced systolic thickening and endocardial motion include focal myocarditis[116] and idiopathic cardiomyopathy. Several studies that have examined the specificity of echocardiographic wall motion abnormalities for diagnosis of acute myocardial infarction are worth noting. Among 65 patients presenting to the emergency room with chest pain, there were 5 false-positive echocardiograms, demonstrating regional asynergy in patients without infarction for a specificity of 85%.[117] In a more recent study by Peels et al[118] of 43 patients with chest pain and normal or nondiagnostic electrocardiogram, the specificity of echocardiographic wall motion abnormalities was 78% for ischemia and only 53% for infarction. The apparent discrepancy between the two studies is probably due to differences in prevalence of disease in the population studied. Sabia et al[105] used echocardiography to study 202 patients presenting to the emergency room with acute shortness of breath or chest pain. Of the 140 patients who were ruled out for myocardial infarction, 60 had regional wall motion abnormalities detected by echocardiography. Of those patients, 52% (31 of 60) had had a prior infarction and 53% (32 of 60) were found to have evidence of coronary artery disease on subsequent testing. Although the development of electrocardiographic Q waves is usually associated with a transmural infarction, the absence of Q waves does not always signify a nontransmural or subendocardial infarction.[119] Non–Qwave infarctions are usually smaller, are associated with smaller enzyme leaks,[120] and more often are in the distribution of the left circumflex artery. [121] Two-dimensional echocardiographic evidence of a wall motion abnormality is present in 90% to 100% of patients with Q-wave infarctions [117] [122] [123] [124] compared with 75% to 85% in patients with non–Q-wave [104] [114] [117] [123] [124] [125] infarctions. , The most widely used scoring system for grading the severity of a wall

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motion abnormality is that recommended by the American Society of Echocardiography, in which normal = 1, hypokinesis = 2, akinesis = 3, dyskinesis = 4, and aneurysm = 5[38] (Table 12-1) . Unlike other published scales,[106] hyperkinesis is not distinguished from normal contraction. Weiss et al[124] demonstrated that the finding of akinesis or dyskinesis is most common in the setting of transmural infarction, with milder degrees of wall motion abnormalities (i.e., hypokinesis) most likely representing nontransmural infarction or ischemia. Localization of Infarction Clinical studies have documented the accuracy of echocardiography in identifying the site of coronary occlusion. Echocardiographic localization has significant advantages TABLE 12-1 -- Scoring System for Grading Wall Motion[38] Score 1 2 3 4 5

Wall Motion Normal Hypokinesis Akinesis Dyskinesis Aneurysmal

Endocardial Motion * Normal Reduced Absent Outward Diastolic deformity

Wall Thickening * Normal (>30%) Reduced ( 13 mm Hg; n = 9) with those without (JVP < 13; n = 15). There was no difference in the frequency of detectable wall motion abnormalities between the two groups (77% versus 66%). However, the group with higher estimated JVP had less descent of the base (.7 cm versus 1.3 cm); less inspiratory collapse of the inferior vena cava (22% versus 45%) and a greater right-to-left ventricular size ratio (1.1 versus 0.6). The pressure half-time of the pulmonary regurgitant jet reflects the compliance of the right ventricular Figure 12-4 Four-chamber view of an echocardiogram from a patient after an inferior infarction with right ventricular involvement. There is enlargement of the right ventricle (RV) and right atrium (RA). The left ventricle (LV) appears small and the interatrial septum is deviated from right to left, suggesting elevated right atrial and right ventricular enddiastolic pressures.

chamber. In a recent study, a short pressure half-time of the pulmonary regurgitant jet ( inferior 39 (28) Anterior > inferior

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172 30 (17)

Peaked on 3rd day Echo at 72 hr

[164]

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185 44 (24)

Inferior MIs only; higher incidence with RV infarct Widimsky and 192 82 (43) Peaked 5th day; CHF or [167] Gregor death more common; no increase with thrombolysis or heparin CHF, congestive heart failure; MI, myocardial infarction; RV, right ventricular. [163]

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incidence of congestive heart failure and mortality is higher in those patients with effusions apparent on echocardiography.[167] In almost all cases the effusions are small and hemodynamically insignificant. Thus, the effusion did not cause the increase in morbidity and mortality but serves as yet another marker of a large infarction. Mitral Regurgitation Ischemic mitral regurgitation can be defined as valvular incompetence associated with myocardial ischemia or infarction in the absence of primary leaflet or chordal pathology (Fig. 12-6) . Acute mitral valve incompetence may occur in the setting of myocardial infarction owing to necrosis and rupture of papillary muscle tissue or incomplete coaptation of the mitral valve leaflets owing to distortion of ventricular architecture. Mitral regurgitation is common in the setting of acute myocardial infarction, with a reported incidence rate between 10% and 50%. Of almost 12,000 postinfarction patients catheterized at Duke University, 19% had evidence of mitral regurgitation by angiography.[168] [169] Hemodynamically significant mitral regurgitation occurs equally in anterior and inferior infarcts. Risk factors for significant postinfarction mitral regurgitation include advanced age, female gender, diabetes, and prior infarction.[170] [171] In patients with myocardial infarction, moderate to severe mitral regurgitation is associated with substantially reduced short- and long-term survival, with up to a 24% early and 54% 1-year mortality rate.[171] [142]

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Severe postinfarction mitral regurgitation also is an independent risk factor for coronary artery bypass surgery operative mortality. [168] Moreover, in patients presenting to the emergency room with chest pain, moderate or severe Figure 12-6 (color plate.) Mitral regurgitation in a patient with an inferior myocardial infarction and resultant inferobasal aneurysm. A, Diastolic deformity in this apical two-chamber view (arrow). B, Lack of thickening in this region during systole (arrow). C, Moderately severe mitral regurgitation (double arrow).

mitral regurgitation by echocardiography was associated with high risk for overall and cardiovascular mortality (risk ratio = 2.0).[172] Among these patients, only 60% had audible murmurs. The clinical recognition of mitral regurgitation in the setting of myocardial infarction may be confounded by several variables. Up to 50% of patients with hemodynamically significant mitral regurgitation do not have an audible murmur owing to rapid equalization of left ventricular and left atrial pressures (especially in a low output state) or because the murmur is obscured by lung sounds in a patient with pulmonary edema or mechanical ventilation.[171] In view of the adverse prognosis, early diagnosis is desirable to institute medical or surgical interventions that potentially improve outcome. Although some authors have advocated TTE in all patients admitted with myocardial infarction, this approach is probably not costeffective. However, echocardiography is mandatory in the postinfarction patient with a new systolic murmur, pulmonary edema, or sudden cardiac decompensation. In this situation, TTE is 100% sensitive in detecting mitral regurgitation and in distinguishing mitral regurgitation from ventricular septal defect.[173] Detection and grading of mitral regurgitation is accomplished with 2D, Mmode, color, and spectral Doppler techniques. Two-dimensional imaging detects abnormalities in the mitral valve apparatus, including flail leaflets or ruptured chordae. Although color flow parameters are those most often used, accurate grading of mitral regurgitation severity should encompass other echo-Doppler signs as well.[174] [175] In the patient with pulmonary edema, the unexpected findings of a small infarction, a hyperdynamic left ventricle, increased early mitral inflow velocity, or all three [176] should prompt a careful search for mitral regurgitation even when color flow Doppler mapping is unrevealing.

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263

Papillary muscle necrosis with rupture and a flail leaflet is a life-threatening complication of myocardial infarction that requires surgical intervention. The more frequent involvement of the posteromedial papillary muscle is thought to be due to its blood supply from a single coronary artery. Chordae to both leaflets arise from each of the papillary muscles so that in cases of "complete" rupture of the entire trunk of a papillary muscle, both leaflets are affected. In less severe cases, the rupture is "incomplete" and only a single head is torn. The 2D echocardiographic findings include prolapse of one or both leaflets, a flail leaflet, and liberation of a portion of the papillary muscle.[177] In some patients, the ruptured muscle may remain tethered to the chordae and chaotic motion is not present. Spectral and color flow Doppler imaging of the jet is usually easily accomplished with surface imaging, but an eccentric path of flow may complicate its identification. In our experience, TEE is superior in this regard,[36] supported by multiple case reports in the literature[16] [19] [21] (Fig. 12-7) . When only a single head of the papillary muscle is affected (incomplete rupture), medical stabilization often is possible. Initial treatment should include afterload reduction with diuretics, angiotensin converting inhibitors, nitroprusside, and (in cases of severe cardiac decompensation) inotropic support and intra-aortic balloon pump. When rupture is complete, involving the main trunk of the papillary muscle, the complication is uniformly fatal without immediate recognition and prompt repair.[177] [178] In the other forms of ischemic mitral regurgitation, reperfusion therapy with thrombolytics or angioplasty should be considered first-line therapy because reperfusion may improve regurgitant severity and patient prognosis. Coronary bypass in conjunction with mitral valve surgery should be considered in patients who show benefit from medical therapy or nonsurgical revascularization. Coronary bypass with mitral valve surgery is necessary in patients who develop circulatory collapse as a result of mitral regurgitation, despite the relatively high operative mortality in this patient group. In those patients who receive surgery for severe ischemic mitral regurgitation, there is evidence that early surgery, concomitant revascularization, and repair, rather than replacement, improve survival.[179] [180] In the recent SHOCK trial (SHould we use emergently revascularized Occluded Coronaries in cardiogenic shocK?), the survival rate in patients with

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Figure 12-7 (color plate.) Transesophageal echocardiogram of a patient with papillary muscle rupture after an acute inferior myocardial infarction. The papillary muscle rupture was incomplete and the head of the papillary muscle remained tethered to the mitral chordae. A, The triangular density representing the head of the papillary muscle (arrow) can be seen within the body of the left ventricle during systole. B, Associated severe mitral regurgitation with a prominent area of proximal isovelocity surface acceleration (double arrow).

acute severe mitral regurgitation who underwent surgery (40%) was higher than in those treated medically (71%, P < .003).[181] Ventricular Septal Rupture Ventricular septal defect owing to myocardial rupture complicates 1% to 3% of all acute myocardial infarctions and up to 5% of all fatal infarctions. In the GUSTO-1 trial (Global Utilization of Streptokinase and TPA for Occluded coronary arteries), the incidence of ventricular septal rupture was only 0.2% (84 of 41,021 enrolled patients), suggesting that thrombolytic therapy has reduced the incidence of rupture.[182] Ruptures occur only in the presence of transmural infarction and result from hemorrhage within the necrotic zone. Independent risk factors for the development of a ventricular septal defect are similar to those for papillary muscle rupture and include first infarction, advanced age (>65), hypertension, and female gender.[183] [184] There appears to be a higher incidence in patients without a history of prior angina and with infarcts in the distribution of a single vessel.[183] [184] [185] Thus, septal rupture appears to be more likely following abrupt occlusion of a single artery that vascularizes a territory for which there is little collateral flow.[184] Unlike papillary muscle rupture, ventricular septal rupture occurs with equal frequency among patients with anterior (LAD) and inferior (RCA) infarctions but less frequently in those with lateral (left circumflex artery) infarctions.[186] Conflicting evidence exists as to the effect of thrombolytic therapy on the development and outcome of postinfarction ventricular septal defect. Thrombolytic administration that is delayed more than 12 hours following the onset of chest pain may increase the incidence of ventricular septal rupture.[97] However, in most cases the slight increase in the risk of rupture is outweighed by the overall benefit of reperfusion therapy. In the GUSTO1 study, the onset of rupture was earlier on average (1 day) than that reported previously, suggesting that although thrombolytic therapy reduced the rate of rupture, it tended to occur earlier after thrombolysis.

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Ventricular septal defects usually present 3 to 6 days after infarction with recurrent chest pain, dyspnea, and sudden hypotension or shock. A new harsh pansystolic murmur is present in approximately 50% of patients. Bedside 264

echocardiography has been demonstrated to be highly sensitive and specific in the diagnosis of ventricular septal defect. The defect can be visualized by transthoracic 2D imaging in 40% to 70% of patients.[177] [187] The use of contrast and color flow Doppler imaging improves the sensitivity to 86% and 95%, respectively.[21] [97] [173] [177] When TTE is suboptimal, TEE is highly accurate with a reported 100% sensitivity and specificity, [188] [189] with improved delineation of the site of defect, the morphology, and presence of multiple defects[190] (Fig. 12-8) . The most common site for a ventricular septal rupture is the posteroapical septum. Visualization of the area of myocardial dropout is most often accomplished in the parasternal short-axis view just below the level of the papillary muscles or in the apical four-chamber view with slight posterior angulation of the probe. Anterior septal defects most often occur in the distal one third of the septum and are visualized in the apical four-chamber view with anterior angulation or in an apical short-axis view. Postmyocardial infarction ventricular septal defects may be multiple and often have a serpiginous course through the myocardium.[191] Associated echocardiographic findings include evidence of elevated right ventricular pressure including right ventricular dilation, decreased right ventricular systolic function, and paradoxical septal motion. Signs of increased right atrial pressure include right atrial dilation, bowing of the interatrial septum toward the left throughout the cardiac cycle, and plethora of the inferior vena cava. Color flow Doppler imaging is particularly useful in demonstrating the exact position of the defect; the width of the jet correlates with the size of the defect as measured at surgery.[191] Although the peak gradient across the ventricular septal defect measured with continuous wave Doppler allows an estimate of right ventricular systolic pressure, the measurement should be used with caution in patients with complex defects involving indirect tracts through the myocardium. [191] A recent study demonstrated a fair correlation between this Doppler estimate of right ventricular systolic pressure and that measured at catheterization (r = 0.71); the values were similar to those estimated from the tricuspid

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regurgitant jet. Echocardiography provides prognostic and diagnostic information in patients with ventricular septal rupture. Rupture Figure 12-8 (color plate.) Transesophageal echocardiogram showing a large ventricular septal defect (VSD) involving the posterior septum in a patient with a large inferior myocardial infarction and right ventricular extension. Left, The area of discontinuity can be visualized as a large, irregularly shaped area of myocardial dropout. Right, Color flow demonstrates left-to-right shunting across this ventricular septal defect. LV, left ventricle; RV, right ventricle.

of the posterior septum after inferior myocardial infarction is associated with a higher mortality rate, apparently related to the degree of associated right ventricular dysfunction.[186] [192] Moreover, posterior septal ruptures tend to be more complex and associated with remote myocardial involvement. In contrast, anterior septal defects more often have a direct course and involve a discrete myocardial region. Overall mortality is 95% to 100% without surgical intervention.[193] The strongest indicator of poor prognosis is the development of cardiogenic shock associated with as much as a 90% mortality rate.[192] Although early surgery appears to improve survival when cardiogenic shock is present, results in the recent SHOCK trial were disappointing. In the surgically treated group, the survival rate (19%) was only slightly better than that of the medically treated group (5%).[186] Right ventricular systolic pressure tended to be higher and right atrial pressure lower, among the survivors. When the patient can be stabilized medically, operative mortality may be improved when surgical repair is delayed until 6 weeks following the event.[184] In summary, the value of echocardiography in patients with suspected ventricular septal rupture is its ability to provide an accurate, timely diagnosis and important prognostic information that may assist in therapeutic decision making. Rupture of the Ventricular Free Wall and Pseudoaneurysm Free wall rupture occurs in approximately 3% of all acute myocardial infarctions,[194] and it is one of the leading causes of fatality (8% to 20%).[195] [196] [197] [198] [199] Risk factors for free wall rupture are similar to those for papillary muscle and ventricular septal rupture; however, this complication is more likely to occur in patients with a transmural myocardial infarction involving the posterolateral wall associated with a left circumflex occlusion

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or with a LAD occlusion.[201] Early successful reperfusion appears to decrease the risk of rupture. In one study of approximately 1300 patients, the overall incidence of cardiac rupture was lower in those receiving thrombolytic therapy (1.7%) than in those in the conventional therapy group (2.7%). Among

[200]

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patients who receive thrombolytic therapy, patients older than 70 years of age and women had higher rates of rupture.[202] Moreover, patients in whom reperfusion was unsuccessful had a significantly higher rate of rupture than those who were successfully reperfused (5.9% versus 0.5%).[203] Conversely, late reperfusion appears to increase the risk of myocardial rupture though decreasing overall mortality.[97] [204] The use of nitrates in acute myocardial infarction may decrease the risk of rupture by as much as 30%.[205] The intensity of post-thrombolytic anticoagulation with heparin or hirudin does not appear to affect the rate of rupture. [202] Although ventricular free wall rupture usually presents clinically as an acute catastrophic event leading to rapid demise, several recent pathologic and clinical studies have suggested that many cases may involve subacute dissection and tearing of the myocardium before hemodynamic collapse.[194] [196] [200] [205] , Intramural hematoma or hemorrhage at the junction of the necrotic and the normal myocardium results in a small endocardial rent. The tear usually takes a circuitous pathway through the myocardium, ending in a small epicardial opening. Clinically, a prodrome of ongoing or recurrent chest pain (in the absence of an elevation in creatinine kinase), repetitive large volume emesis, unexplained agitation, hypotension or syncope may be associated with the initial small tear.[194] [196] [200] A small amount of hemorrhage into the pericardial space of blood may precede the final catastrophic event. Patients diagnosed during this subacute phase and taken promptly to surgery have a greater chance of survival. A second mechanism of rupture through the wall of an aneurysm has been described. [206]

Echocardiography has a high sensitivity for rupture[194] when the diagnosis is sought and all the echocardiographic findings are considered. The most frequent finding is pericardial effusion; the absence of pericardial effusion virtually excludes rupture. Increasing size of effusion and the presence of thrombus in the pericardial space significantly increases the specificity for rupture (>98%). [194] [204] , [207] An intrapericardial thrombus appears as an

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echo-dense mass; it may be mobile, undulating within the pericardial space or immobile, impinging on the cardiac chambers.[208] Direct visualization of the myocardial tear is possible with TTE in as many as 40% of patients.[201] Other echocardiographic findings include evidence of Figure 12-9 The difference between a true aneurysm (A) and a false aneurysm (B). Note that in the true aneurysm there is continuity of myocardium in the region of dilation, in contrast to the loss of this continuity in the pseudoaneurysm. (Modified from MacKenzie JW, Lemole GM: Tex Heart Inst J 1994;21:296–301.)

tamponade with right atrial and right ventricular diastolic collapse (40%), [201] respiratory variation of the tricuspid and mitral inflow pattern, and plethora of the inferior vena cava. Echocardiographic guidance of pericardiocentesis of the hemopericardium may be life saving in the patient with hemodynamic collapse before the patient can be transported to surgery. Patients at risk for rupture may be identified by evidence of infarct expansion with significant wall thinning at the infarct site. The mortality rate of free wall rupture in the absence of surgical intervention approaches 100%,[199] although recent series report as much as a 50% survival rate in patients who underwent pericardiocentesis and conservative medical management.[201] [209] The in-hospital mortality rate for those who undergo surgical repair is in the range of 40%.[193] [201] [204] Those who survive until hospital discharge appear to have a good long-term prognosis. Thus, early echocardiographic diagnosis with prompt surgical or percutaneous drainage is mandatory in patients who develop postinfarction myocardial rupture. A pseudoaneurysm is a myocardial rupture contained by pericardial adhesions resulting in a pouch that communicates with the left ventricular cavity. [177] A distinguishing echocardiographic feature is the narrow neck, compared with the broader "entrance" to the body of a true aneurysm, with a "neck" diameter-to-maximum diameter ratio less than 0.5. An echocardiographic study showed that this sign was only 60% sensitive in patients with post-myocardial infarction pseudoaneurysms.[210] The majority of post-myocardial infarction pseudoaneurysms were located in the inferoposterior or posterolateral regions (associated with right coronary or left circumflex coronary occlusions).[210] The walls of the pseudoaneurysm are composed of pericardium rather than

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the thin-walled myocardial scar of true aneurysm (Fig. 12-9A) . Occasionally a pseudoaneurysm may occur after rupture of the thin wall of a true aneurysm with the development of a "mixed" aneurysm (see Fig. 129B) . [211] Spectral and color Doppler imaging demonstrate characteristic flow in and out of the pericardial cavity at the site of the tear, as well as abnormal flow within the pseudoaneurysm. Respiratory variation of the peak systolic velocity has also been demonstrated.[212] A meta-analysis suggested that TEE has a higher diagnostic accuracy (>75%) than TTE (26%), although data 266

was available in only a small number of patients[213] (Fig. 12-10) . Surgical repair is the preferred treatment, although new reports have demonstrated that conservative medical treatment in certain high-risk patients is not associated with an increased risk of cardiac rupture.[210] [213] Infarct Expansion and Aneurysm Formation Infarct expansion is an increase in the circumferential extent of the area of infarction that results from stretching and thinning of the infarcted zone. Early clinical studies demonstrated that this phenomenon with a consequent increase in left ventricular volume and wall stress was associated with an adverse prognosis.[85] The importance of infarct expansion has been underscored by clinical trials using angiotensin converting enzyme inhibitors in patients with left ventricular dysfunction after myocardial infarction. In the SAVE trial (Survival and Ventricular Enlargement), which showed a 21% reduction in cardiovascular mortality with the use of captopril,[214] echocardiography demonstrated that ventricular enlargement and reduced fractional area change were independent risk factors for cardiac events. Patients treated with captopril had a lower incidence of ventricular enlargement, which was associated with the lower risk of events,[50] a finding that has been confirmed in subsequent studies.[141] [215] The final expression of infarct expansion is aneurysm formation. In the Coronary Artery Surgery Study (CASS) there was a 7.6% incidence of angiographically documented left ventricular aneurysms.[216] In a study by Visser et al,[218] the incidence of aneurysm was 22% (35 of 158), and most of those occurred in patients with anterior infarction. Formation of an aneurysm occurs only with transmural infarction with a full-thickness scar and, thus, is more frequent following a Q-wave than a non-Q-wave

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infarction. An aneurysm is more likely to complicate an infarct in the LAD distribution than in the right or circumflex arteries.[218] Spontaneous rupture of an acute aneurysm is rare (see "Rupture of the Ventricular Free Wall"), and late rupture virtually never occurs. Serial 2D echocardiographic studies show that aneurysmal dilation is present as early as 5 days after myocardial infarction (15 of 35, 43%, in the Visser study), and new aneurysms after 3 months are unlikely.[218] Despite the Figure 12-10 Transgastric views in transesophageal echocardiogram showing a large pseudoaneurysm involving the inferolateral wall. Left, short-axis view (horizontal plane); right, long-axis view (longitudinal plane).

beneficial clinical course attributed to delayed reperfusion with thrombolytic therapy, there has been no reduction in the frequency of ventricular aneurysms.[219] [220] The echocardiographic appearance of a ventricular aneurysm parallels the pathology. A true aneurysm is defined as a deformity of the thinned infarct segment that is apparent during diastole as well as during systole (see Fig. 12-6) and demonstrates a diastolic contour abnormality. In contrast, a dyskinetic myocardial segment deforms during systole, extending beyond the normal contour of the myocardium. The involved myocardial segment is scarred with thin walls (20 µg/kg/minute) has been shown to be a less reliable predictor of recovery.[8] Although some investigators start at lower doses, or use only a low-dose protocol for the assessment of viability, and others use 5-minute rather than 3-minute increments, [174] there does not appear to be a clear benefit in favor of any of these alternatives. Dipyridamole has been shown to enhance both segmental shortening and load-independent indices of ventricular function in stunned myocardium.[175] The mechanism of this phenomenon is unclear, but a "local Frank-Starling response" (whereby augmentation of myocardial blood volume leads to increased sarcomere separation) appears to be the most likely explanation. Additionally, an indirect sympathomimetic response to dipyridamoleinduced ischemia may contribute to improvement of regional function, as may resolution of ischemia secondary to improvement of coronary perfusion. Dipyridamole appears to be an effective alternative in low-dose and "infra-low-dose" protocols[176] the choice of agent is dependent on local expertise and preference. The interpretive criteria are similar, irrespective of the stressor. Viable segments are characterized by reduced resting function, which augments in response to low-dose dobutamine (usually 7.5 to 10 µg/kg/minute). There is continued augmentation if there is a patent infarct-related artery or the tissue is well collateralized. In the presence of a stenosed infarct-related artery, an increasing proportion of segments become ischemic at dobutamine doses greater than 10 µg/kg/minute.[177] This initial

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improvement followed by deterioration in function constitutes the "biphasic response," which is strongly predictive of eventual functional recovery of the tissue.[177] A uniphasic response is less predictive of recovery, and a classic ischemic response is not very predictive of the recovery of resting function. Because the biphasic response is the most reliable finding (Fig. 14-10) , our preference is to induce ischemia whenever possible by proceeding to maximal stress (i.e., 40 µg/kg/minute dobutamine with or without atropine), rather than using a discreet "viability" or low-dose protocol. In patients with severe left ventricular dysfunction, this approach warrants caution, and early termination may be needed if ischemia is progressive or if other responses might induce instability. Finally, viability studies are the most difficult to interpret, and we commonly use both digital display, including doses of both 5 and 10 µg/kg/minute, and videotape for review of the study. The response of regional function to dobutamine is influenced by the extent of viable tissue, the degree of residual stenosis, the extent and magnitude of collateral vessels, the size of the risk area (which influences tethering), and the presence of drug therapy,[178] of which the extent of viable tissue and perfusion warrant further attention. The uniphasic response is an ambiguous signal that may be caused by part of the wall mounting a dobutamine response (i.e., admixture of scar and normal tissue) or all of the wall mounting a partial response (i.e., viable myocardium). The ability to discriminate the extent of subendocardial damage, with its implications for the likelihood of subsequent functional recovery, is poor. With respect to perfusion, augmentation of function is dependent on delivery of more substrate; thus, tissue supplied by more severe stenosis may become ischemic before it augments function. This may compromise the recognition of viability. The accuracy of dobutamine for prediction of regional functional recovery is summarized in Table 14-10 , although there is a large evidence base, most studies are relatively small and derive from expert centers. The overall sensitivity of dobutamine (approximately 80%) appears greater than that of dipyridamole stress (approximately 60%), although the specificity of the former is less (78% vs. 87%). Moreover, the nuclear approaches are more sensitive but less specific than these echocardiographic techniques.

324

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Figure 14-10 Apical four-chamber diastolic (right) and systolic (left) views at rest (top), with low-dose dobutamine (middle), and with peakdose dobutamine (below), illustrating a "biphasic" response to dobutamine stress (reduced systolic thickening at rest, increment with low dose, and deterioration at peak dose) in the lateral wall.

Prediction of Recovery of Global Function and Outcome Improvement of left ventricular function within individual segments is not usually the goal of revascularization, whereas improvements in ejection fraction, exercise capacity, and outcome are therapeutic goals. Recent work has sought to address the ability to predict these parameters. Stress echocardiography can be used to predict improvement of global left ventricular function after revascularization. Cornel et al[179] has reported an 89% sensitivity and 81% specificity for prediction of a significant (5%) improvement in ejection fraction, using a cut-off point of 4 of 16 viable (biphasic) segments at dobutamine echocardiography. Similarly, the global ventricular response to low-dose dobutamine is a strong predictor of global functional recovery.[180] Other factors clearly influence the likelihood of recovery, including an inverse relationship with the number of thinned and akinetic segments or ventricular volumes. [181] The revascularization of patients with adequate amounts of viable myocardium (usually >25% of left ventricular mass) is associated with improved functional class. The presence of viable myocardium may influence outcome in two ways. First, revascularized viable tissue may lead to improved function and thereby improved outcome.[182] Second, non-revascularized viable tissue may be unstable and act as a substrate for recurrent events,[183] including mortality.[184] These outcomes have not been reported in all series,[185] probably because of heterogeneity in populations studied and responses; for example, a uniphasic response early after infarction may be a benign finding.

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New Technologies that May Solve Limitations of Stress Echocardiography Image Quality Although perfect image quality is certainly not essential for a stress echocardiographic study to be interpretable, 325

TABLE 14-10 -- Sensitivity and Specificity of Dobutamine Echocardiogra for Identification of Myocardial Viability (Segmental Analysis) * Study Pierard †

Stress Dobutamine

Smart * [8]

Dobutamine

Previtali[30]

Dobutamine

Cigarroa ‡ Marzullo[275] Alfieri § Watada

Dobutamine Dobutamine Dobutamine Dobutamine

La Canna ¶ Dobutamine Dobutamine Charney[276] Perrone-Filardi Dobutamine

Patients, Sensitivity, Specificity, N % (n) % (n) Comm 17 83 (6) 73 (8/11) Early p MI 51 86 (22) 90 (26/29) Early p MI 42 79 (63) 70 Early p (109/158) MI 25 82 (11) 86 (12/14) 14 82 (49) 92 (24/26) 14 91 (93) 78 (25/32) 21 83 (66) 86 (43/50) Early p MI 33 87 (205) 82 (89/109) 17 71 (31) 93 (27) 18 88 (48) 87 (27/31)

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Afridi Arnese[70]

Dobutamine Dobutamine

20 74 (38) 38 74 (33)

Senior[110] Bolognese[202]

Dobutamine Dobutamine

45 87 (45) 30 89 (27)

73 (55/76) 95 (130/137) 82 (123) 91 (45)

Poli #

Dobutamine

51 72 (78)

68 (176)

Dipyridamole

51 51 (78)

82 (176)

40 40 36 73

40 79 (73)

94 (133) 94 (133) 63 (65) 86 (238/277) 83 (36)

53 69 (32) 86 (50) 30 89 (62) 18 68 (46)

100 (26) 57 (46) 82 (106) 83 (63)

Varga[10]

Dipyridamole Dobutamine Dobutamine Bax[283] Vanoverschelde Dobutamine

78 (40) 76 (40) 85 (27) 76 (167)

[285]

Perrone-Filardi Dobutamine

Early p MI Early p MI Early p MI

[282]

Furukawa[67] Cornel[87] Nagueh[279]

Dobutamine Dobutamine Dobutamine Dobutamine

Total

Dobutamine Dipyridamole

Akinet Hypok Biphas respon

726 81 78 (1065/1312) (1401/1796) 91 60 (71/118) 87 (269/309)

MI, myocardial infarction. * Average ejection fraction approximately 35%. † Pierard et al: J Am Coll Cardiol 1990;15:1021–1031 ‡ Cigarroa et al: Circulation 1993;88:430–436 § Alfieri et al: Eur J Cardiothoracic Surgery 1993;7:325–330 Watada et al: J Am Coll Cardiol 1994;24:624–630 ¶ La Canna et al: J Am Coll Cardiol 1994;23:617–626 £ Perrone-Filardi et al: Circulation 1995;91:2556–2565

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Afridi et al: Circulation 1995;91:663–670 # Poli et al: Heart 1996;75:240–246

it certainly favors concordance between observers[73] and facilitates an accurate diagnosis of disease extent and distinction of ischemia and scar. Major improvements in image quality obtained from harmonic imaging have translated into improvements in the accuracy of stress echocardiography.[58] Likewise, the use of contrast echocardiography may facilitate delineation of the endocardial border; the implications of this finding are addressed in another chapter. Quantitative Approaches to Interpretation As mentioned earlier, the current qualitative algorithm for interpretation of stress echocardiograms requires a significant level of expertise on the part of the observer. A less subjective means of interpretation would be attractive on the grounds of feasibility and reproducibility. Either semiquantitative or fully quantitative strategies of examining wall motion can be used to evaluate global and regional left ventricular function. Global indices (ejection fraction or end-systolic volume) are insensitive to milder degrees of ischemia and are not an answer to the shortcomings of qualitative interpretation. Wall motion scoring offers a semiquantitative regional approach, which may improve the reproducibility of observers, but this does not constitute a major deviation from the regional approach used by most experienced readers and does not measure function independent of the observer. True quantitation of regional function may be based on following either radial or longitudinal myocardial motion (see Chapter 5) . The simplest approach involves tracing of endocardial (and for some methods, epicardial) interfaces and their superimposition using a fixed or floating reference system and measurement of endocardial excursion or myocardial thickening. Historically, this approach has been limited by three major technical limitations, but recent developments have addressed some of these limitations. First, excellent border definition of both endocardium and epicardium (especially in the apical views) was obtainable in less than 50% of images, but harmonic imaging has improved image quality substantially, and contrast echocardiography may also be of value. Second, failure to

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compensate for rotational or translational cardiac movement may be associated with false-positive results, but correction for movement of the heart may also compromise sensitivity. A postprocessing approach (using color-enhanced digitized cine-loops) may be used to correct translational movement.[186] Third, the 326

process of tracing multiple systolic and diastolic frames is tedious, timeconsuming, and unattractive for clinical practice. However, recent developments in edge-tracking have led to automated programs for measuring endocardial excursion. Along similar lines, Perez has developed an online quantification of ventricular function during dobutamine echocardiography using acoustic quantification.[187] The feasibility and accuracy of this approach has now been documented in several studies[188] [189] (Fig. 14-11) (Figure Not Available) . Myocardial tissue Doppler may provide another means of quantifying regional function. A unique aspect of this approach is that it can be used to quantify motion in the longitudinal (base-apex) direction, which corresponds to the contribution of longitudinal subendocardial muscle fibers.[190] Tissue Doppler measurements can be obtained using color or pulsed wave modalities to gather peak velocity and timing parameters. Pulsed wave Doppler, although useful for resting imaging,[191] is less feasible during stress because of the need to acquire all values online within a limited time at peak stress. Tissue velocity profiles within each segment of a color myocardial Doppler image may be obtained by postprocessing, but this requires a high frame-rate (at least 80 to 100 frames per second) to ensure that true peak systolic velocity is captured (Fig. 14-12) . The development of ischemia causes a reduction of peak velocity and transmyocardial velocity gradient and a delay in the development of peak velocity, of which the first is the most reproducible. Peak velocity has been shown to correlate with wall motion interpretation[192] [193] and ischemia with dual isotope SPECT.[194] More recently, normal ranges at peak stress have been described, and these ranges have been applied to the identification of angiographically defined coronary disease, [195] providing comparable accuracy to an expert reader. This technique presents some unresolved problems; it appears to be more amenable to dobutamine than exercise stress, and further efforts are needed to remove the contribution of translational movement.

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Another quantitative approach that is independent of edge detection is the analysis of myocardial backscatter. Cyclic variation of backscatter has been shown to change during ischemia,[196] [197] but, until recently, backscatter analysis was strictly a research technique that was dependent Figure 14-11 (Figure Not Available) (color plate.) Color kinesis images with color coding showing sequential frames in systole and diastole in short-axis and apical fourchamber views. The graphics express regional fractional area change in each segment. (From Mor-Avi V et al: Circulation 1997;95:2087–2097.)

on the ability to export and process voluminous raw data from the echocardiography machine. Recent developments in computer technology, especially storage, have made this approach more feasible,[198] although whether it can be incorporated into clinical imaging remains to be seen. Stress Doppler Echocardiography Stress Doppler echocardiography has been used to examine systolic or diastolic blood flow alterations caused by ischemia. Unfortunately, because compensatory hyperkinesis of the nonischemic wall tends to preserve overall ventricular function, changes in stroke volume occur mainly in the presence of extensive ischemia,[199] and stress-induced alterations in global cardiac function are not specific for coronary disease. The development or worsening of mitral regurgitation on color flow mapping (which may explain the occurrence of dyspnea disproportionate to the severity of coronary disease) is another systolic parameter that may be predictive of ischemia during dobutamine stress testing,[33] but the frequency of this finding is low,[200] as vasodilation at peak dobutamine dose tends to reduce left ventricular cavity size and therefore regurgitation. Left ventricular relaxation is an active process that may be altered by the development of myocardial ischemia. These changes can be examined by transmitral flow measurements of the peak E and A wave velocities, E/A ratio, E wave deceleration time, diastolic time intervals, and flow-velocity integrals of passive and active flow.[201] Unfortunately, tachycardia causes the E and A waves to merge at higher heart rates. Nonetheless, reductions in passive left ventricular filling (probably reflecting impaired relaxation secondary to ischemia) have been correlated with ischemia during dobutamine stress echocardiography.[202] The same pattern has been recorded with other stressors that provoke ischemia without tachycardia, such as dipyridamole and pacing with cessation after the development of ischemia.[203] Unfortunately, however, the effects of ischemia (delayed

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relaxation) may be pseudonormalized by ischemia-induced increases in left atrial pressure (Fig. 14-13) . Tissue Doppler assessment may be of value in 327

Figure 14-12 (color plate.) Importance of high frame-rate to tissue Doppler velocity. Doppler velocity profiles are shown in the same segment at different frame-rates. A high frame-rate (>100 frames per second [f/s]) is necessary to obtain the true peak velocity as well as timing variables.

examining regional diastolic function with less influence from left atrial pressure. [204] Changes of diastolic function in response to stress are not specific for ischemia, however, and may be induced by left ventricular hypertrophy, for example.

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Alternatives to Nonexercise Stress Echocardiography Exercise Stress Echocardiography Nonexercise stress approaches are invaluable in patients who are unable to exercise maximally. Attempts to use exercise stress in such patients are attended by suboptimal sensitivity, and this is true also of isometric exercise. [205] Pharmacologic stressors have also been used in patients who are able to exercise, among whom the results of Figure 14-13 Development of a pseudonormal pattern, probably due to ischemia-induced increment in left atrial pressure. This patient with resting left ventricular dysfunction developed extensive ischemia by wall motion assessment. However, there is an increment of E wave velocity and shortening of the deceleration time, rather than development of a delayed relaxation pattern.

exercise and pharmacologic techniques can be compared. Table 14-11 summarizes several studies that compared exercise and nonexercise stress echocardiography on a "head-to-head" basis. Most studies have shown no significant differences in sensitivity or specificity between exercise and nonexercise stress echocardiography. Some of these comparisons have suggested that the nonexercise technique has greater feasibility, although this may be colored by greater expertise in pharmacologic than in exercise echocardiography at some centers. However, several of these comparisons have involved designs that do not replicate the usual clinical scenario, such as exclusion of patients with technically difficult studies, as well as cessation of antianginal therapy before the test. The latter may have an important influence on this analysis; in one comparison of dobutamine and exercise echocardiography, the sensitivity of dobutamine stress was significantly less than that obtained with bicycle exercise in patients who

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were treated with beta receptor blockers, or who failed to complete the dobutamine protocol because of the development of side effects. Interestingly, among the patients with coronary disease in whom both tests were positive, the extent of ischemia was reliably greater with exercise than with dobutamine, reflecting the greater cardiac workload imposed by exercise. This more extensive ischemia may lead the observer to be more confident in the results of exercise than dobutamine stress testing, despite the image quality being better with dobutamine. The advantages of pharmacologic approaches are feasibility, better image quality, and ability to image the heart during stepwise increments of stress as well as at peak stress. These are balanced by a number of considerations that favor the use of exercise stress in those who can perform it. Exercise stress testing provides a greater level of stress on the heart, renders electrocardiographic data useful (the results of which are less useful with pharmacologic stressors), and gives results regarding functional capacity and data about stress that are readily extrapolated to everyday life. Exercise also offers important prognostic 328

TABLE 14-11 -- Sensitivity and Specific

Study Picano et al[265]

Myocardial CAD Multivessel, Infarction, Patients, CAD, Diameter, n (% all n (% all N n % CAD) CAD) EXERCI 55 34 >70 18 (53) 6 (18) 76

Hoffman et al[81]

50 >70

21 (42)

0 (0)

Cohen et al[76]

37 >70

21 (57)

11 (30)

136

119 >50

11 (9)

41 (34)

Beleslin et al[79]

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Marangelli et al[123]

35 >75

19 (54)

—

Marwick et al[77]

56 >50

34 (61)

0 (0)

Dagianti et al[219]

25 >70

15 (60)

0 (0)

Rallidis et 85 85 >70 [266] al CAD, coronary artery disease.

40 (47)

42 (49)

329

data. Based on these considerations, exercise echocardiography appears to offer more data than the nonexercise approaches, and we limit the use of exercise-simulating techniques to patients who are unable to perform maximal exercise. However, the new techniques that are adjunctive to stress echocardiography (for example, contrast, tissue Doppler, and acoustic quantification echocardiography) are more easily performed in the stationary patient and may lead to an increase in the number of nonexercise studies in the future. Stress Electrocardiography In the current medical-economic climate, much attention is being paid to using less expensive diagnostic and therapeutic methodologies. Because stress electrocardiography is substantially less expensive than stress imaging tests, it might be considered as an alternative to stress echocardiography. In this respect, it is important to differentiate between the stress electrocardiographic component of the pharmacologic tests and

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the exercise electrocardiogram. The latter is an option only if the patient can exercise maximally, and in this situation, both dobutamine and dipyridamole stress echocardiography are as sensitive as or more sensitive than the exercise electrocardiography. Nonetheless, the discussion suggests that if the patient can exercise, the choice should be between the exercise echocardiogram and the exercise electrocardiogram. If the use of nonexercise stress is restricted to patients who cannot exercise, there is little to recommend the use of the pharmacologic stress electrocardiogram, which has poor sensitivity for the diagnosis of coronary artery disease, even if the standard exercise electrocardiographic criteria are altered for use with nonexercise approaches. Although this test should not be performed in isolation, the presence and characteristics of ischemic electrocardiographic changes add useful information about the severity and prognostic implications of an abnormal stress echocardiogram.[206] TABLE 14-12 -- Comparison of Pharmacologic Stress Echocardiography Coronary Arte Patients, Study N Stress 25 Adenosine Nguyen et [267] al Amanullah 40 Adenosine [268] et al Marwick 97 Adenosine [99] et al Marwick 217 Dobutamine [99] et al Forster et 21 Dobutamine [269] al Gunalp et 19 Dobutamine [270] al 61 Dobutamine Senior et [216] al Ho et al[271] 54 Dobutamine Huang et 93 Dobutamine

Sensitivity, % NUC ECHOCARDIOGRAPHY IMA 60 90

Dose 0.14 mg/kg/min 0.14 74 mg/kg/min 0.18 58 mg/kg/min 40 µg 72

94 86 76

40 µg + atropine 30 µg

40 µg

40 µg 40 µg

93 93

98 90

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al[126] Santoro et al[272] San Roman et al[273] Perin et al [274]

Simonetti et al[232] Santoro et al[272] San Roman et al[273]

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60 Dobutamine 40 µg

102 Dobutamine 40 µg + atropine

25 Dipyridamole 0.56 mg/kg 35 Dipyridamole 0.84 mg/kg 60 Dipyridamole 0.84 mg/kg 102 Dipyridamole 0.84 mg/kg

Pharmacologic Stress Echocardiography versus Perfusion Scintigraphy Thallium (or technetium MIBI) imaging has the advantage of being the most widely used imaging technique for the noninvasive diagnosis of coronary artery disease and is technically easier to perform and interpret than is stress echocardiography. However, nuclear imaging has disadvantages pertaining to specificity, cost, and inconvenience to the patient. As there is a substantial variation in the reported accuracy of both stress echocardiography and nuclear imaging, based on variations in the population studied, the relative accuracies of each test can only be addressed by direct comparison in the same patient population. The relative abilities of the tests to deal with the diagnosis of coronary disease, identification of viable myocardium, and prognostic assessment are discussed separately. Bearing in mind the preceding discussion regarding the selection of patients for nonexercise stress, this discussion is confined to patients who are for some reason unable to exercise. Diagnosis of Coronary Artery Disease

Several studies focusing on the comparison of stress echocardiography and scintigraphy using dipyridamole, adenosine, dobutamine, or atrial pacing stress for the diagnosis of coronary disease have been published (Table 14-

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12) . The concordance rates between scintigraphy and echocardiography for the presence or absence of disease range from 80% to 90% in most studies. There are several pertinent points in the interpretation of this literature. First, it is important to have a reference standard (coronary angiography) to judge which test is "wrong" if the results are discordant, despite the inherent selection bias that this design produces toward studying patients with more severe disease, as well as the imperfections of using angiography as the arbiter of disease. Second, because both techniques may be technically demanding and require 330

considerable interpretive skill, studies coming from centers with expertise in one or the other are unlikely to be meaningful. The corollary of this observation is that for the choice even to be considered routine practice, high-quality nuclear and echocardiographic laboratories should be available; if a center has expertise in only one methodology, the alternative should not be considered. Simply put, good scintigraphy is always better than poor stress echocardiography and good stress echocardiography is always better than poor scintigraphy. Using dobutamine or pacing stress, the sensitivities of both tests for the identification of coronary artery disease are comparable, with most studies showing slightly greater sensitivity with scintigraphy (see Table 14-12) . This difference is most evident in patients with single-vessel disease,[207] a finding that might be expected from the identification of flow heterogeneity with perfusion imaging, which is an earlier event in the ischemic cascade than regional dysfunction, identified by echocardiography. For the same reason, antianginal therapy influences the results of echocardiography because it prevents the development of ischemia[115] but does not influence the results of perfusion scintigraphy.[208] On the other hand, the better spatial resolution of echocardiography and the ability to categorize wall motion independently in each segment (contrasting with the relative flow comparisons used in myocardial perfusion imaging) may compensate for its requirement of ischemia. Thus, the similarities in the sensitivity of echocardiography and scintigraphy reflect the balance between the underlying physiology of the tests and their imaging characteristics. In contrast, studies with adenosine and dipyridamole have shown vasodilator stress echocardiography to be significantly less sensitive than perfusion scintigraphy.[209] This

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Figure 14-14 (Figure Not Available) Prognostic content of single photon emission computed tomography (201 TI SPECT) and stress echocardiography scans. The correlation with outcome of the extent of perfusion defect (PDS) and wall motion abnormality (WMS) appears comparable in this exercise stress study. (From Olmos LI, et al: Circulation 1998;98:2679–2686.)

difference is most marked in patients with single vessel coronary disease and reflects failure to develop coronary steal in the absence of extensive coronary disease. This difference in sensitivity is less prominent in patients with multivessel disease. With either dobutamine or vasodilator stress, the specificities of stress echocardiography and perfusion scintigraphy are also comparable, with most series showing a small benefit for echocardiography. Whereas the high sensitivity of myocardial perfusion imaging with SPECT may have been gained at the cost of a sacrifice in specificity, two important sources of false-positive results are patients with left bundle branch block and patients with left ventricular hypertrophy. The influence of left bundle branch block has been investigated in a small number of patients,[210] among whom stress echocardiography produced more favorable results for specificity, although insufficient numbers of patients have been studied to reliably address sensitivity. Patients with hypertension and left ventricular hypertrophy are prone to false-positive SPECT results, probably owing to small vessel disease. Stress echocardiography, especially with dobutamine stress, appears to offer greater levels of accuracy.[211] Prognostic Assessment

Stress myocardial perfusion scintigraphy is widely used for risk stratification of patients undergoing vascular surgery, patients with chronic coronary disease, and patients who have had a myocardial infarction. Unfortunately, although a substantial amount of literature regarding the individual predictive abilities of echocardiography and 331

TABLE 14-13 -- Comparison of Nuclear and Stress Echocardiographic T (Evidenced by Improvement of Regional Left Ventric Sensitivity, % Dobutamine

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DOBUTAMINE Thallium Protocol, THALLIUM SPECT ECHOCARDIOGRA Study Technique µg/kg/min Low-dose, 86 82 Marzullo et al Rest[275] redistribution 10 Low-dose, 95 71 Charney et al Rest[276] redistribution 10 Kostopoulos et RestLow-dose, 90 87 [277] al redistribution 10 Qureshi et al[278] RestHigh-dose, 90 74 redistribution 40 Nagueh et al[279] RestHigh-dose, 91 68 redistribution 40 Low-dose, 92 87 Senior et al[280] Stress (dobutamine)- 10 rest/NTG Arnese et al[281] Stress Low-dose, 89 74 (dobutamine) 10 reinjection Low-dose, 100 79 Perrone-Filardi Stress [282] (dobutamine) 10 et al reinjection Stress Low-dose, 93 85 Bax et al[283] (dobutamine) 10 reinjection Low-dose, 100 94 Haque et al[284] Stress (exercise) 20 reinjection Vanoverschelde Stress High-dose, 72 88 [285] et al (exercise) 40 reinjection High-dose, 87 95 Elsasser et al[286] Stress (dobutamine) 40 reinjection SPECT, single photon emission computed tomography. * Average ejection fraction 38%.

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perfusion imaging is available, comparative data are sparse. In patients undergoing surgery for vascular disease, dipyridamole stress thallium imaging has been shown to have a negative predictive value of more than 90% in most studies.[130] The occurrence of unexpected cardiac events in some patients is probably due to intracoronary thrombus formation on nonsignificant stenoses (which do not cause abnormal perfusion results). The predictive value of ischemia at scintigraphy ranges from 30% to 50%, this result being attributable to positive perfusion studies in the context of mild (prognostically benign) coronary disease and falsepositive results. Overall, these results are comparable to those of pharmacologic stress echocardiography (see Table 14-7) . There are few comparative studies between stress echocardiography and SPECT. The group of Pierard[135] compared the ability of dobutamine stress echocardiography and dobutamine technetium-99m sestamibi SPECT to predict postoperative cardiac events in 156 patients, among whom the adverse event rate was 5.6%. Both tests were characterized by a high negative predictive value (96% for echocardiography; 97% for SPECT). Postoperative cardiac events were predicted by previous cardiac symptoms, a Detsky score of 15 or greater (RR, 3.0), a positive dobutamine echocardiogram (RR, 3.7), and a positive dobutamine SPECT scan (RR, 7.4). In contrast, work by Pasquet et al[212] suggests that the specificity of stress echocardiography exceeded that of SPECT for the prediction of subsequent events. In patients with chronic stable coronary disease and after myocardial infarction, the relative prognostic roles of stress echocardiography and myocardial perfusion scintigraphy appear comparable (Fig. 14-14) (Figure Not Available) . Ischemia may be difficult to identify within segments having abnormal resting function, and this is a source of discrepancy from the findings of perfusion scintigraphy. Because the territory is supplied by the infarct-related artery, the analysis of sensitivity and specificity does not permit discrimination of which test is correct. Preliminary data comparing dipyridamole stress echocardiography and MIBI-SPECT in patients after recent myocardial infarction have shown the finding of ischemia at echocardiography (and not at scintigraphy) to be predictive of subsequent hard events.[213] Diagnosis of Viable Myocardium

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Positron emission tomography, thallium reinjection techniques, and dobutamine echocardiography have all been shown to reliably identify viable myocardium. A significant evidence base has been accumulated regarding the comparison of these variables (Table 14-13) . In one of the initial studies of patients after thrombolysis, dobutamine responsiveness and spontaneous improvement at follow-up were detected in stunned myocardium (normal flow with reduced function), and no dobutamine response correlated with failure to improve at follow-up was seen in infarcted tissue (reduced flow and reduced fluorodeoxyglucose activity). Hibernating tissue (reduced flow with preserved fluorodeoxyglucose activity) was responsive to dobutamine but failed to improve at follow-up, although not all patients in this category underwent myocardial revascularization. The majority of the comparative studies show SPECT techniques to be more sensitive but of lower specificity for the prediction of functional recovery.

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Consequences of Special Characteristics In addition to the effects noted earlier, there are other differences in intravascular ultrasound owing to the use of high frequencies and size constraints. The strength of backscattered ultrasound relative to the incident ultrasound strength is called the backscattering coefficient. This coefficient is determined not only by the composition of the tissue but also by the frequency of the ultrasound. The backscattering coefficient increases with higher frequencies for virtually all tissues, but the rate of increase is different for each tissue, depending on the microscopic structure.[4] In particular, the strength of the backscattered signal from fibrous tissue increases at a rate greater than that of the other tissues in the arterial wall.[5] A fibrous plaque may have strong echogenicity compared with other tissues at 10 MHz, but it still may be less than calcified tissue. At 30 MHz, however, the strength of the signal from fibrous tissue may be equal to or even greater than that from calcified tissue (Fig. 15-7) . Strong echo alone cannot be used to identify the presence TABLE 15-2 -- Comparison of Characteristics of Systems Type of System Electronic Cable, direct Cable, mirror Motor, direct

Resolution Good Very good Very good Very good

Nonuniform Rotation No Yes Yes No

Ring Down Yes Yes No Yes

Figure 15-7 Calcified and fibrous tissue can have very similar echo intensities. This clinical intracoronary image shows an area of dense fibrosis with some calcification. The area of fibrosis extends from 10 to 4 o'clock, but the area from 11 to 1 o'clock, which has the brightest echo

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intensity, also has the least shadowing. This finding indicates that there is calcification in the plaque in all areas except 11 to 1 o'clock. Note the "halo" surrounding the catheter, owing to ring-down artifact.

of calcium in the wall of the vessel, because fibrous tissue may mimic this. Calcified tissue can be distinguished by the additional presence of "shadowing," a profound weakening of signal strength distal to the calcified tissue, owing to the intense attenuation caused by the calcification. Fibrous tissue does not cause this same degree of attenuation, regardless of the intensity of the backscattered signal. Thus, if we see a very bright echo without shadowing, we should suspect that it is fibrous tissue, whereas a bright structure with shadowing should be identified as calcification. It should be noted, however, that the actual classifications are not so clearcut. Fibrous tissue may have microscopic calcifications, which also cause shadowing. Size constraints lead to other practical issues as well. Intravascular ultrasound catheters need a guidewire for placement, and of the several different types that have been developed, the simplest and least flexible is a fixed guidewire at the tip of the catheter. This type of guidewire does not interfere with the imaging function, but it cannot be used for the exchange of catheters over it. A much more adaptable approach is a removable guidewire, but this approach poses the problem of where to place the guide in the already tight constraints of space at the tip of the catheter. For catheters with electronic beam steering, the center of the catheter is free for use by a guidewire because there is no motor or drive cable. For mechanical systems, there is a space problem, which can be solved in one of two ways. The first solution is to have a channel on the outside of the imaging portion of the catheter through which the guidewire can pass. This approach leaves the imaging portion relatively unchanged, but the guidewire is present in the imaging field, causing a bright echo. The second solution is to use the same channel for the guidewire and an imaging core consisting of the transducer and drive cable, alternately withdrawing one to 345

allow passage of the other. This approach has the advantage of a concentric design with no echo from an adjacent guidewire. Because the imaging core

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and the guidewire do not have to occupy the tip at the same time, the tip size can be much smaller. For this reason, this design enables the use of the smallest catheters now available. One final consideration is the need to prepare the catheter. All the mechanical designs must be flushed with fluid before use to provide sound transmission from the transducer to the blood; the presence of even microscopic bubbles can adversely affect image quality. The various designs also differ in how easy they are to flush, depending on the size of the catheter and the size of the flushing channel. This consideration is not applicable with electronically steered systems, because the blood itself provides the contact with the transducer.

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340

Chapter 15 - Principles of Intravascular Ultrasound David T. Linker MD

Intravascular ultrasound is a relatively new technique for imaging a vascular structure from a catheter placed within that structure.[1] The basic physical principles are the same as those for other ultrasound techniques, but the physical constraints and characteristics of a catheter-based imaging technique lead to solutions different from those normally employed in other forms of ultrasound examination. This chapter examines the ways in which the constraints and characteristics of intravascular ultrasound dictate certain forms of design solutions and their consequences on the resultant capabilities of the systems used. The practical consequences for clinical application and future development are also outlined.

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Special Ultrasound Characteristics The principles governing all types of ultrasound imaging are the same, whether the transducers are outside the body, as in transthoracic ultrasound, or within the body, as in transesophageal or intravascular ultrasound. The major differences are transducer size, the distance to the structure being imaged, and the intervening tissues (Table 15-1) . For intravascular ultrasound, these parameters are significantly different. The transducer itself must be very small so that it can be placed inside a catheter, which is inside the arteries or veins. Typical catheter sizes range from less than 1 up to 2.6 mm in diameter. The distance to the structures being imaged is very short, and there is an enveloping layer of fluid (blood) surrounding the transducer at all times. This hom*ogeneous layer of fluid TABLE 15-1 -- Comparison of Intravascular Ultrasound with Other Ultrasound Techniques Technique Transthoracic Transesophageal Intravascular

Transducer Size (cm) >2 45%).[35] In patients with left ventricular systolic dysfunction, a normal pulmonary venous systolic flow pattern indicates a small (0.3 cm2 ) regurgitant orifice, consistent with severe regurgitation. However, blunted systolic flow is much less predictive, as it may be associated with a broad spectrum of regurgitant severity, ranging from trivial to severe regurgitation (Fig. 17-4) .

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To optimize the sensitivity of pulmonary venous systolic flow reversal as an indirect marker of mitral regurgitation severity, it is important to sample both right and left pulmonary veins, since jet direction can influence the pulmonary venous flow pattern.[36] Discordant flow patterns have been observed in the right and left pulmonary veins, with systolic flow reversal demonstrated more 370

Figure 17-2 Summary of the relationship between left atrial pressure hemodynamic and pulmonary venous flow Doppler profiles in 2+, 3+, and 4+ mitral regurgitation (MR). As MR increases, the v wave and v-y descent increase, and the a wave and x-y descent decrease, which is coincident with decreased pulmonary venous systolic (S) flow, increased diastolic (D) flow, and reversed systolic flow (RSF) in 4+ MR. AR, atrial reversed flow velocity. (From Klein AL, Stewart WJ, Bartlett J, et al: J Am Coll Cardiol 1992;20:1345–1352. Reprinted with permission from the American College of Cardiology.) Figure 17-3 Reversal of systolic flow by pulsed Doppler sampling of the pulmonary vein during transesophageal echocardiography in a patient with severe mitral regurgitation.

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Figure 17-4 Regurgitant orifice area and regurgitant stroke volume in three different pulmonary venous flow patterns. Open triangles, normal flow; open circles, blunted flow; solid circles, reversed patterns. Dashed lines indicate regurgitant orifice area of 0.3 cm2 . (From Pu M, Griffin BP, Vandervoort PM, et al: J Am Soc Echocardiogr 1999;12:736–743.)

often in the right pulmonary vein.[33] [34] Other limitations of this indirect method include the influence of other factors on pulmonary venous flow pattern, in addition to left ventricular systolic and diastolic function, including atrial fibrillation, mitral stenosis, ventricular loading conditions, left atrial compliance, and left atrial contractile function.[37] [38] In an effort to account for these other factors, it has been proposed that the systolic component of the pulmonary inflow pattern be expressed as a percentage of

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the total (systolic and diastolic) velocity time integral and then corrected for left atrial filling volume measured from single-plane transthoracic echocardiography. This approach correlated well with Doppler-derived regurgitant fraction[39] however, it remains unclear whether this combined method can be used reliably in patients with acute severe mitral regurgitation, patients with eccentric jets, or patients in atrial fibrillation. Peak E Wave Velocity

Early diastolic mitral inflow is represented by the E wave velocity, which is directly related to the pressure gradient between the left atrium and the left ventricle at the time of mitral valve opening. The added regurgitant volume in mitral regurgitation increases the initial atrial-to-ventricular pressure gradient, thus increasing the peak E wave velocity.[40] A recent retrospective study showed a modest positive predictive value (75%) for an E velocity greater than 1.2 m per second for identifying patients with severe chronic mitral regurgitation. This relationship was independent of other variables such as heart rate, age, and restrictive left ventricular diastolic function.[41] However, increased mitral inflow velocity has also been observed in patients with severe aortic regurgitation.[42] Moreover, the predictive value of this marker has not been tested in patients with acute mitral regurgitation. Therefore, although peak E wave velocity may be a simple screening method for hemodynamically significant mitral regurgitation, it should be not used in isolation to judge regurgitant severity. Aortic Regurgitation Pressure Half-Time

The pressure half-time index represents the time for the peak gradient across the aortic valve in diastole to decay to half of its initial value. Doppler velocity and catheterization pressure half-times have been demonstrated to be linearly related (r = 0.91), with Doppler pressure halftime inversely related to the angiographic grade of aortic regurgitation.[43] Patients with severe aortic regurgitation have a shortened pressure half-time because of the rapid rate of decline in aortic diastolic pressure and rise in left ventricular diastolic pressure, resulting in rapid equalization of aortic and left ventricular pressures (Fig. 17-5) . A Doppler pressure half-time of 400 msec separates mild (1+, 2+) from significant (3+, 4+) aortic regurgitation by angiographic grading with a specificity of 92% and positive predictive value of 90%.[43] Aortic regurgitant severity may be overestimated, however, if the left ventricular end-diastolic pressure is

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elevated because of depressed left ventricular systolic function resulting in a significant overlap in pressure half-times between patients with mild, moderate, and severe regurgitation.[43] In addition, other factors such as stroke volume, aortic and left ventricular compliance, and systemic vascular resistance influence the pressure half-time.[44] Pressure half-time is most useful as an additional method to classify and monitor progression of chronic aortic regurgitation when color flow Doppler methods are discrepant. [45] Deceleration Slope

With increased severity of aortic regurgitation, the diastolic aortic pressure falls rapidly while left ventricular filling pressure rises rapidly, resulting in a steeper deceleration slope on a continuous wave Doppler echocardiogram. Although deceleration slope and pressure half-time both are measured from the continuous wave Doppler curve, deceleration slope is not dependent on the initial pressure gradient. Deceleration slope has been reported to be a better index of regurgitant severity than pressure halftime, demonstrating a close correlation with angiographic grade of regurgitation even in patients with associated aortic stenosis, mitral valve disease, or low cardiac output.[46] A deceleration slope greater than 3 m/sec2 suggests severe aortic regurgitation. Unfortunately, a deceleration slope less than 3 m/sec2 can be seen with mild, moderate, or severe regurgitation. [46] [47] Left ventricular compliance influences the reliability of deceleration slope as an index of aortic regurgitant severity, since a steep slope can be observed in a patient with only mild aortic 372

Figure 17-5 (color plate.) Color Doppler image (A) and continuous wave Doppler image (B) demonstrate severe aortic regurgitation with a pressure half-time of 49 msec and deceleration slope of 18 m per second2 resulting from rapid equalization of pressure between the aorta and left ventricle. (Courtesy of Brad Roberts, RDCS.)

regurgitation but a stiff left ventricle. As with pressure half-time, deceleration slope is influenced by systemic vascular resistance.[44] Thus, pressure half-time and deceleration slope are unreliable methods to assess changes in aortic regurgitation severity in response to vasodilators. However, these approaches may be helpful in assessing whether aortic regurgitation is chronic and well-compensated (flat slope), as compared

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with the steep slope in patients with acute, decompensated regurgitation. Diastolic Flow Reversal

Severe aortic regurgitation is associated with diastolic reversal of flow in the aorta (Fig. 17-6) [48] as well as Figure 17-6 Diastolic flow reversal demonstrated by pulsed Doppler interrogation of the descending aorta in the same patient shown in Figure 17-5 with severe aortic regurgitation. (Courtesy of Brad Roberts, RDCS.)

systolic augmentation of flow within the central aorta.[49] Pandiastolic reversal of flow in the superior abdominal aorta using pulsed Doppler echocardiography from a subcostal window is highly specific and sensitive for predicting severe aortic regurgitation.[50] It is possible to calculate aortic regurgitant fraction from the ratio of reversed to forward flow in the aortic arch using M-mode measurements to account for the systolic and diastolic changes in aortic diameter.[49] However, diastolic flow reversal in the aorta is directly related to aortic compliance, as well as to regurgitant volume. Abnormal diastolic flow patterns can be observed in subjects with abnormal compliance in the proximal aorta or in patients with left to right shunt from the aorta 373

(such as a patent ductus arteriosus).[49] Compared with the ascending aorta, pulsed Doppler interrogation of the descending aorta has been reported to more reliably reflect severity of aortic regurgitation, owing, in part, to the more uniform velocity profiles more distally in the aorta.[51] Other Indirect Markers

High left ventricular diastolic pressure associated with severe acute aortic regurgitation results in echocardiographic findings such as premature closure of the mitral valve or diastolic mitral regurgitation.[52] However, these markers of severe aortic regurgitation are poorly sensitive, being present in fewer than half of the patients with this condition.[42] [52] Increased E/A ratio was reported to be more sensitive for severe symptomatic aortic regurgitation, with greater sensitivity than pressure half-time, M-mode, or color flow mapping for predicting regurgitant severity. [42] [52]

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Tricuspid Regurgitation A reliable marker of severe tricuspid regurgitation is systolic reversal of flow in the hepatic veins and venae cavae (Fig. 17-7) .[53] Another index of severe tricuspid regurgitation is an associated annular diameter greater than 34 mm or greater than 21 mm/m.[28] Intracardiac Pressure Gradients Continuous wave Doppler echocardiography can be utilized to measure instantaneous and mean pressure gradients to assess the hemodynamic effects of regurgitant valvular lesions by using the modified Bernoulli equation. Left atrial pressure can be derived from the mitral regurgitant Doppler signal by subtracting the peak gradient from systolic blood pressure.[54] Similarly, left ventricular end-diastolic pressure can be calculated from the diastolic blood pressure and the aortic regurgitant enddiastolic pressure gradient.[47] [55] However, Doppler consistently overestimates left ventricular end-diastolic pressure because of suboptimal angulation of the interrogating ultrasound beam, resulting in underestimation of the peak velocity and gradient. [47] Therefore, the main limitation of this technique is suboptimal angulation and the inability to obtain a complete high-quality Doppler spectral envelope. When there is a rapid rise in left atrial pressure (V wave), the mitral regurgitant jet may appear asymmetric and cut off in late systole (Fig. 17-8) . Although right ventricular systolic pressure can be estimated from continuous wave Doppler interrogation of flow across a regurgitant tricuspid valve, [54] it is of little value in assessing the severity of tricuspid regurgitation, since increased regurgitant severity results in increased right atrial pressure and decreased peak tricuspid velocity and pressure gradient.

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Quantitative Analysis of the Proximal Flow Convergence Region Principle of Conservation of Mass Accelerating laminar flow patterns have been observed proximal to stenotic, regurgitant, and shunt orifices by Doppler color flow mapping by transthoracic and transesophageal echocardiography.[56] [57] [58] [59] [60] Regurgitant flow rate can be calculated from these laminar flow patterns based on the conservation of mass, which assumes that fluid converges uniformly and radially toward a restrictive orifice, forming a series of concentric isovelocity layers. These isovelocity surfaces are hemispheric for orifices that are small relative to the region of acceleration.[61] Compared to the turbulent downstream jet, this more predictable pattern of flow in the proximal flow convergence region makes quantitation of regurgitant severity possible. By Doppler color flow mapping, the radius (r) of the isovelocity surface is measured as the distance from the orifice to the point of color aliasing (Fig. 17-9) . Instantaneous flow rate can be calculated as the product of the aliasing velocity VA at any of these hemispheric contours times the surface area (2πr2 ) of that shell: Peak flow rate = VA (2πr2 ) (6) This calculation is based on the conservation of mass, which assumes that the accelerating flow through each isovelocity surface equals flow through the regurgitant orifice, since all flow through the isovelocity surface must pass through the orifice.[57] It is also assumed that the isovelocity hemispheric shells in the proximal flow convergence region demonstrate increasing velocity and decreasing surface area as the regurgitant orifice is approached. Each shell is associated with a particular velocity relative to its surface area. In theory, the proximal isovelocity surface area (PISA) derived from this zone of accelerating laminar flow is less dependent on

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instrument[62] and hemodynamic factors that influence the spatial extent of the regurgitant jet in the receiving chamber. Furthermore, unlike the volumetric method, the PISA method has the practical advantage of being independent of other associated regurgitant lesions. Initial in vitro and animal studies have demonstrated the validity of the hemispheric assumption for proximal isovelocity surfaces of small planar orifices relative to the acceleration zone.[57] [59] [63] There have been several clinical studies in patients with mitral or tricuspid regurgitation validating the PISA method using two-dimensional and quantitative Doppler techniques[64] [65] or color Doppler flow mapping.[66] The cause of mitral regurgitation did not affect the correlation of proximal flow acceleration estimates with angiography and quantitative Doppler calculations.[67] The PISA method was less useful in patients with aortic regurgitation in whom the Doppler beam angle exceeded 30 degrees.[66] By multiplane transesophageal echocardiography, comparison of flow rate calculations from the proximal convergence zone with angiographic grades of mitral regurgitation revealed that the proximal flow convergence method better distinguished severe from mild regurgitation than color Doppler area 374

Figure 17-7 (color plate.) Systolic flow reversal in the hepatic veins demonstrated by M-mode (A) and pulsed Doppler images (B) in a patient with severe tricuspid regurgitation. (Courtesy of Brad Roberts, RDCS.)

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Figure 17-8 Continuous wave Doppler with V wave cut-off sign in severe mitral regurgitation (A) with simultaneous hemodynamic tracings (B) demonstrating the pressure relationship that causes the alteration in the deceleration slope of the time-velocity signal (arrows). Note the dark signal intensity of the Doppler signal. In the same patient, increased E wave velocity in A is additional evidence for severe mitral regurgitation. (Courtesy of Rick Nishimura, MD.)

and ratio of systolic to diastolic pulmonary venous flow velocities.[68]

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Technical Considerations The accuracy of the proximal flow convergence method is highly dependent on precise measurement of the PISA Figure 17-9 (color plate.) Color Doppler image of a patient with severe tricuspid regurgitation illustrating the proximal flow convergence zone with the hemispheric blue-to-yellow aliasing contour (blue-yellow interface or Nyquist limit) on the ventricular side of the tricuspid leaflets. (Courtesy of Brad Roberts, RDCS.)

radius, which requires high-resolution imaging and zoom magnification.[63] Furthermore, the proximal flow convergence region is not optimally visualized in all patients with regurgitant lesions, particularly in those with mild regurgitation. [66] [67] , [69] [70] Regurgitant Flow Rate and Aliasing Velocity

Adequate visualization of proximal flow acceleration thus depends on the severity of regurgitation and the aliasing velocity. Patients with very mild mitral regurgitation (regurgitant flow rate less than 20 m per second or regurgitant stroke volume less than 4.5 mL) do not have a visible proximal acceleration zone at the typical Nyquist velocity (VN ) of 49 to 58 cm per

second.[67] Because flow rate is underestimated unless the Nyquist velocity is much less than the orifice velocity, the hemispheric assumption for calculating regurgitant flow rate cannot be used with larger Nyquist velocities.[61] In in vitro models, the measured radius is always higher at lower aliasing velocities for a given flow rate (Fig. 17-10) . [69] Thus, the hemispheric model is most accurate with larger volume flow rates or with lower aliasing velocities. To improve accuracy, the aliasing velocity can be optimized to better define the hemispheric contour. [71] [72] Regurgitant flow rate is systematically overestimated furthest from the orifice and underestimated closest to the orifice because of progressive flattening of the flow convergence region (Fig. 17-11) . Therefore, the hemielliptical model may more accurately reflect flow rates closer to the orifice.[69] In the hemielliptical PISA method, radii from the orifice to the aliasing boundary are measured from long-axis (minor) and short-axis (major) views. This method correlates well with actual volume flow rates under

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Figure 17-10 (color plate.) In this patient with severe mitral regurgitation, the radius of the proximal flow convergence zone appears larger at a lower aliasing velocity of 22 cm per second (A) compared with an aliasing velocity of 33 cm per second (B). (Courtesy of Brad Roberts, RDCS.)

both constant and pulsatile flow conditions. When a flattened proximal convergence zone exists near the orifice, with a major-to-minor axis ratio greater than 2.0, the hemispheric model underestimates the actual volume flow rate by more than 50%. [69] Based on in vitro models, correction factors have been proposed to adjust for errors in flow rates calculated by the PISA method. [61] Orifice Size and Shape

The initial assumption that fluid converges toward an orifice in concentric hemispheric shells applies to an infinitesimally small orifice but cannot be applied to the finite orifice size of regurgitant orifices. In vitro models have demonstrated that the velocity distribution is independent of orifice size if measured at least two orifice diameters from the orifice, in situations in which the hemispheric assumption is valid.[61] In the clinical setting, a discrete Figure 17-11 Diagram of flow converging toward a finite orifice (bottom) showing the streamlines (dotted lines) and the consecutive isovelocity contours (solid lines), illustrating progressive contour flattening as the orifice is approached. (From Vandervoort PM, Thoreau DH, Rivera JM, et al: J Am Coll Cardiol 1993;22:535–541. Reprinted with permission from the American College of Cardiology.)

circular regurgitant orifice is rarely seen. Moreover, irregular or multiple orifices may make application of the PISA method more difficult. It has been proposed, however, that the PISA method can be consistently applied with irregular or multiple orifices if the measurements are obtained at greater distances (at least two orifice diameters) from the orifice.[59] [63] These studies conclude that measurements obtained far from the regurgitant orifice eliminate the influence of orifice size and shape. Other studies have demonstrated that orifice shape does not influence the accuracy of flow rate calculations if the aliasing velocity is small (220-degree) proximal flow convergence angle [83] and overestimation in patients with mitral valve prolapse.[82] Overestimation of EROA in patients with mitral valve prolapse can be explained in part by dynamic changes in the effective orifice area.[84] [85] The PISA method provides instantaneous measurement of regurgitant flow and EROA and thus may not accurately reflect the overall severity of mitral regurgitation over the entire cardiac Figure 17-14 Line plot showing the correlation between effective regurgitant orifice area calculated by the proximal flow convergence method (y-axis) and the Doppler echocardiographic method (x-axis) in the clinical setting of mitral regurgitation. (From Vandervoort PM, Rivera JM, Mele D, et al: Circulation 1993;88:1150–1156.)

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Figure 17-15 Typical examples of the types of dynamic changes in the

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regurgitant orifice area obtained by the electromagnetically determined flow method (EM). The regurgitant orifice size usually increases to maximal size in early to mid-systole (arrow) and decreases in late systole. (From Shiota T, Jones M, Teien DE, et al: J Am Coll Cardiol 1995;26:528–536. Reprinted with permission from the American College of Cardiology.)

cycle. Furthermore, the dynamic changes in EROA do not necessarily parallel the changes in regurgitant volume.[84] In late systole, despite continued increase in EROA, there is a decrease in the ventriculoatrial gradient and regurgitant velocity.[53] Experimental and clinical data further support the observation that the mitral regurgitant orifice changes dynamically during systole (Fig. 17-15) .[80] [86] Furthermore, the temporal variation in mitral regurgitant orifice area during systole varies according to the underlying cause.[86] Thus the PISA method of calculating EROA has the potential advantage of identifying the dynamic changes in regurgitant orifice area during the cardiac cycle. Changes in EROA are measured sequentially during the cardiac cycle by color M-mode echocardiography from the zenith of the isovelocity hemisphere.[80] [85] [86] The clinical implications of these data are that the EROA is not completely independent of hemodynamic variables and its changes may explain the beneficial effects of vasodilator therapy on functional mitral regurgitation.[77] In contrast, the existence of dynamic changes in aortic regurgitant orifice area is controversial.[87] [88] Dynamic changes have also been observed in the tricuspid regurgitant orifice area using the proximal flow convergence method.[89] Regurgitant Volume Although the calculation of regurgitant flow rate by the PISA method is relatively simple, requiring only the measurement of the isovelocity radius and aliasing velocity in a single view, it estimates peak, but not mean, flow rate. The measurement of regurgitant volume (RV) may be more accurate and clinically useful because the inclusion of the time velocity integral (TVI) by continuous wave Doppler may better reflect regurgitant jet dynamics during the cardiac cycle[64] [90] [91] RV = EROA × TVI (10) When regurgitant volume and flow rate by the PISA method are compared with angiographic grading of mitral regurgitation, PISA-derived regurgitant volume is better than flow rate at distinguishing 4+ mitral regurgitation from the other regurgitant grades.[71]

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In addition to the technical considerations that affect the validity of the hemispheric assumption of the PISA method, there are a number of limitations of this method for estimating regurgitant volume and flow rate. Since the PISA method relies on color Doppler to identify the region of proximal flow convergence, it is limited by technical factors that influence the accuracy of color Doppler flow mapping. Of these factors, the angle between the Doppler beam and direction of blood flow is most critical. The angle of the central PISA radius and the ultrasound beam must approach zero for optimal accuracy.[66] Other technical factors to be optimized include wall filter settings, interrogation depth, pulse-repetition frequency, and spatial beam expansion.[92] Furthermore, translational motion of the valve annulus affects the apparent PISA velocity, with overestimation with movement in the same direction[93] and underestimation with movement away from the PISA velocity shift.[94] Moreover, when the entire flow crossing the aliasing boundary does not pass through the restrictive orifice, as in ventricular septal defects,[93] the conservation of mass principle is not strictly applicable. Although attempts have been made to standardize the PISA method to calculate regurgitant flow, the optimal instrument settings for aliasing velocity and its corresponding radius remain unclear.[72] [91] [95] Furthermore, the accuracy of the PISA method is highly dependent on precise measurement of the radius from the orifice. Theoretically, the higher frequency imaging of transesophageal echocardiography provides improved spatial resolution and lower color aliasing velocity, which should improve the accuracy of the radius measurement.[96] Although attempts have been made to better define the radius by high-resolution imaging with zoom magnification, the exact position of the regurgitant orifice may still remain elusive.[70] [97] Errors in measurement of the PISA radius could result in significant errors in the estimation of volume flow. Vandervoort et al[97] propose an automated algorithm to locate the regurgitant orifice from a computer-simulated flow field, but this approach is not widely available.

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Vena Contracta Width Experimental and Clinical Validation The vena contracta width is defined as the narrowest diameter of regurgitant flow immediately downstream from the flow convergence region (Fig. 17-16) . Although, like proximal jet size, it is relatively unaffected by flow rate and driving pressure,[21] [98] vena contracta width is not identical to proximal jet size, since vena contracta width requires measurement of the diameter at the narrowest portion of regurgitant flow between the flow convergence region and the downstream turbulent jet.[99] Furthermore, the vena contracta width more directly reflects 379

Figure 17-16 (color plate.) Transesophageal imaging in the long-axis view demonstrates the vena contracta width as the narrowest extent of regurgitant flow immediately downstream from the flow convergence region in this patient with severe mitral regurgitation.

changes in the size of the regurgitant orifice.[100] Unlike proximal jet width, vena contracta width remains accurate in the presence of eccentric jets (Fig. 17-17) . [99] [101] [102] [103] [104] [105] The feasibility of measuring the vena contracta is 92% to 97% in patients with mitral regurgitation with minimal inter-observer variability.[100] [104] [106] Multiplane transesophageal echocardiography was shown to be more accurate than single plane imaging.[106] [107] Thus, the vena contracta method has been proposed to be a simple yet accurate method of assessing mitral regurgitant severity intraoperatively.[107] [108] Furthermore, vena contracta width is more predictive of the severity of mitral regurgitation than color Doppler jet area, left atrial size, and pulmonary venous flow.[104] Since mitral regurgitation worsens in the anteroposterior

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Figure 17-17 Linear regression plot showing good correlation between vena contracta width in the parasternal long-axis view and regurgitant volume (left) and regurgitant orifice area (right). Solid circles represent eccentric mitral regurgitation jets; open circles central jets. (From Hall SA, Brickner ME, Willett DL, et al: Circulation 1997;95:636–642.)

direction of the mitral valve orifice, accurate measurement of the vena contracta is obtained from long-axis views by transthoracic and transesophageal echocardiography. [100] [104] , [106] For mitral regurgitation, a vena contracta width of 5 mm or greater identifies severe mitral regurgitation, and a vena contracta width of 3 mm or less identifies mild mitral regurgitation.[104] In clinical and animal studies of aortic regurgitation, the vena contracta width correlates well with quantitative Doppler and electromagnetic flowmeter measurements, [103] [105] so that a vena contracta width of 6 mm or greater predicts severe aortic regurgitation, whereas mild aortic regurgitation is identified by vena contracta width of less than 5 mm.[105] EROA is estimated from the vena contracta width (VCW) by the following equation: EROA = π(VCW/2)2 (11) The estimated EROA and regurgitant volume flow correlated well with reference measurements by electromagnetic flowmeter (Fig. 17-18) .[103] A vena contracta width of 6.5 mm or greater predicts severe tricuspid regurgitation and correlates with EROA significantly better than visual estimates of jet area, which are influenced by right atrial pressure.[99] Clinical Considerations Accurate measurement of the vena contracta width is critically dependent on imaging with optimized axial resolution. Imaging views with poor lateral resolution result in artifactual widening of the flow signal and overestimation of regurgitant lesion severity. Precise imaging of the vena contracta requires smaller sector angles, high frame-rates, high resolution, appropriate color and tissue priority, and zoom mode magnification. However, the vena contracta width may be difficult to measure with poor acoustic windows, orifice movement, or rapid divergence of the jet beyond the orifice. Vena contracta width is not a direct measurement of regurgitant orifice area and is actually smaller than the anatomic orifice by a factor 380

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Figure 17-18 Correlation between peak regurgitant flow rates calculated by color Doppler vena contracta and electromagnetic flow meter methods. (From Ishii M, Jones M, Shiota T, et al: Circulation 1997;96:2009–2015.)

of 0.8 (coefficient of contraction). There is considerable overlap of actual regurgitant orifice areas in the intermediate mitral regurgitant vena contracta width range between 3 and 5 mm.[104] Therefore, regurgitant lesions in the intermediate vena contracta range may require additional methods of quantitation to more fully assess regurgitant severity.[109] In addition, the vena contracta width as a single measurement does not reflect dynamic changes in the regurgitant orifice during the cardiac cycle. In the presence of an irregular regurgitant orifice, multiple vena contracta width measurements in more than one plane may be necessary to improve accuracy.[103] [106] [109] , [110] Three-dimensional imaging of the vena contracta area accurately measures mitral regurgitant orifice by transesophageal echocardiography intraoperatively and may become the approach of choice as three-dimensional methods become clinically feasible.[108] The value of vena contracta width in the presence of multiple or diffuse regurgitant jets or atrial fibrillation is not known.

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Conservation of Momentum Theoretical Background Based on experimental studies of fluid dynamics of turbulent jet flow, the velocity distribution of the jet in the receiving chamber is best characterized by its momentum, which combines several factors such as flow rate, driving pressure, orifice velocity, and orifice area.[111] In the absence of a pressure gradient within the receiving chamber because of an adjacent wall or counterflow from another orifice, momentum should remain constant within the turbulent jet.[112] The principle of momentum conservation states that the momentum measured anywhere in the downstream jet is the same as the momentum of the jet at its orifice: Momentumorifice = Momentumjet (12) At the orifice, momentum is calculated by the product of jet velocity (Vo ) and flow rate (Q):

Momentumorifice = Vo Q (13) Thus, the regurgitant orifice flow rate (Q) can be calculated from jet momentum (M) measured anywhere along the extent of the jet, divided by orifice velocity (Vo ), measured by continuous wave Doppler[113] Q = M/Vo (14) Methods for Quantitation of Momentum In an in vitro model, when jets are formed through 0.005 to 0.5 cm2 orifices at a driving pressure of 1 to 81 mm Hg, the velocity distribution

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downstream conforms to a gaussian (bell-shaped) profile with the centerline velocity decaying inversely with distance from the orifice.[113] Jet momentum (M) flux can be calculated across the transverse plane of the jet by integrating flow velocity (v) across the area (A) of the jet in that plane: M = ∫A v2 dA (15) For an axisymmetric jet (circular cross section), momentum can be calculated from a single velocity profile across the jet: M = 2 π∫0 ∞v2 rdr (16) where r is the radial distance from the jet centerline to a point at which each velocity is measured. Thus, orifice flow rate can be accurately calculated by dividing momentum by the orifice velocity using equation 14. Effective regurgitant orifice areas then can be calculated by dividing momentum by the square of the orifice velocity: EROA = M/Vo 2 (17) An alternative approach, based on data from an in vitro pulsatile model, is to measure only the centerline velocity (Vc ), which is inversely proportional to the distance (x) from the orifice[114]

Vc (x) = 7.8√M/x (18) Then flow rate (Q) can be calculated by recording a single centerline velocity (Vc ) at a distance x from the orifice as well as orifice velocity

(Vo ):

Q = Vc 2 x2 /60.8Vo (19) The flow convergence centerline velocity/distance methods correlated well with reference methods in small

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381

clinical[115] and animal[116] studies that quantitated mitral and aortic regurgitation. The proposed benefit of the centerline velocity method over the PISA method is that the use of several data points instead of a single velocity data point improves accuracy.[116] Clinical Practice In spite of experimental validation and proposed theoretical advantages of using jet momentum or centerline velocity methods to quantitate valvular regurgitation, these methods are rarely used in the clinical setting for several reasons. First, since it has been reported that free jets are observed in only 60% to 70% of patients with mitral regurgitation,[10] the critical assumption of a free axisymmetric jet may not apply to a significant number of patients with eccentric jets in whom momentum is not conserved because of jet impingement on an adjacent wall or interference from pulmonary venous counterflow. It has been demonstrated that eccentrically directed jets are significantly underestimated by the momentum quantification method.[117] Moreover, application of the centerline velocity profile method requires accurate resolution of velocities within the turbulent jet, which is difficult because aliasing due to high velocities is often seen with mitral regurgitation. The considerable variation in the instantaneous velocity and position of the jet axis during the cardiac cycle requires data averaging using the simplified centerline velocity equation. Finally, the applicability of these methods is not known with varying size and compliance of the receiving chamber. Thus, these practical considerations limit the routine use of these momentum-based methods of quantification in the clinical setting.

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Amplitude-Weighted Mean Velocity Amplitude-weighted mean velocity is a nonvolumetric method for calculating the ratio of flow in shunt and regurgitant lesions based on the theory that the amplitude of the recorded Doppler signal is proportional to the number of erythrocytes contributing to the backscattered signal. This approach assumes a hematocrit within the normal range.[118] The amplitudeweighted mean velocity is calculated as the sum of the individual velocities of the erythrocytes within the continuous wave Doppler spectrum multiplied by their respective signal amplitudes.[118] Therefore, the basis of this approach is that each velocity is weighted according to the strength of its signal. Applying this concept over the cardiac cycle, the flow volume during a given time interval is proportional to the time integral of the average weighted mean velocity. Therefore, regurgitant fraction (RF) can be calculated as follows:

where the amplitude-weighted mean flow (AWMF) is measured at the regurgitant valve (regurg. valve) and at a competent reference valve (ref. valve). [119] The advantages of this method are that measurement of valvular surface areas is not necessary and its accuracy is not impaired in the presence of mitral valve prolapse. Regurgitant fraction calculated by the amplitudeweighted mean velocity method has been shown to correlate with ventriculographic[118] [120] and quantitative Doppler and two-dimensional echocardiographic findings.[119] There are technical considerations that limit the amplitude-weighted mean velocity method for calculation of regurgitant severity, however. These include the requirements that the continuous wave Doppler beam be of adequate width to include the entire area of the regurgitant signal (for example, the entire mitral annulus). In addition, the beam must be directed

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properly to avoid inclusion of adjacent flows, and the transducer must be maintained in the same position throughout the recording period to avoid translational motion from one valve to another. Furthermore, determination of the amplitude-weighted mean velocity varies with instrument gain settings and the effect of depth on signal strength. Thus, the ratio of amplitude-weighted mean velocity from the mitral valves to that from the aortic valves may not yield a value of 1.0, even in the absence of valvular regurgitation.[119] In addition to requiring a normal hematocrit, this method is applicable only in the setting of isolated regurgitant lesions, since separation of erythrocytes from blood plasma may falsely elevate the signal amplitude recorded from stenotic lesions.[118] Because the amplitude-weighted mean velocity is dimensionless, its measurement does not represent a physiologic variable and does not allow calculation of regurgitant volume or regurgitant orifice area. Thus, amplitude-weighted mean velocity may best be used as an adjunctive tool to quantitate valvular regurgitation. Finally, the requirement of special software limits the use of this approach in the clinical setting.

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Three-Dimensional Echocardiography Three-dimensional echocardiography is an evolving technique that has been applied for the assessment of intracardiac anatomy,[121] [122] for quantification of intracardiac volumes, [123] and to better characterize mitral valve morphology by multiplane transesophageal echocardiography.[124] Initial three-dimensional reconstruction of color Doppler flow mapping for shunts and valvular regurgitant jets could only be visualized in gray scale and did not include quantitative information or comparison with actual flow rates.[125] [126] However, more recent in vitro studies have demonstrated that regurgitant flow may be accurately quantitated by three-dimensional reconstruction for bioprosthetic valves[127] and for varying native valve orifice shapes and jet morphologies.[110] In a preliminary clinical study, three-dimensional reconstruction has also been shown to accurately quantitate mitral regurgitant orifice area compared with the proximal flow convergence method intraoperatively in patients undergoing mitral valve repair.[108] Although early attempts to obtain color-coded images from threedimensional reconstruction required manual digitization of Doppler flow signals,[125] more recent studies 382

have demonstrated three-dimensional reconstruction of Doppler signals in original color coding by using direct digital data, which allows separate visualization of intracardiac flow and cardiac structures.[128] [129] These threedimensional images reveal the complex geometry of eccentric regurgitant jets in patients with mitral valve prolapse and demonstrate how misleading two-dimensional visual assessment or planimetry of regurgitant jets can be ( Fig. 17-19 and Fig. 17-20 ).[128] , [129] Since recent three-dimensional volumes are measured by an automated segmentation and voxel count procedure, they are independent of manual planimetry or subjective

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estimation. The technical and hemodynamic factors that influence color Doppler flow imaging also influence three-dimensional Doppler images.[129] However, the main limitation of three-dimensional echocardiography is the need for stable positioning of the transducer during image acquisition or a method to continuously track transducer position relative to cardiac structures. Another limitation is that three-dimensional reconstruction is time consuming, and the presence of irregular heart rhythms such as atrial fibrillation can significantly prolong the process. Furthermore, the timerelated changes of three-dimensional jet Figure 17-19 (color plate.) A, Transesophageal color Doppler images in a patient with a mitral regurgitant jet recorded at different rotational angles (0 and 90 degrees). B, Three-dimensional reconstruction of the central regurgitant jet in a patient with atrioventricular septal defect. (From De Simone R, Glombitza G, Vahl CF, et al: Eur Heart J 1999;20:619–627.)

areas and volumes have not yet been characterized. Some of these limitations will be overcome in the future with the advent of real-time three-dimensional echocardiography.

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Clinical Implications The quantitation of valvular regurgitation is important, not only for the early detection of hemodynamically significant lesions but also for monitoring of therapeutic success. It has been suggested that not all patients respond favorably to vasodilator therapy, and quantitative methods can thus assist in differentiating patients by their response to therapeutic interventions.[130] [131] [132] However, the quantitative assessment of valvular regurgitation is a far more complex issue than the measurement of such variables as regurgitant volume, regurgitant fraction, and regurgitant orifice area. In addition to the anatomy of the regurgitant lesion, its hemodynamic impact should also be taken into account, since symptoms are not necessarily related to regurgitant severity.[32] [133] A semiquantitative index has been proposed that incorporates variables reflecting 383

Figure 17-20 (color plate.) A, Transesophageal color Doppler images show a wall-impinging mitral regurgitant jet at different angles (0 and 90 degrees). None of these conventional views is able to visualize the regurgitant jet entirely. B, Three-dimensional Doppler reconstructions show that the regurgitant jet resembles a spoon. The lower panel shows the convex face of this spoon jet. (From De Simone R, Glombitza G, Vahl CF, et al: Eur Heart J 1999;20:619–627.)

384

TABLE 17-1 -- Calculation of the Mitral Regurgitant Index Characteristic Jet penetration

Score Description 0 No jet

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1 2

PISA

CW jet

3 0 1 2 3 0 1 2 3

Pulmonary artery pressure Pulmonary venous flow

0 1 2 3 0

Central jet that does not impinge on lateral wall in any view Eccentric jet that extends to the pulmonary vein Eccentric jet that encircles the atrium No PISA visualized PISA ≤0.5 cm radius PISA 0.5–1.0 cm PISA ≥1.0 cm No jet detected Incomplete jet envelope Complete envelope, jet density 20%–50% of mitral inflow Complete envelope, jet density 50%–70% of mitral inflow 45 mm Hg Systolic flow exceeds diastolic flow by ≥50%

1 Systolic flow exceeds diastolic flow by systolic flow 3 Systolic flow reversal Left atrial 0 None enlargement 1 Mild 2 Moderate 3 Severe The mitral regurgitant index = total score/number of variables CW, continuous wave Doppler ultrasonography; PISA, proximal isovelocity surface area. From Thomas L, Foster E, Hoffman JIE, et al: J Am Coll Cardiol

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1999;33:2016–2022. the hemodynamic impact as well as characteristics of the regurgitant jet (Table 17-1) .[133] The same regurgitant volume may be associated with changing valve structure and varying degrees of chamber dilation and function. Furthermore, echocardiographic signs of severe chronic regurgitation may not be applicable in the acute setting. Although volumetric and proximal isovelocity surface area methods have been validated both clinically and experimentally, these methods are rarely applied in routine clinical practice because they are time consuming and highly dependent on operator experience. Indirect TABLE 17-2 -- Proposed Doppler Criteria for Identifying Severe Valvular Regurgitation by the Transesophageal Approach Mitral Regurgitation Jet area/left atrium area >40% Regurgitant fraction >40% Vena contracta width >5.5 mm Systolic pulmonary vein flow reversal Present Aortic Regurgitation Vena contracta width >12 mm Pressure half-time of regurgitant flow 18 cm/sec Modified from Tribouilloy C, Shen WF, Leborgne L, et al: Éur Heart J 1996;17:272–280.

TABLE 17-3 -- Summary of Echocardiographic Methods to Quantify Valvular Regurgitation Method Doppler color flow mapping

Volumetric Doppler

Limitations Jet area represents velocity not volume and is influenced by driving pressure, receiving chamber compliance, regurgitant orifice size, and instrument factors. Underestimation of severity occurs with eccentric jets. Accurate in experienced hands, yet time consuming. Greatest measurement of mitral or

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aortic cross-sectional area. Requires competent valve to measure forward stroke volume. Pulmonary venous In addition to severe MR, systolic-to-diastolic flow pulmonary flow ratio may be influenced by other variables, such as LV function, LA compliance, atrial fibrillation, mitral stenosis, loading conditions, sampling of left vs. right pulmonary vein. AR pressure half-time Both markers are less reliable when systemic and deceleration slope vascular resistance is altered or in the presence of LV dysfunction with significant overlap of values for varying degrees of AR severity. Aortic diastolic flow Related to regurgitant volume and aortic reversal compliance. Proximal flow Relies on hemispheric geometric assumptions. convergence Requires selection of optimal aliasing velocity and identification of the orifice for precise measurement of the radius. Overestimation of flow is observed with eccentric jets. Vena contracta width Simple and accurate but requires optimal axial resolution and imaging plane for clear definition. Limited with rapidly divergent jets and overlap in lesion severity between 3–5 mm. Momentum Measures flow rate and ROA from a single velocity profile across an axisymmetric jet. Validated in vitro but rarely used clinically. Not applicable to eccentric jets. Amplitude-weighted Nonvolumetric method for calculating ratio of flow mean velocity based on the amplitude of the Doppler signal. Requires special software. Three-dimensional Reveals the complex geometry of regurgitant echocardiography lesions. Requires stable positioning of transducer and patient during image acquisition, which may be time consuming. AR, aortic regurgitation; LA, left atrium; LV, left ventricle; MR, mitral regurgitation; ROA, regurgitation orifice area.

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markers are affected by other variables and should not be used in isolation to determine regurgitant severity (Table 17-2) . Although there are many proposed echocardiographic methods to quantify valvular regurgitation (Table 17-3) , the main limitation has been the lack of a true gold standard for comparison.[27] [134] The challenge to future investigations in this area is to develop a better gold standard for quantifying valvular regurgitation by extracting more reproducible yet accurate spatial, temporal, and velocity information from color Doppler imaging.

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389

Chapter 18 - The Role of Echocardiography in the Timing of Surgical Intervention for Chronic Mitral and Aortic Regurgitation David J. Meier MD Carolyn K. Landolfo MD Mark R. Starling MD

The optimal timing of surgical intervention in patients with chronic mitral and aortic regurgitation remains controversial and challenging. Historically, mitral and aortic regurgitation have been considered hemodynamically equivalent as conditions of left ventricular (LV) volume overload.[1] Although mitral regurgitation is a condition of primary LV volume overload, aortic regurgitation generates both a pressure and a volume overload on the left ventricle. In both conditions, preload is elevated because of excess volume, resulting in the development of eccentric hypertrophy. In aortic regurgitation, however, afterload is also increased secondary to LV pressure overload, resulting in the development of concomitant concentric hypertrophy. These fundamental hemodynamic differences are responsible for the observed differences between mitral and aortic regurgitation in the natural history of the disease processes, mechanisms for LV systolic dysfunction, response to surgery, and the appropriate timing of surgical intervention.

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After a long asymptomatic period, often lasting several years, prolonged mitral or aortic regurgitation inevitably leads to LV pump dysfunction, which is characterized by decreased LV ejection fraction and contractile dysfunction. [2] [3] [4] [5] [6] [7] [8] In assessing LV pump performance in valvular regurgitation, it is important to distinguish between ejection performance and contractile performance of the left ventricle. Left ventricular ejection performance, commonly measured by indices such as ejection fraction and percent fractional shortening, refers to the global pumping capability of the left ventricle. Because LV ejection phase indices are affected by multiple variables, such as contractility, heart rate, preload, and afterload, an abnormal LV ejection fraction does not necessarily imply abnormal contractility. Likewise, LV ejection fraction may be normal, despite significant underlying contractile dysfunction. Left ventricular contractility, on the other hand, refers specifically to the performance of the contractile apparatus of the left ventricle, independent of loading conditions. Although both mitral and aortic regurgitation eventually lead to LV pump dysfunction, the mechanisms underlying decreased LV pump performance differ between the two conditions. Wisenbaugh et al[9] evaluated the hemodynamic characteristics of patients with severe aortic regurgitation (n = 9) and severe mitral regurgitation (n = 8) and compared the findings to those of normal subjects (n = 7) (Fig. 18-1) . Despite a similar volume of regurgitation between the patients with aortic and mitral regurgitation, afterload (end-systolic stress) was found to be significantly increased above control in patients with aortic regurgitation, but not in patients with mitral regurgitation. Conversely, LV contractile dysfunction, measured by the ratio of end-systolic stress to end-systolic volume index, was found to be more depressed in patients with mitral regurgitation than in patients with aortic regurgitation, despite comparable reductions in LV ejection fraction. These data suggest that the mechanism for decreased LV pump performance in aortic regurgitation is afterload excess, in contrast to mitral regurgitation, in which LV contractile dysfunction is the primary mechanism. Because 390

Figure 18-1 The relationship between left ventricular ejection fraction (EF) and end-systolic stress, constructed from the data of Wisenbaugh et al,[9] is illustrated for normal subjects and patients with mitral (MR) or aortic (AR) regurgitation. End-systolic stress or afterload is increased only in the AR group. (From Devlin WH, Starling MR: Cardiol Rev 1994;3:16–28.)

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of the favorable loading conditions in mitral regurgitation, however, ejection phase indices of LV systolic performance often remain normal, thereby masking the severity of LV contractile dysfunction. Although afterload excess is the primary mechanism for LV pump dysfunction in aortic regurgitation, contractile dysfunction also contributes to decreased LV pump performance, but typically as a late manifestation of severe, prolonged regurgitation.[11] These hemodynamic differences between mitral and aortic regurgitation have very important clinical implications, both in terms of disease progression and in response to corrective surgery. Because afterload excess is responsible for the early decline in LV pump performance in aortic regurgitation, the decrease in afterload that follows aortic valve replacement favors improvement in LV systolic performance, even when preoperative LV ejection phase indices are depressed.[12] [13] [14] [15] [16] [17] Later in the course of the disease, however, significant contractile dysfunction also develops, resulting in progressive and potentially irreversible LV failure. In contrast, contractile dysfunction develops relatively early in the natural history of mitral regurgitation, but it may be masked by the favorable preoperative loading conditions and the compensatory activation of the sympathetic nervous system with resultant beta-adrenergic stimulation.[18] [19] [20] [21] [22] [23] [24] Postoperatively, as loading conditions change with elimination of the regurgitant leak into the low-resistance left atrium, this underlying contractile dysfunction becomes unmasked, resulting in a decreased in LV ejection fraction.[5] [6] [7] [16] [25] [26] [27] [28] [29] Patients with mitral regurgitation who have even a mildly depressed LV ejection fraction preoperatively often have severe contractile dysfunction and are, therefore, at risk for significant LV systolic dysfunction, congestive heart failure, and death in the postoperative period.[4] [5] [6] [7] [8] However, in patients with occult contractile dysfunction marked by a mildly elevated end-systolic dimension in the presence of a normal LV ejection fraction, recovery of contractile function often does occur postoperatively.[30] Thus, these data highlight the clinical imperative in mitral regurgitation to identify early, occult, but potentially reversible contractile dysfunction to optimize the long-term results of mitral valve surgery. This is important because there appear to be two populations of patients: those in whom contractility improves and those in whom contractility does not improve following mitral valve surgery.

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Therefore, because reduced LV ejection fraction reflects more severe contractile dysfunction in mitral compared with aortic regurgitation, a greater degree of preoperative LV pump dysfunction is tolerated without adverse clinical outcome in aortic regurgitation, provided that the duration of LV pump dysfunction is brief. Prolonged LV pump dysfunction reflects severe contractile dysfunction in both mitral and aortic regurgitation and is associated with an adverse postoperative outcome. The ability to identify contractile dysfunction and correct the regurgitant lesion before contractile dysfunction becomes irreversible is critical to the timing of surgical intervention for both regurgitant valve lesions. Although contractile dysfunction is the mechanism for the early decrease in LV ejection fraction in mitral regurgitation, the type of operation performed also significantly affects the degree of postoperative LV pump dysfunction. [31] [32] [33] [34] [35] [36] [37] [38] [39] [40] [41] LV ejection fraction almost always declines after conventional mitral valve replacement with removal of the submitral apparatus, even when preoperative indices of LV pump performance are normal.[31] [32] [33] [36] [37] This decline of LV ejection fraction has been attributed to an alteration in LV geometry resulting from transection of the chordae tendineae and removal of the papillary muscles. Conversely, LV ejection fraction is not decreased to the same extent after mitral valve reconstruction or mitral valve replacement with preservation of the submitral apparatus.[31] [32] [33] , [40] Therefore, because mitral valve reconstruction preserves LV pump performance and can be performed with a low operative morality rate and low risk for thromboembolism and endocarditis, earlier surgical intervention has been advocated in all patients in whom valve repair is feasible, particularly those with reduced LV pump performance. [42] The major challenge in the management of patients with valvular regurgitation is the ability to identify contractile dysfunction and to correct the regurgitant lesion before irreversible contractile dysfunction develops. The purpose of this chapter is to present the echocardiographic parameters that can be used to guide timing of surgical intervention in aortic and mitral regurgitation. Because LV contractility dysfunction is the most important determinant of survival and postoperative outcome in valvular regurgitation, the primary goal guiding the timing of surgical intervention is assumed to be preservation of contractility. Unfortunately, many noninvasive variables currently used to guide surgical intervention identify patients likely to do poorly after surgery, but they do not pinpoint the onset of occult, reversible contractile dysfunction when timely operative

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intervention would be warranted. [11] [18] , [26] [28] The proposed algorithms presented in this chapter for the evaluation of patients with valvular regurgitation incorporate clinical, hemodynamic, and echocardiographic variables into rational guidelines for 391

appropriate timing of surgical intervention directed toward the long-term preservation of contractility.

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Pathophysiologic Mechanisms Although LV volume overload is the primary hemodynamic abnormality in mitral regurgitation, both pressure and volume overload exist in aortic regurgitation. [1] Significant elevations in preload caused by increased regurgitant volume in both mitral and aortic regurgitation lead to the development of eccentric hypertrophy, characterized by LV enlargement and increased myocardial mass.[2] [3] [20] The degree of hypertrophy is commensurate with the degree of LV dilation, maintaining the ratio of LV mass to end-diastolic volume within the normal range. In addition to eccentric hypertrophy, increased systolic wall stress (afterload) in aortic regurgitation also leads to the development of concentric hypertrophy.[1] [9] The differences in the compensatory mechanisms of the left ventricle to pure volume overload in mitral regurgitation and both pressure and volume overload in aortic regurgitation account for the observed difference in disease progression, changes in LV pump performance, and response to operation. Mitral Regurgitation Acute Mitral Regurgitation.

The pathophysiologic mechanisms underlying mitral regurgitation have been well reviewed by Carabello.[43] [44] Left ventricular ejection fraction increases in acute mitral regurgitation as a result of increased preload and decreased afterload. In acute mitral regurgitation, the left ventricle compensates for the sudden increase in volume by increasing sarcomere diastolic length (preload). Left ventricular end-diastolic volume increases, leading to augmentation of LV stroke work by the Frank-Starling mechanism. In addition to increased preload, systolic ejection of blood through the incompetent mitral valve into the low-impedance left atrium lowers systolic wall stress (afterload). Decreased afterload, in turn, augments ventricular emptying, resulting in reduced end-systolic volume,

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increased total stroke volume, and increased ejection fraction. In acute mitral regurgitation, therefore, the left ventricle compensates for the volume overload by emptying more completely. Chronic Compensated Mitral Regurgitation.

The transition from the acute to the chronic state of mitral regurgitation is characterized by LV enlargement and compensatory eccentric hypertrophy, resulting in an increase in LV end-diastolic volume and mass. The increase in LV end-diastolic volume enables augmentation of total stroke volume, helping to return forward stroke volume toward the normal range. With the development of eccentric hypertrophy, the radius of the left ventricle increases without a significant change in wall thickness, increasing wall stress into the normal range, in accordance with the law of Laplace. As wall stress increases into the normal range, LV emptying decreases and endsystolic volume increases. In the compensated phase, therefore, the increase in LV end-diastolic volume produced by increased preload and the increase in end-systolic volume result in an ejection fraction that is within the normal range, but less than that of the acute stage. Chronic Decompensated Mitral Regurgitation.

As a result of these compensatory mechanisms and the stimulation of the sympathetic nervous system, patients with chronic mitral regurgitation may remain asymptomatic for long periods of time and LV ejection phase indices may remain normal, despite underlying contractile dysfunction. Eventually, contractility declines beyond the compensatory capabilities of the left ventricle and the sympathetic nervous system.[24] With LV decompensation, ejection fraction decreases because of an increase in endsystolic volume. Left ventricular end-diastolic pressure increases, resulting in further eccentric hypertrophy and LV dilation. With progressive increases in the radius of the left ventricle, wall stress increases above normal, resulting in a significant increase in end-systolic volume. A vicious cycle thus evolves, leading to a progressive decline in LV pump performance. Response to Operation.

In compensated mitral regurgitation, correction of the regurgitant lesion results in a decrease of LV end-diastolic volume and end-diastolic dimension into the normal range. Although postoperative end-systolic stress remains normal, LV ejection fraction decreases in nearly all patients

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after mitral valve replacement with removal of the submitral apparatus.[45] Left ventricular ejection fraction generally remains unchanged in patients with compensated mitral regurgitation who undergo mitral valve reconstruction or mitral valve replacement with preservation of the submitral apparatus.[31] [32] [33] [34] , [40] In decompensated mitral regurgitation, there is marked preoperative LV enlargement, elevation in end-systolic wall stress, and decreased fiber shortening. [45] Postoperatively, the left ventricle remains persistently dilated, end-systolic wall stress increases, and ejection fraction declines significantly. Interestingly, in children and young adults, the early postoperative course of LV systolic dysfunction is similar to that in adults, but the long-term occurrence of LV systolic dysfunction is significantly different. In a recent study by Krishnan et al,[46] long-term postoperative LV systolic dysfunction was found to be rare, but it occasionally occurred. Better clinical postoperative results were associated with a shorter duration of mitral regurgitation. Aortic Regurgitation Acute Aortic Regurgitation.

In acute aortic regurgitation, because the normal LV chamber cannot acutely adapt to the large regurgitant volume, forward stroke volume is reduced, resulting in significant elevation in LV end-diastolic pressure.[47] Prolonged regurgitation eventually leads to the development of LV dilation and eccentric hypertrophy.[20] Chronic Compensated Aortic Regurgitation.

In the transition from acute to chronic compensated aortic regurgitation, LV dilation and eccentric hypertrophy accommodate a larger end-diastolic volume. [20] [48] The increased LV end-diastolic volume, in turn, allows for 392

increases in both total and forward stroke volume, thereby returning LV filling pressures to normal. These compensatory mechanisms maintain LV ejection fraction and end-systolic volume within the normal range. In addition, vascular adaptation, as measured by total arterial elastance, has been found to occur in response to chronic aortic regurgitation. This LV-

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arterial coupling occurs in a heterogeneous pattern. In some patients it decreases, thereby maximizing LV work and performance, whereas in others it increases, causing "double loading" of the left ventricle and progressive pump dysfunction. [49] Concentric hypertrophy also develops in aortic regurgitation in response to pressure overload.[1] [9] [20] Unlike mitral regurgitation, in which the excess volume is unloaded into the low-impedance left atrium, in aortic regurgitation, the forward and regurgitant volume must be pumped into the higher pressure arterial system, resulting in an increase in end-systolic pressure and wall stress.[50] In accordance with the Laplace relationship, an increased end-systolic wall stress results in concentric hypertrophy, leading to an increase in wall thickness, returning the ratio of cavity radius to wall thickness to within the normal range. Chronic Decompensated Aortic Regurgitation.

The transition to decompensated aortic regurgitation is characterized by progressive LV dilation and deterioration in LV pump performance resulting from intrinsic contractile dysfunction.[2] [51] At this stage, the left ventricle has reached its limit of compensation and can no longer increase wall thickness to compensate for increases in preload. The ratio of cavity dimension to wall thickness increases, resulting in elevated end-systolic wall stress and afterload mismatch. Total and forward stroke volumes decrease and end-systolic volume increases, resulting in a decline in ejection fraction and elevation in left-sided filling pressures. Response to Operation.

In chronic compensated aortic regurgitation, valve replacement results in a reduction in end-diastolic volume and regression of LV hypertrophy. [16] [17] , [52] [53] [54] [55] [56] [57] Afterload also decreases, resulting in improved LV pump performance, even if LV ejection fraction was reduced preoperatively. In chronic decompensated aortic regurgitation, there is marked LV enlargement, significant elevation in end-systolic wall stress, and decreased LV pump performance.[59] [60] Despite successful valve replacement, LV dilation and hypertrophy persist, end-systolic wall stress remains elevated, and systolic performance remains depressed, indicating the development of irreversible contractile dysfunction.

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Assessment of Left Ventricular Function in Valvular Regurgitation Although the pathophysiologic mechanisms differ between the two regurgitant valve lesions, LV pump performance is the most important determinant of survival and postoperative outcome in both mitral and aortic regurgitation. As a result, most of the variables used to predict outcome in valvular regurgitation relate to LV ejection phase indices. How, then, is LV systolic performance best evaluated in chronic valvular regurgitation? Ejection Phase Indices. Left ventricular pump performance is often gauged by indices such as ejection fraction and percentage of fractional shortening. These LV ejection phase indices can be altered dramatically, however, by changes in loading conditions, heart rate, and contractility.[18] Alteration in any one of these factors can change LV ejection fraction without necessarily implicating abnormal contractility as the mechanism.[22] Likewise, LV ejection fraction can remain normal, despite markedly impaired contractility. [26] [28] Because mitral and aortic regurgitation are states of altered load, LV ejection phase indices may not accurately assess contractility in these conditions. End-Systolic Indices. To overcome the limitations of LV ejection phase indices in the assessment of contractile state in valvular regurgitation, investigators have alternatively used load-independent variables.[18] [21] [22] [23] [46] Because preload is elevated in valvular regurgitation, preload-independent variables, particularly the end-systolic indices, are commonly employed to assess contractility in mitral and aortic regurgitation.[19] [61] [62] [63] [64] [65] [66] [67] [68] [69] The endsystolic indices have been classified according to those that measure afterload, including end-systolic stress and end-systolic pressure; and those that indicate LV size, including end-systolic volume and end-systolic

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dimension. The ratio of end-systolic stress (or end-systolic pressure) to endsystolic volume (or end-systolic dimension) are preload-independent indices of contractility that also correct for afterload. The basic principle underlying the use of these indices of contractility is that for a given afterload, a ventricle that can shorten to a smaller end-systolic volume has greater contractility than a ventricle with a larger end-systolic volume. End-Diastolic Indices. End-diastolic indices, including end-diastolic dimension and end-diastolic wall stress (the product of end-diastolic pressure and dimension divided by the wall thickness) have also been used to evaluate LV performance in valvular regurgitaton. [59] [66] Left ventricular end-diastolic dimension increases in valvular regurgitation in response to volume overload. In mitral regurgitation, end-diastolic dimension increases without significant changes in wall thickness, whereas in aortic regurgitation both end-diastolic dimension and wall thickness increase. Progressive increases in enddiastolic dimension and end-diastolic wall stress are suggestive of decompensation in both conditions of valvular regurgitation. Pressure-Volume Relationship. The slope of the LV end-systolic pressure-volume relationship has also been used as a load-independent measure of contractility.[11] [20] [21] , [26] [69] [70] [71] Unfortunately, determination of this slope requires measurement of endsystolic volume at different levels of afterload, typically using pharmacologic stress during cardiac catheterization. In most clinical settings, therefore, the pressure-volume relationship cannot be used as a routine tool for serial assessment of contractility in valvular regurgitation. Importantly, however, it can be used to provide insights into the occurrence of contractile dysfunction that can be translated into better use of ejection phase indices to determine the appropriate timing of surgical intervention, particularly in mitral regurgitation.

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Chronic Mitral Regurgitation 393

Traditionally, surgery for chronic mitral regurgitation has been delayed until the onset of symptoms. Unfortunately, by the time symptoms have developed, severe irreversible contractile dysfunction may already be present. Contractile dysfunction typically develops during the asymptomatic period when ejection phase indices of LV pump performance remain within the normal range. Because survival is reduced in patients with mitral regurgitation who have irreversible contractile dysfunction, current management strategies have been directed toward the timing of surgery to prevent progression to irreversible contractile dysfunction. Advances in detection of occult contractile dysfunction, better knowledge of the preoperative predictors of surgical outcome, reduction in mortality for mitral valve replacement using chordal-sparing techniques, and advances in mitral valve repair are leading to earlier surgical intervention in this population of patients. Etiology The mitral valve apparatus consists of the annulus, the anterior and posterior leaflets, the chordae tendineae, and the papillary muscles. Mitral regurgitation develops from alterations in one or more components of the mitral apparatus. [72] Causes of chronic mitral regurgitation are listed in Table 18-1 .[73] The most common causes of pure isolated mitral regurgitation include myxomatous degeneration (62%) (Fig. 18-2) , ischemia-related papillary muscle dysfunction (30%), infectious endocarditis (5%), and rheumatic disease (3%).[72] Changing Etiology of Mitral Regurgitation.

The spectrum of surgical mitral valve disease has changed significantly

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since the 1970s, with a decline in surgical referral for rheumatic valvular disease and an increase for myxomatous degenerative disease.[74] [75] [76] [77] In one review, TABLE 18-1 -- Causes of Chronic Mitral Regurgitation Mechanism Condition Inflammatory Rheumatic heart disease Systemic lupus erythematosus Takayasu's arteritis Scleroderma Degenerative Myxomatous degeneration of mitral valve leatlets Mitral valve annular calcification Marfan's syndrome Ehlers-Danlos syndrome Pseudoxanthoma elasticum Infectious Bacterial endocarditis Structural Ruptured chordae tendineae Rupture or dysfunction of the papillary muscles Dilation of the mitral valve annulus Hypertrophic cardiomyopathy Paravalvular prosthetic leak Congenital Mitral valve clefts or fenestrations Parachute mitral valve abnormality Adapted from Haffajec CI: Chronic mitral regurgitation. In Dalen JE, Alpert JS (eds): Valvular Heart Disease, 2nd ed. Boston, Little, Brown. 1987, pp 111–119. Figure 18-2 (color plate.) Transesophageal echocardiogram in the longitudinal plane (two-chamber view) from a patient with myxomatous degenerative mitral valve disease who presented with a 3-month history of dyspnea. Demonstrated is mitral valve prolapse (A) with a flail posterior leaflet secondary to a ruptured chordae tendineae, resulting in severe mitral regurgitation (B).

rheumatic valvulitis accounted for 46% of all surgically treated cases of

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mitral regurgitation from 1970 through 1974, but only 15% from 1985 through 1989. Conversely, myxomatous degenerative disease accounted for only 37% of cases in the earlier years, but it represented 60% of cases in the latter years.[75] Changes in the etiology of mitral regurgitation have been paralleled by changes in surgical therapy for the disease. The number of valves being repaired has steadily increased, particularly in centers experienced in valve reconstruction. At the Cleveland Clinic, 80% of patients referred for correction of mitral regurgitation in 1988 underwent valve repair (see Chapter 19) .[74] Because of the potential for valve repair, the specific anatomic defect responsible for mitral regurgitation, defined by twodimensional and transesophageal echocardiography, has become an integral part of the evaluation of patients with mitral regurgitation. The potential to repair myxomatous degenerative valves has been further stratified according to the specific anatomic defect. Because operative mortality and overall complication rates are lower with mitral valve repair procedures,[72] [77] the ability to repair a valve favors earlier surgical intervention to prevent development of occult contractile dysfunction. Natural History Importance of Left Ventricular Pump Performance.

394

The natural history of mitral regurgitation is variable and depends on multiple factors, including the volume of regurgitation, LV pump performance, contractile state, and the underlying etiology of the disease.[3] [78] [79] The most important determinant of survival, however, is LV contractile state. Chronic mitral regurgitation represents a state of volume overload in which elevated preload and compensatory eccentric hypertrophy maintain overall LV ejection fraction within the normal range for extended periods of time.[43] [44] In addition, recent evidence suggests that LV pump performance in chronic mitral regurgitation is also maintained by activation of the sympathetic nervous system. Nagatsu and colleagues[24] used a canine model to show that indices of LV ejection and contractile performance could be maintained in the normal or near-normal range by beta-adrenergic stimulation in surgically created chronic mitral regurgitation, despite the

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presence of significant underlying contractile dysfunction.[49] This implied that by the time contractile dysfunction is detected in the absence of betaadrenergic blockade, severe contractile dysfunction is already present. In human subjects, Mehta and colleagues[80] [81] found that the sympathetic nervous system was activated in proportion to the increase in LV endsystolic volume and the reduction in ejection fraction, rather than the severity of mitral regurgitation (Fig. 18-3) . Activation of the sympathetic nervous system was found to increase and was clearly evident at echocardiographic LV end-systolic dimensions of 40 mm or more. Despite the initial compensatory function of beta-adrenergic stimulation in mitral regurgitation, chronic stimulation may have adverse effects on LV contractility. Canine models of surgically created mitral regurgitation have shown that sustained beta-adrenergic blockade resulted in Figure 18-3 The relationship between the extravascular norepinephrine release rates (NE2 ) and echocardiographically determined left ventricular end-systolic dimension (ESD) is shown. Note that sympathetic tone is markedly elevated in mitral regurgitation patients with a left ventricular ESD of greater than 40 mm. (From Mehta RH, Supiano MA, Oral H, et al: Am J Cardiol 2000;86:1193–1197.)

improved LV pump performance. This effect was associated with an improvement in cardiocyte contractility secondary to an increased number of contractile elements in isolated cardiocytes.[82] These compensatory mechanisms allow patients to remain asymptomatic for many years. Eventually, a transition phase ensues, during which time insidious contractile dysfunction begins to develop. During this transition phase, however, patients generally remain asymptomatic or are just beginning to develop mild symptoms of fatigue. The development of atrial fibrillation often heralds the onset of this decompensation.[83] [84] By the time patients become overtly symptomatic, with exhaustion, decreased exercise tolerance, and congestive heart failure, severe irreversible contractile dysfunction may have already developed.[3] , [78] It is important to understand that, despite significant and potentially irreversible contractile dysfunction, LV ejection fraction may be reduced to only 40% to 50%. [26] [28] Right heart failure, characterized by congestive hepatomegaly, ascites, and peripheral edema, may develop late in the course of the disease.[77] [85] Medical versus Surgical Therapy.

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Overall survival in chronic mitral regurgitation appears to be improved with surgical therapy in patients with normal or reduced LV pump performance. Because the natural history of severe mitral regurgitation has been significantly altered by surgical advances, only a few studies exist that directly compare medical with surgical therapy[86] [87] [88] [89] (Table 18-2) . Rapaport[86] studied the natural history of 70 patients with mitral regurgitation treated medically over a 5- and 10-year period. The survival rate at 5 and 10 years was reported to be 80% and 60%, respectively, for patients with isolated mitral regurgitation. Hammermeister et al[87] reported much lower 5- and 9- to 10-year survival rates for 36 medically treated patients at 55% and 22%, respectively. Survival was significantly improved in the 61 patients who underwent mitral valve replacement, with 5- and 9to 10-year survival rates of 72% and 63%, respectively. Delahaye et al[89] also reviewed the outcomes of 216 patients with chronic mitral regurgitation. Actuarial survival at 8 years for the surgical group (n = 116) was 74%, compared with 33% for the medical group (n = 54). For mixed mitral regurgitation and stenosis, survival with medical therapy has ranged from 45% to 65% at 5 years and 27% to 32% at 9 to 10 years. Surgery also improves mortality in this subset of patients, with survival rates reported at 61% to 84% at 5 years and 75% at 9 to 10 years. Although survival is reduced in patients with impaired LV pump performance, overall mortality is improved with surgery compared with medical therapy. [87] Therefore, surgery should not be withheld in patients with chronic mitral regurgitation on the basis of reduced LV ejection fraction. Mitral Valve Replacement Importance of Preservation of the Submitral Apparatus.

Left ventricular ejection fraction frequently decreases after surgical correction of chronic mitral regurgitation, 395

TABLE 18-2 -- Survival in Chronic Mitral Regurgitation: Comparison Surgical Therapy Medical Therapy

Sur

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PATIENTS, Study Condition n MR 70 Rapaport[86] MR/MS 102 Hammermeister MR 36 [87] et al MR/MS 22 99 Munoz et al[88] MR/MS Delahaye et al MR 54

9- TO 10YEAR 5-YEAR SURVIVAL, SURVIVAL, PATIENTS, % % n 80 60 65 32 55 22 61 63 45 33

45 45 116

[89]

MR, mitral regurgitation; MS, mitral stenosis. even if preoperative indices of LV pump performance are normal.[16] [25] [29] Traditionally, it was believed that afterload (end-systolic wall stress) was decreased in mitral regurgitation by systolic "unloading" into the lowimpedance left atrium. Correction of mitral regurgitation with elimination of the low-resistance leak into the left atrium was thought to acutely increase afterload, resulting in the decrease in LV ejection fraction observed postoperatively.[29] It is now known that for the majority of patients with severe mitral regurgitation, afterload is normal before surgical correction. Furthermore, changes in afterload are not solely responsible for the observed decrease in LV pump performance after surgical correction of mitral regurgitation. Rather, primary contractile dysfunction, resulting from chronic volume overload, and alterations in LV geometry secondary to removal of the submitral apparatus during conventional mitral valve replacement are also responsible for the post-operative decline in LV pump performance. Conventional mitral valve replacement with transection of the chordae tendineae and removal of the subvalvular apparatus almost always results in a postoperative decline Figure 18-4 Preoperative (PRE) and postoperative (POST) left ventricular (LV) ejection fractions depicted for patients undergoing mitral valve replacement with transection (open squares) and preservation (solid circles) of the chordae tendineae. Data for individual

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patients are represented by smaller symbols; mean ± SEM is represented by larger symbols. Mitral valve replacement with transection of the chordae tendineae resulted in a decrease in LV ejection fraction, but mitral valve replacement with chordal preservation did not. (From Rozich JD, Carabello BA, Usher BW, et al: Circulation 1992;86:1718–1726.)

in global and regional LV ejection fraction, even when preoperative indices of LV pump performance are normal.[90] LV ejection fraction decreases immediately after removal of the subvalvular apparatus[34] and persists over the long term after excision.[89] For the majority of patients, however, this decline in LV ejection fraction does not occur with mitral valve reconstruction[34] [91] [92] or mitral valve replacement with preservation of the chordae tendineae and papillary muscles [31] [33] , [40] (Fig. 18-4) . In addition to preservation of LV systolic performance, postoperative survival and exercise capacity have been shown to improve in patients who undergo mitral valve replacement with chordal preservation.[37] The mechanisms for preservation of LV pump performance after mitral valve replacement with chordal preservation have been defined by Rozich et al[40] using two-dimensional echocardiography. Disruption of the functional components of the submitral apparatus during conventional mitral valve replacement disturbs the continuity between the mitral annulus and LV wall through the leaflets, chordae tendineae, and papillary muscles, resulting in significant increases in end-systolic volume and 396

end-systolic stress. In addition, the ratio of the LV major axis to minor axis dimension decreases significantly, suggesting a loss of LV geometry with assumption of a more spherical shape.[33] [40] [45] Mitral valve replacement with chordal preservation maintains LV systolic performance by preserving LV geometry, resulting in a smaller LV cavity and a decrease in endsystolic wall stress.[35] Although the decline in LV pump performance after conventional mitral valve replacement can be attributed, at least in part, to disruption of LV geometry after removal of the submitral apparatus, underlying contractile dysfunction secondary to long-standing volume overload is still the major determinant of postoperative LV pump dysfunction. Left ventricular pump performance declines postoperatively in patients with significant preoperative LV enlargement, despite mitral valve replacement with preservation of the submitral apparatus. Wisenbaugh et al[93] demonstrated

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that patients with an end-systolic diameter of greater than 50 mm had a poor long-term outcome after mitral valve replacement, despite chordal preservation. Similar data have been reported by Enriquez-Sarano et al[5] for patients undergoing mitral valve reconstruction, with a decline in postoperative LV ejection fraction demonstrated for patients with a preoperative LV ejection fraction of less than 60%. These data confirm the fact that occult contractile dysfunction secondary to long-standing volume overload is an important mechanism for the observed postoperative decline in LV ejection fraction after correction of mitral regurgitation. Mitral Valve Reconstruction Left Ventricular Systolic Performance.

The long-term success of mitral valve reconstruction for mitral regurgitation has been reported in numerous series.[37] [77] [79] , [91] , [94] [95] [96] [97] [98] [99] [100] [101] [102] [103] [104] [105] [106] [107] [108] In addition to preservation of LV geometry, mitral valve reconstruction has been shown to confer additional operative and long-term survival advantages over mitral valve replacement for chronic mitral regurgitation. The reduction in LV pump performance that has been observed after conventional mitral valve replacement has not been observed with mitral valve reconstruction, provided that the preoperative contractile state remains intact (Table 18-3) . TABLE 18-3 -- Preoperative and Postoperative Ejection Fraction: A Comparison of Mitral Valve Repair and Mitral Valve Replacement with Chordal Transection and Preservation

Study Duran et al[91] David et al[33] David et al[31] Goldman et al[34] Hennein et al[37] Sakai et al[92]

Repair, % PREOP POSTOP 47 54 63 63 44 65

49 68

Replacement with Chordal Transection, % PREOP POSTOP 54 47 62 51 55 48 64 40 46 31 64 57

Replacement with Chordal Preservation, % PREOP POSTOP 64 53

65 52

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Rozich et al[40] 60 63 54 69 Enriquez-Sarano et al[5] Preop, preoperative; Postop, postoperative.

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36 49

Mortality.

Operative mortality and long-term survival rates are also better after mitral valve repair compared with mitral valve replacement (Table 18-4) . Mitral valve reconstruction has been compared to replacement in several studies. The first large retrospective study was reported by Duran et al [91] in 1980 for 562 patients undergoing mitral valve surgery predominantly for rheumatic heart disease. Operative mortality for the 255 patients undergoing mitral valve repair was 1.9% compared with 11.4% for the 307 patients in the replacement group. Survival at 2 years was better for the repair group (98.3%) than for the replacement group (92.9%), largely due to the differences in operative mortality. Only one prospective trial exists comparing mitral valve reconstruction with replacement. Perier[110] studied 400 patients with mitral regurgitation predominantly of rheumatic origin. Patients were divided into four groups of 100 patients each, with one group undergoing mitral valve repair and the remaining three groups treated with valve replacement using different prostheses. The 7-year survival rate was 82% for the repair group versus 56%, 61%, and 60% for the three replacement groups. Yacoub et al[108] reported long-term results for mitral valve reconstruction versus replacement for the "floppy mitral valve syndrome." Survival rates at 5 and 10 years were 91% and 81%, respectively, for the repair group, versus 81% and 39% for the replacement group. In addition to preservation of LV pump performance, therefore, mitral valve reconstruction also confers a survival advantage over mitral valve replacement. Thromboembolism.

In addition to the decreased operative mortality and increased long-term survival associated with mitral valve repair, the thromboembolic and hemorrhagic complications associated with mitral valve reconstruction are also significantly decreased compared with mitral valve replacement. Several studies have reported that approximately 95% of patients are free from thomboembolic complications at 5 to 10 years after surgery.[111] In contrast, 10% to 35% of patients with mechanical prostheses have thromboembolic events within 5 to 10 years of surgery.[112]

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Hemorrhage.

Because only a minority of patients who undergo valve reconstruction are maintained on chronic anticoagulation therapy, the incidence of significant bleeding complications is also extremely small,[101] [111] in contrast 397

TABLE 18-4 -- Operative Mortality and Long-Term Survival: Mitral Valve Repair versus Replacement Operative Mortality

Long-Term Survival YEARS AFTER

REPAIR, REPLACEMENT, REPAIR, REPLACEMENT, n (%) n (%) OPERATION % % Study Duran et 255 1.8 307 11.4 4 96 81 [91] al 86 3.1 46 7.0 5 91 62 Yacoub [108] et al Oliveira 82 4.9 101 5.0 6 88 68 [106] et al Adebo 21 0 44 6.8 5 85 78 and Ross [96]

100 2.0 100(SE)

100(BS) 100(BP) 131 6.1 106

12 12 7.5

60(BS) 56(BP) 72

222

4.0

Angell et 112 5.4 72 al[95] 75 4.0 63 Cohn et [97] al

18.1

5/10

90/75

55/40

3.0

Perier et al[110]

Orszulak et al[107] Sand et al

48 0

61(SE)

[94]

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Galloway 280 2.0 169(ME) et al[101] 975(BP) Craver et 65 1.5 65 al[99] Kawachi 43 2.3 48 [103] et al Enriquez- 151 1.3 175 * * Sarano et al[7]

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6.6

72(ME)

8.5 4.6

69(BP) 82

8.3

5/8

91/91

82/75

5.7

79; EF > 60

71; EF > 60

48; EF < 60 68

50; EF < 60

Enriquez- 44 † 6.8 39 † 30.8 10 52 Sarano et al[5] BP, bioprosthesis; BS, Björk-Shiley; EF, ejection fraction; ME, mechanical; SE, Starr-Edwards. *Age ≤ 75 years. †Age > 75 years.

to relatively frequent episodes of bleeding after valve replacement.[112] Endocarditis.

The risk of endocarditis is also decreased after mitral valve repair compared with replacement. In the series of Duran et al,[91] infectious endocarditis occurred at a rate of 0.4% per year after repair and at 2.2% per year after replacement. Late endocarditis after mitral valve reconstruction is negligible, in contrast to the 3% to 6% incidence after mitral valve replacement. [111] Predictors of Postoperative Outcome and Survival As previously stated, patients with mitral chronic regurgitation who have reduced LV pump performance prior to surgery are at risk for a suboptimal postoperative outcome, characterized by persistent LV systolic dysfunction, congestive heart failure, and death. Presumably, operation in such patients

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is being performed late in the hemodynamic course at a time when severe, irreversible contractile dysfunction has already developed. So, should surgery be performed "prophylactically" in all asymptomatic patients to prevent occult contractile dysfunction? The optimal time for surgery is at the onset of LV contractile dysfunction, justifying the surgical risk, but early enough in the course to be reversible. If it were possible to pinpoint this critical moment in the natural history of chronic mitral regurgitation, then it would be simple to plan the timing of surgery in these patients. Unfortunately, no variable that can be routinely measured in the clinical setting is able to define the precise onset of reversible contractile dysfunction in chronic mitral regurgitation. Several markers, however, have been identified that predict a poor outcome after mitral valve surgery. These variables, in conjunction with those that have recently been identified to predict an optimal outcome, can be used to provide a rational framework for the timing of surgery in this valve disease for the purpose of preservation of contractility. Table 18-5 summarizes the preoperative clinical, hemodynamic, angiographic, and echocardiographic parameters that have been used to predict postoperative outcome in patients with mitral regurgitation. Clinical Predictors.

Among 177 surgically treated patients with mitral valve disease, Hammermeister et al[87] found age to be the only independent predictor of survival after mitral valve replacement. Patients older than 61 years had a 5-year survival rate of 40%, compared with 74% in patients 41 to 60 years old and 87% in patients younger than 40 years. In a study by Phillips et al,[8] patient age was also found to predict survival. Patients younger than 60 years at the time of surgery had a 5-year survival rate of 91%, compared with 72% for those 61 years old or older. In several studies by EnriquezSarano and colleagues,[5] [7] age was also found to be an important predictor of operative morality in patients undergoing mitral valve surgery. Operative mortality in elderly patients (older than 75 years) was 30.8% for valve replacement and 6.8% for valve repair versus 5.7% for valve replacement and 1.3% for valve repair in patients younger than 75 years of age. In addition to age, Enriquez-Sarano and colleagues[5] [6] [7] also found the following clinical variables to be predictive of overall survival, operative mortality, and postoperative LV ejection fraction in patients undergoing mitral valve replacement or reconstruction: creatinine (no level specified), New York Heart Association (NYHA) functional class greater than II, atrial

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fibrillation, and concomitant coronary artery disease. Recently, in a study of 576 consecutive postoperative survivors, Dujardin et al[113] found that preoperative LV ejection fraction ( 60 years > 75 years > Class II

8 5 5–7, 114, 116 5–7 5–7

> 20 mm Hg

< 2.0 L/m/m2 > 12 mm Hg

116

≥ 30 mL/m2

116 8 19 4

≥ 50 mL/m2

≥ 60 mL/m2

< 50%

< 2.6 dyne × 103 /cm2

ES volume index Echocardiography LV ejection fraction

References

mL/m2 < 50% < 60% < 63%

6 7 25

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Fractional shortening End-diastolic dimension End-systolic dimension

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< 31% > 70 mm > 50 mm > 45 mm ≥ 40 mm

69 25 25, 93 6, 7 30 69

End-systolic dimension > 2.6 cm/m2 index End-systolic stress index > 195 mm Hg 69 Doppler-derived LV dP/dt < 1343 mm Hg/sec 118 Radionuclide Right ventricular ejection < 30% 119 fraction ES, end systolic; LV, left ventricular; NYHA, New York Heart Association.

coronary artery disease were each positively associated with postoperative mortality and congestive heart failure. Ramanthan et al[114] likewise found NYHA functional class to be an important predictor of survival in medically treated patients with mitral regurgitation followed for a 4-year period, with mortality rates of 53% and 44% for class III and class IV patients, respectively. Similarly, in a recent study of 478 patients with organic mitral regurgitation corrected surgically, Tribouilloy et al[115] found preoperative functional class III/IV symptoms to be independently associated with decreased immediate and long-term postoperative survival. The excess mortality associated with NYHA class III/IV as compared to class I/II was demonstrated regardless of LV ejection fraction (Fig. 18-5) . These researchers concluded that surgical intervention should be considered when no or minimal symptoms are present in low operative risk patients. Salomon et al[116] retrospectively analyzed multiple patient-related risk factors to determine survival after mitral valve replacement in 897 patients, 240 with mitral stenosis, 352 with mitral regurgitation, and 305 with mixed stenosis and regurgitation. In addition to patient age of less than 60 years, preoperative NYHA class of III or lower, cardiac index of 2.0 or greater, and LV end-diastolic pressure of 12 or less were also found to predict improved perioperative as well as long-term survival. Similarly, Crawford et al[4] found that a mean preoperative pulmonary artery pressure of 20 mm Hg or greater predicted a reduced LV ejection fraction after

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mitral valve replacement. Left Ventricular Ejection Fraction.

Although it does not identify asymptomatic patients with early contractile dysfunction, LV ejection fraction has been used extensively to predict outcome after surgery. As mentioned earlier, Dujardin et al[113] found, in a study of 576 consecutive postoperative survivors of mitral valve surgery, that Figure 18-5 Overall survival is compared between patients in New York Heart Association (NYHA) class I/II and those in class III/IV who had a preoperative left ventricular ejection fraction (EF) of 60% or greater (A) or less than 60% (B). (From Enriquez-Sarano M, Tajik AJ, Schaff HV, et al: Circulation 1995;91:1022–1028.)

399

Figure 18-6 Postoperative survival following mitral valve surgery on organic mitral regurgitation based on patients' preoperative left ventricular ejection fraction is shown. (From Enriquez-Sarano M, Tajik AJ, Schaff HV, et al: Circulation 1994;90:830–837.)

LV ejection fraction of 60% or greater was associated with improved survival (adjusted risk ratio 0.49) and reduced incidence of congestive heart failure (adjusted risk ratio 0.30). In a study by Enriquez-Sarano et al[7] of 409 patients with isolated mitral regurgitation undergoing mitral valve surgery, preoperative LV ejection fraction was found to be the most important predictor of long-term survival. Survival at 10 years was 72% for patients with a mean preoperative LV ejection fraction of 60% or greater, 53% for patients with an ejection fraction in the range of 50% to 60%, but only 32% percent for those with an ejection fraction of less than 50% (Fig. 18-6) . Enriquez-Sarano et al[6] also reviewed the echocardiographic predictors of postoperative LV pump performance in 266 patients undergoing mitral valve replacement for mitral regurgitation. Independent predictors of postoperative LV pump dysfunction (defined as an ejection fraction of less than 50%) included a preoperative LV ejection fraction of less than 50% or an end-systolic dimension of greater than 45 mm. Postoperative LV pump

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dysfunction (ejection fraction of less than 50%) was associated with an increased mortality rate evidenced by an 8-year survival rate of 38% in patients with decreased postoperative LV ejection fraction, compared with 69% for patients with a postoperative LV ejection fraction of greater than 50%. In a study of 150 patients undergoing mitral valve replacement for isolated mitral regurgitation, Phillips et al[8] also demonstrated the value of preoperative LV ejection fraction in predicting long-term survival. Fiveyear survival rates for patients with a preoperative LV ejection fraction of 50% or greater, 40% to 49%, and less than 40% were 89%, 71%, and 38%, respectively. These data suggest that by the time LV ejection fraction had decreased to below the lower limits of normal, severe contractile dysfunction had already developed, and recovery was unlikely after surgery. Reduced LV ejection fraction, therefore, identifies patients who are likely to do poorly after surgery, but a normal LV ejection fraction does not distinguish between patients with normal contractility and those with occult early contractile dysfunction, who might benefit from prompt surgical intervention. Crawford et al[4] studied 48 patients with mitral regurgitation and 23 patients with mixed mitral stenosis and regurgitation to determine the role of LV size, pump performance, and clinical status in predicting survival and LV pump performance after mitral valve replacement. Mortality and increased NYHA functional class due to congestive heart failure were significantly higher in patients with mitral regurgitation and a postoperative LV ejection fraction of less than 50% and in patients with mixed stenosis and regurgitation and postoperative LV enlargement, defined by an enddiastolic volume index of greater than 101 mL/m2 . The strongest predictor of postoperative LV ejection fraction was the preoperative ejection fraction. Preoperative predictors of postoperative LV enlargement included an endsystolic volume index of greater than 50 mL/m2 and a mean pulmonary artery pressure of greater than 20 mm Hg. Similarly, Starling[30] studied 15 patients with chronic mitral regurgitation with micromanometer LV pressures and radionuclide angiograms for LV volumes over a range of loading conditions before and 1 year after successful mitral valve surgery. This study demonstrated that LV contractile impairment is reversible in many patients with chronic mitral regurgitation and that the best predictors of this reversibility include a normal preoperative LV ejection fraction and less LV dilation as manifest

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by end-systolic volume (Fig. 18-7) . Thus, following mitral valve surgery for chronic mitral regurgitation, LV contractility improved in those patients with an average preoperative LV ejection fraction of 0.63 ± 0.09 and an end-systolic volume index of 44 ± 12 mL/m2 , whereas it remained abnormal in those patients with an LV ejection fraction of 0.49 ± 0.12 and an end-systolic volume index of 89 ± 28 mL/m2 . This implies that early surgical intervention can preserve LV contractility and portend an excellent long-term outcome in some patients with mitral regurgitation.

400

Figure 18-7 The left ventricular (LV) end-systolic pressure-volume relationship (Ees ) both before and after successful mitral valve surgery uncorrected (A) and corrected (B) for LV size is shown. A substantial increase in contractility occurs on the postoperative study compared with the preoperative study in the majority of patients, although a small group of patients shows either a decline or no change in this contractile index. *P < .05. (From Starling MR: Circulation 1995;92:811–818.)

The percentage of fractional shortening has also been used to assess LV pump performance in mitral regurgitation. Zile et al[69] found that a preoperative fractional shortening of less than 31% predicted postoperative congestive heart failure and death after mitral valve replacement in patients with mitral regurgitation. Despite the fact that survival is decreased in patients with reduced LV pump performance, patients with a decreased LV ejection fraction have improved survival with surgery over medical therapy.[87] The 5-year survival rate in patients with a reduced LV ejection fraction (31% to 50%) was 82% with valve repair or replacement, compared with 45% for the medically treated group. The 10-year survival rate was 82% for the repair group, 74% for the replacement group, and less than 20% for medically treated patients. Therefore, despite reduced overall survival in patients with mitral regurgitation and impaired LV pump performance, mitral valve surgery, particularly valve repair, should not be withheld in this subset of patients, as survival is significantly worse with medical therapy alone. End-Systolic Dimension.

Using two-dimensional echocardiography, Schuler et al[25] demonstrated the

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importance of the preoperative LV end-systolic dimension as a predictor of postoperative LV pump dysfunction in 16 patients with mitral regurgitation who underwent conventional mitral valve replacement. Group I consisted of those patients with a normal preoperative LV ejection fraction and mild LV enlargement; group II included those patients with a low normal LV ejection fraction and moderate LV enlargement. Postoperatively, at a mean follow-up of 15 months, group I patients demonstrated a significant decrease in mean echocardiographic LV end-diastolic and end-systolic dimension, a slight decline in LV ejection fraction, and regression of LV hypertrophy. In contrast, group II patients had no significant decrease in LV end-diastolic dimension, an increase in end-systolic dimension, and a marked reduction in LV ejection fraction. A preoperative LV end-diastolic dimension of greater than 70 mm, end-systolic dimension of greater than 50 mm, and LV ejection fraction of less than 55% identified the majority of patients with postoperative LV pump dysfunction and lack of regression of LV hypertrophy. Wisenbaugh et al[93] evaluated the outcome of 66 patients after mitral valve replacement with preservation of the submitral apparatus. At a mean follow-up period of 24 months, postoperative death or severe heart failure were predicted by a preoperative echocardiographic end-systolic dimension of 50 mm or greater. A preoperative LV end-systolic dimension of less than 40 mm identified all patients with an excellent postoperative outcome. The importance of echocardiographic end-systolic dimension in predicting adverse postoperative outcome has also been reported by Enriquez-Sarano and associates[6] [7] for an end-systolic dimension of greater than 45 mm and by Zile et al[69] for an end-systolic dimension index of greater than 26 mm/m2 . Similarly, in a recent study by Flemming et al,[117] 27 patients were evaluated with micromanometer LV pressures, radionuclide angiography, and echocardiographic parameters prior to and at 3 and 12 months after mitral valve surgery. They found that the most predictive echocardiographic indicator of early occult LV contractile dysfunction was an end-systolic dimension of 40 mm or more (Fig. 18-8) . This index was also able to predict a unique response to mitral valve surgery that was characterized by a short-term fall in LV pump performance, but a long-term recovery to normal LV pump performance, possibly because of a recovery of LV contractile function. They concluded that this measure may be useful to separate those with and without early occult LV contractile dysfunction and normal LV pump performance and to identify those patients who may

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benefit from early mitral valve surgery with or without mild symptoms to preserve LV systolic performance. End-Systolic Volume.

Borow et al[19] have evaluated the 401

Figure 18-8 Receiver operator characteristic curves were generated using sensitivity and 100-minus specificity for echocardiographic left ventricular (LV) end-systolic dimension (ESD), fractional shortening (FS), and end-diastolic dimension (EDD) to identify contractile dysfunction in mitral regurgitation (MR) patients with a normal LV ejection fraction. An LV ESD of 40 mm or greater was optimal for identifying patients with MR and a normal LV ejection fraction and early occult contractile dysfunction. (From Flemming MA, Oral H, Rothman ED, et al: Am Heart J 2000;140:476–482.)

role of the preoperative end-systolic volume index as a predictor of postoperative LV pump performance and survival in chronic mitral regurgitation. Abnormal postoperative LV pump performance was predicted by a preoperative end-systolic volume index of greater than 60 mL/m2 . Furthermore, a preoperative end-systolic volume index of greater than 90 mL/m2 predicted increased postoperative mortality. Specifically, four of five patients with an end-systolic volume index of greater than 60 mL/m2 died in the perioperative period, whereas no patients with an endsystolic volume index of less than 60 mL/m2 died of cardiac failure. All patients with an end-systolic volume index of less than 60 mL/m2 achieved NYHA class I or II postoperatively. In the study by Crawford et al,[4] an end-systolic volume index of 50 mL/m2 or greater was similarly found to predict postoperative LV pump dysfunction. End-Systolic Wall Stress.

In addition to an echocardiographic LV end-systolic dimension index of greater than 26 mm/m2 and percentage fractional shortening of less than 31%, Zile et al[57] have also demonstrated that an echocardiographic LV end-systolic wall stress index of greater than 195 mm Hg can be used to predict postoperative congestive heart failure and death after mitral valve replacement for chronic mitral regurgitation.

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End-Systolic Wall Stress/End-Systolic Volume Index.

Variables predictive of reversible LV contractile dysfunction have been identified in mitral regurgitation, but such measurements have required complex invasive hemodynamic protocols. In a study of 21 patients with mitral regurgitation, Carabello et al[64] found that the ratio of end-systolic wall stress to end-systolic volume, a preload-independent index of contractility, was the best predictor of outcome after mitral valve replacement for mitral regurgitation. The end-systolic wall stress to endsystolic volume index was 5.6 in normal subjects, 3.3 in patients with a favorable postoperative outcome (NYHA class II or lower), and 2.2 in patients with an unfavorable postoperative outcome, including NYHA class III or IV symptoms or death. The fact that the absolute value of the ratio of LV end-systolic wall stress to end-systolic volume index was lower in patients with a favorable postoperative outcome than in normal subjects suggests that preoperative contractility was abnormal in this subset of patients with mitral regurgitation, but to an extent that did not adversely affect postoperative outcome. A significant decrease in the LV end-systolic wall stress to end-systolic volume index, on the other hand, appeared to identify a patient group with severe, irreversible contractile dysfunction. The LV end-systolic wall stress to end-systolic volume index may, therefore, be useful in identifying patients with early contractile dysfunction in whom timely operative intervention would be warranted. In a subsequent study, Carabello et al [62] further demonstrated that an endsystolic wall stress to end-systolic volume index ratio of 2.6 or less predicted poor surgical outcome, defined as postoperative death or NYHA class III or IV symptoms. Pressure-Volume Relationship.

Starling et al[26] have demonstrated that the slope of the end-systolic pressure-volume relationship (chamber elastance), a load-independent measure of contractility, can be used to identify occult reversible contractile dysfunction in patients with mitral regurgitation who have a normal LV ejection fraction. Patients with a normal preoperative LV ejection fraction but impaired contractility (reduced elastance) had an initial decline in ejection fraction in the immediate postoperative period, but it improved within 1 year of surgery. In contrast, patients who had both impaired contractility and a reduced ejection fraction preoperatively had persistent postoperative LV pump dysfunction. These data suggested that the combination of abnormal elastance and normal ejection fraction can identify a patient group in whom contractile dysfunction is present but still

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reversible. In this particular group of patients, prompt surgical intervention is indicated to avoid progression to irreversible dysfunction. Unfortunately, because measurements of elastance require complex hemodynamic protocols, elastance cannot be used as a routine tool for serial assessment of patients with mitral regurgitation. However, the information gained using elastance has helped to interpret the clinical data used to determine the appropriate timing for surgical intervention in patients with mitral regurgitation. In a preliminary analysis of patients with mitral regurgitation and normal LV ejection fraction, patients with impaired contractility could be separated from those with normal contractility on the basis of echocardiographic indices of LV size and performance.[117] An LV end-systolic dimension of greater than 40 mm approximated a reasonable separation of these patients and may, therefore, represent a reasonable surrogate for the elastance concept in patients with mitral regurgitation. Doppler-Derived dP/dt.

The spectral velocity pattern of mitral regurgitation obtained by continuous wave Doppler echocardiography can also be used to assess LV systolic performance in mitral regurgitation. The spectral velocity curve represents the instantaneous pressure difference between the left ventricle and the left atrium. When systolic performance is reduced, the rate of rise of LV 402

Figure 18-9 Spectral Doppler signal of mitral regurgitation from a patient with depressed left ventricular function, demonstrating a slow rate of acceleration to peak regurgitant velocity, reflecting a low dP/dt. The dP/dt is estimated from the time interval (dt) required for the mitral regurgitant velocity to rise from 1 to 3 m per second. In this case, the dP/dt measured 800 mm Hg per second.

pressure is decreased, resulting in a concomitant decrease in the rate of increase in the velocity of mitral regurgitation. The slope of the mitral regurgitant velocity curve, designated as dP/dt, is decreased when LV systolic performance is decreased (Fig. 18-9) . Pai et al [118] studied the Doppler-derived index of the rate of LV pressure rise (dP/dt) in 25 patients with mitral regurgitation before and 6.5 weeks after mitral valve surgery. The LV dP/dt was found to be the best independent predictor of postoperative LV ejection fraction. A preoperative dP/dt of 1343 mm Hg

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per second or less predicted a postoperative ejection fraction of 50% or less. Right Ventricular Ejection Fraction.

Hochreiter et al[119] assessed the prognostic importance of right ventricular ejection fraction in 35 medically treated and 21 surgically treated patients with chronic mitral regurgitation. Patients with a right ventricular ejection fraction of 30% or less had a markedly reduced 4-year survival rate (18%) when treated medically compared with those treated surgically (84%). Left Atrial Size.

Reed et al[120] studied the role of left atrial size in predicting postoperative outcome in 176 symptomatic patients who underwent mitral valve replacement with a mean follow-up of 3.8 years. An abnormal left atrial size index (defined as the product of the major and minor atrial dimensions measured in the apical four-chamber view) was found to predict postoperative death. The left atrial size index, however, predicted mortality independent of LV systolic performance only in patients with a supernormal LV ejection fraction (>75%). Since patients with an LV ejection fraction in this range have an excellent prognosis, regardless of the left atrial size, this index appears to offer no additional prognostic information to LV systolic performance. Timing of Surgery Before discussing a rational approach to the proper timing of surgical intervention for chronic mitral regurgitation, the following key points should be emphasized: 1. Chronic severe mitral regurgitation leads to a progressive decline in LV pump performance. 2. Patients may remain asymptomatic with a normal LV ejection fraction for extended periods of time. 3. Occult contractile dysfunction generally develops at a time when patients remain asymptomatic and LV ejection fraction remains normal, and it may be reversible after surgical intervention. 4. Patients with normal LV ejection fraction and occult reversible contractile dysfunction who undergo mitral valve replacement or reconstruction have a favorable long-term prognosis. 5. Patients with LV pump dysfunction and irreversible contractile dysfunction are at risk for postoperative LV systolic dysfunction,

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7. 8. 9.

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death, and congestive heart failure. Although reduced LV pump performance is associated with an overall decrease in long-term survival for patients with mitral regurgitation, survival is improved with surgical therapy compared with medical therapy. Compared with conventional mitral valve replacement, mitral valve reconstruction preserves LV pump performance and reduces mortality and comorbid complications. If feasible, mitral valve reconstruction should be the procedure of choice in patients with reduced preoperative LV pump performance. Long-term postoperative LV pump dysfunction due to mitral regurgitation in children and young adults is rare, but it does occur. However, a shorter duration is associated with improved postoperative results.

Since long-term survival in chronic mitral regurgitation is dependent on the contractile state of the left ventricle, the primary goal of surgical intervention should conceptually be to preserve contractility. All symptomatic patients with mitral regurgitation should be referred promptly for valve repair or replacement. It is often difficult for clinicians to justify referral of asymptomatic patients for surgical procedures that have a finite risk for death, even when the risk is small. The immediate operative and postoperative risks, on the one hand, must be balanced by the risk for progression to severe, irreversible contractile dysfunction and, thus, reduced long-term survival. Table 18-6 presents a proposed algorithm for the timing of surgery in patients with chronic mitral regurgitation, based on a system in which points are assigned to the different clinical variables that normally play a role in the decision-making process. The major components of the decision analysis, depicted in part A of the algorithm, include clinical and hemodynamic parameters, LV size and pump performance, and the feasibility of valve repair. The measured components of the algorithm, including LV ejection fraction and end-systolic dimension, were selected on the basis of ease and reproducibility of the measurements using two-dimensional echocardiography. The ability to repair a valve should be determined based on the anatomic and pathologic defects of the valve as defined by transesophageal echocardiography. The feasibility of valve repair, based on the echocardiographic findings, should then be determined in consultation with a surgeon experienced in valve reconstruction. In general, symptomatic patients with congestive heart

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403

TABLE 18-6 -- Proposed Algorithm for Timing of Surgery in Patients with Mitral Regurgitation Part A: Assign a point score for each of the four designated categories. LV Function and Size EJECTION * FRACTION, END-SYSTOLIC Feasibility of Valve Clinical DIMENSION, mm Repair Points Symptoms % 0 None > 60 < 40 None 1 I/II 50–60 40–45 Possible 2 III/IV < 50 > 45 Definite Part B: Based on the total point score, follow suggested guidelines regarding timing of surgery. Total Points Decision Regarding Surgical Intervention 0–1 Delay surgery; recommend clinical and echocardiographic followup at 12 months 2 Borderline; recommend clinical and echocardiographic follow-up at 6 months ≥ 3 Proceed with surgery Part C: Although not essential for decision analysis, additional predictors of adverse outcome, all of which can be measured by twodimensional echocardiography, can also be used to support decisions. Additional Predictors of Adverse Outcome in Aortic Regurgitation † Value Fractional shortening < 31% End-systolic volume index > 30 mL/m2 End-systolic stress index End-diastolic dimension Doppler dP/dt of mitral regurgitant jet Right ventricular ejection fraction

> 195 mm Hg > 70 mm < 1343 mm Hg/sec < 30%

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*Add one point for age > 60 and coronary artery disease; add three points for history of atrial arrhythmias. †Add two points for each predictor present.

failure, decreased exercise tolerance, or atrial arrhythmias should be referred for surgery, regardless of the status of the left ventricle, particularly when mitral valve reconstruction can be performed. Asymptomatic patients with an LV ejection fraction in the low-normal range (60%) and small (140 mm Hg) or decreased diastolic pressure ( 65 years ≥ 0.58 ≥ Class III < 8 METs > 18 mo > 18 mo

> 20 mm Hg < 2.5 L/m/m2 < 50% ≤ 45% ≥ 60 mL/m2 ≤110 mL/m2 ≥ 1.72 mm Hg/mL/m2 < 25% < 28% < 29% > 50 mm

References 144, 153 126, 144, 152 126, 153 14, 158 15 147, 156

144 123, 124 123 124 19 62, 168 169

60 66 155 66

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> 55 mm > 60 mm End-systolic dimension index

> 2.6 cm/m2 End-systolic wall stress > 235 mm Hg End-systolic dimension > 80 mm > 72 mm End-diastolic dimension (R) ≥ 3.2 End-diastolic wall thickness (th) ≥ 4.0 LV, left ventricular; NYHA, New York Heart Association.

60 63 59 66 59, 60 66 66 59

functional class III or IV symptoms were found to be independent risk factors for increased early and long-term postoperative mortality, suggesting that the onset of symptoms should warrant a rapid consideration of surgery. This is particularly true for women. Hemodynamic Predictors.

Hemodynamic predictors of adverse postoperative outcome have also been used to stratify patients prior to aortic valve replacement. The 2-year survival rate in patients with a reduced cardiac index ( 2.5 L/m/m2 ) has been reported to be 72%, compared with 94% for those with a normal index.[144] In two other studies,[123] [124] survival rates at 3 and 5 years in patients with a cardiac index of 2.5 L/m/m2 or less were reported to be 63% and 66%, respectively. Elevated LV end-diastolic pressure of 20 mm Hg or greater has also been associated with increased mortality after aortic valve replacement.[144] Indices of Left Ventricular Systolic Performance in Symptomatic Patients Ejection Phase Indices!

Left ventricular pump performance has been shown to be the most important determinant of survival in symptomatic patients with aortic regurgitation. [123] [124] , [153] Forman et al[123] found preoperative LV ejection fraction to be the most important determinant of survival in 90 patients with chronic aortic regurgitation who underwent valve replacement. Patients with an ejection fraction of less than 50% had a poor 3-year survival rate (64%) when compared with those with an LV ejection fraction of 50% or greater (91%). Greves et al[124] similarly demonstrated an adverse outcome

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in patients with a reduced LV ejection fraction secondary to aortic regurgitation, reporting a 5-year survival rate of 54% in patients with an ejection fraction of 45% or less, compared with 87% for those with an ejection fraction of greater than 45%. Duration of Left Ventricular Systolic Dysfunction.

In addition to decreased LV pump performance as an important predictor of adverse outcome in chronic aortic regurgitation, Bonow et al[15] have also demonstrated the impact of the duration of preoperative LV pump dysfunction in determining survival (Fig. 18-13) . Despite comparable reductions in LV fractional shortening and similar exercise tolerance, patients with prolonged LV systolic dysfunction (≥18 months) had a survival rate of only 45%, compared with 100% for patients with a more brief (18 months) LV pump dysfunction. (From Bonow RO, Picone Al, McIntosh CL, et al: Circulation 1985;72:1244–1256.) Exercise Capacity.

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Preoperative exercise capacity has been shown to provide additional prognostic information to LV pump performance in aortic regurgitaton.[14] [158] Poor exercise tolerance (defined by the National Institutes of Health protocol, equivalent to approximately 8 metabolic equivalents [METs]) also predicts survival in symptomatic patients with aortic regurgitation. The 3year survival rate in patients with preserved exercise capacity was 100%, compared with 52% for patients with reduced exercise tolerance. Exercise capacity further stratifies patients with concomitant LV pump dysfunction into low- and high-risk groups. Decreased exercise tolerance in patients with a decreased fractional shortening ( 55 Decreased

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Part B: Based on the total point score, follow suggested guidelines regarding timing of surgery. Total Points Decision Regarding Surgical Intervention 0–1 Delay surgery; clinical and echocardiographic follow-up at 12 mo 2 Borderline; recommend clinical and echocardiographic follow-up at 6 mo ≥ 3 Proceed with surgery Part C: Although not a requisite part of the algorithm, these additional predictors of adverse outcome can also be used in decision analysis. These variables marked with a double-dagger (‡) can be measured by two-dimensional echocardiography. Additional Predictors of Adverse Outcome in Aortic Regurgitation ‡ Value Percentage fractional shortening < 29% End-systolic volume index > 60 mL/m2 End-systolic wall stress End-diastolic dimension End-diastolic dimension (radius) (R)/End-diastolic wall thickness (th)

> 235 mm Hg > 80 mm ≥ 3.2

*Add one point for age > 65; cardiothoracic ratio 0.58; LV hypertrophy on electrocardiogram. †Preserved = ability to complete at least 8 METs on graded exercise treadmill testing or stable exercise performance; Decreased = inability to complete 8 METs on graded exercise treadmill testing or a decline in exercise performance from an established baseline. ‡Add two points for each additional predictor present.

In aortic regurgitation, the timing of surgery in both asymptomatic and symptomatic patients is relatively straightforward. In general, the majority of symptomatic patients have improved survival, functional class, and LV pump performance with aortic valve replacement; therefore, they should be referred promptly for aortic valve replacement, regardless of the status of LV ejection fraction. Asymptomatic patients with impaired LV pump

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performance have a rapidly progressive course and are likely to develop symptoms and require aortic valve replacement within 2 to 3 years. These patients should be referred for elective aortic valve replacement. Asymptomatic patients who have normal exercise tolerance and preserved LV pump performance can be treated medically and followed closely with serial noninvasive assessments of LV ejection fraction. Left ventricular end-systolic dimension and exercise capacity are parameters that can be used to serially assess asymptomatic patients with aortic regurgitation for the development of LV pump dysfunction. A poor or decreasing exercise tolerance, defined as the inability to complete approximately 8 METs on a graded exercise treadmill test or any decline in LV pump performance from a previously established baseline, may signal the onset of LV decompensation. Similarly, patients who develop a progressive increase in end-systolic dimension likely have contractile dysfunction and, therefore, should be referred for surgery. Given that functional class III and IV symptoms are independent predictors of early and long-term postoperative mortality, patients with class II symptoms should be referred for surgical correction before class III or IV symptoms develop. Table 18-10 presents guidelines in the form of an algorithm for timing of surgery in patients with chronic aortic regurgitation based on a system in which points are assigned to different clinical variables. The major components (part A) of this algorithm include hemodynamic variables, including LV ejection fraction, LV size, and exercise capacity. The measured components of the algorithm, including LV ejection fraction and end-systolic dimension, were chosen on the basis of ease and reproducibility of the measurements using two-dimensional echocardiography. Included in this algorithm (part B) are additional parameters, all of which can be measured using two-dimensional echocardiography, that identify patients at high risk for contractile dysfunction. These parameters may, therefore, be used to confirm a decision to proceed with surgery, but they are not considered requisite components of the algorithm. These variables should be considered only supplemental to the decision-making process. The use of this algorithm to gauge the appropriate 412

timing of surgical intervention in aortic regurgitation is illustrated in the following case study. The patient was a 45-year-old construction worker

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with severe aortic regurgitation secondary to a bicuspid aortic valve. At the time of initial evaluation, the patient was able to complete stage III of a Bruce protocol without symptoms. Echocardiographic LV end-systolic dimension measured 45 mm, and the LV ejection fraction measured 55%. According to the algorithm, the patient would be assigned two points, justifying medical therapy with serial clinical and echocardiographic follow-up. The patient was treated with a vasodilator and followed every 6 months for 1 year, and then yearly thereafter. At 5 years after the initial diagnosis, although the patient remained asymptomatic, echocardiography revealed an increase in the LV end-systolic dimension to 55 mm and a decrease in the LV ejection fraction to 48%, resulting in a total of 3 points. The patient was then referred for successful aortic valve replacement.

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Summary After a long asymptomatic period, often lasting several years, severe, chronic mitral and aortic regurgitation eventually lead to reduced LV pump performance. In aortic regurgitation, decreased LV ejection performance is predominantly caused by afterload excess until late in the course of the disease, when contractile dysfunction supervenes. In contrast, contractile dysfunction occurs early in the course of mitral regurgitation, but it is masked by the favorable preoperative loading conditions. For both conditions, the development of irreversible contractile dysfunction is associated with increased risk for postoperative LV pump dysfunction and death from congestive heart failure. To justify the risk of surgery, the ideal timing for surgical intervention in patients with valvular regurgitation is, therefore, at the onset of contractile dysfunction, yet early enough to prevent the development of irreversible contractile dysfunction. Two-dimensional echocardiography, in conjunction with a thorough history and physical examination, provides an accurate, reproducible, and costeffective methodology for the serial screening for the development of contractile dysfunction in patients with valvular regurgitation. In this chapter, all of the major predictors of clinical outcome in valvular regurgitation, including those validated from nonechocardiographic methodologies, have been integrated to create the pathophysiologic framework necessary to develop algorithms for timing of surgical intervention using echocardiographic tools. The proposed algorithms for timing of surgery in patients with chronic mitral and aortic regurgitation guide operative intervention to preserve contractility and thereby improve long-term postoperative outcome and minimize unnecessary risk.

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417

Chapter 19 - Echocardiography in Patient Selection, Operative Planning, and Intraoperative Evaluation of Mitral Valve Repair Brian P. Griffin MD William J. Stewart MD

The advent of transesophageal echocardiography (TEE) and innovations in ultrasound technology have led to progressive improvement in the outcomes of valve surgery, especially mitral valve repair. Echocardiography has been used extensively in the operating room since the early 1980s. It is an essential element of every valve reconstruction operation.

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Indications for Intraoperative Echocardiography Intraoperative echocardiography has both diagnostic and monitoring functions that are useful in mitral valve repair and other valve-sparing operations. The diagnostic functions are used before cardiopulmonary bypass (prepump) to determine the mechanism and severity of the mitral valvular dysfunction, identify lesions of other valves, and refine the surgical mission. The diagnostic functions are used after cardiopulmonary bypass (postpump) to determine the success of the surgical mission. Intraoperative echocardiography is essential in performing valve repair, aortic hom*ograft, and pulmonary autograft implantation.[1] In addition to its use in valve surgery, the diagnostic function of intraoperative echocardiography also is used in the surgical management of congenital heart disease, [2] [3] hypertrophic cardiomyopathy,[4] [5] reconstruction of the ascending aorta,[6] [7] and many other surgeries (Table 19-1) . [8] The monitoring function of intraoperative echocardiography is used to determine the hemodynamic status of the patient before and after surgery, for assessing intravascular volume, and ventricular contractility. Perioperative monitoring of left ventricular function is important in patients with impaired contractility who are undergoing any kind of cardiac surgery, including myocardial revascularization, [9] [10] and in those with significant cardiac disease undergoing high-risk noncardiac surgery such as reconstructive surgery of the descending thoracic and abdominal aorta[11] [12] [13] (see Chapter 3) . Intraoperative echocardiography also is used to help position intravascular and intracardiac catheters,[14] , [15] including those used for retrograde cardioplegia via the coronary sinus. When postpump echocardiography detects intracardiac air, [16] [17] this can be cleared by further venting of the cardiac chambers to prevent embolization to the coronary blood vessels[18] 418

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TABLE 19-1 -- Indications for Intraoperative Echocardiography Mitral Disease Assess feasibility and success of mitral repair for mitral regurgitation. Assess feasibility and success of commissurotomy for mitral stenosis. Determine need for mitral surgery in patients undergoing revascularization or aortic surgery. Assess presence of disease of other valves or other cardiac structures. Aortic Disease Assess feasibility and success of aortic valve repair. Assess size of prosthesis. Assess feasibility and success of hom*ograft implantation or Ross procedure. Tricuspid Disease Assess need for and feasibility and success of tricuspid repair. Prosthetic Function Determine presence and site of paravalvular leak. Assess perivalvular tissue for abscesses or infection. Assess site and presence of pannus or thrombus. Revascularization Assess regional wall motion and global left ventricular function before and after revascularization. Determine sequence of graft placement. Detect and assess complications of infarction (ventricular septal defect, mitral regurgitation). Surgery on Aorta Assess size and extent of aneurysm. Determine the mechanism and severity of associated aortic regurgitation. Determine presence and complications of aortic dissection. Determine presence and extent of aortic atheroma. Transplantation/Devices

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Assess left ventricular function and suture lines postoperatively. Assess appropriate sizing, function, and hemodynamic changes with ventricular assist devices. Congenital Heart Surgery Determine connections (ventriculoarterial, atrioventricular). Assess systemic and nonsystemic ventricular size and function. Assess anatomy of shunts and valvular anatomy. Monitoring Assess ventricular volume and function. Monitor drug effects on ventricular function. Diagnose presence and location of ischemia. or the brain.[19] In patients who are difficult to wean off cardiopulmonary bypass or who remain hypotensive in the early postoperative period, echocardiography is a useful diagnostic and monitoring tool.[20] [21] More recent indications for intraoperative echocardiography include use in patient selection and monitoring for alternative surgical approaches such as the use of smaller incisions, port access techniques for cannulation, and offpump coronary artery grafting without cardiopulmonary bypass. [22] [23] The most frequent indication for intraoperative echocardiography is the postpump assessment of valve reconstruction surgery to determine whether the desired surgical result has been obtained. The availability of online feedback concerning the adequacy of the surgical result has allowed surgeons to become more innovative in repair techniques. Immediately after valve repair and before the chest is closed, the echocardiographer can determine whether the repair is adequate or if there is residual regurgitation or other complications present, requiring further repair or prosthetic implantation. Making this determination before the chest is closed allows the surgeon to perform further surgical procedures during a second run of cardiopulmonary bypass (a "second pump run") to optimize the surgical outcome. This second pump run eliminates the need for another surgical procedure at a later time, which would require another thoracotomy and create an increased mortality risk for the patient. In one study, 11% of patients undergoing valve surgery had inadequate results based on postpump echocardiographic imaging and required further surgery.[24] In our experience, intraoperative echocardiographic findings require a second pump run in 6% of cases.[1]

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It is axiomatic that all elective patients undergoing cardiac surgery have a full diagnostic work-up and a definite surgical plan before arriving in the operating room. Despite this, there are findings on the prepump echocardiogram that alter management by refining the preoperative diagnosis and the surgical mission. In our unpublished series of 436 consecutive prepump echocardiograms in patients with various valve problems, the surgical procedure was changed in 40 cases (9.2%). In a series of 154 consecutive patients undergoing valvular surgery, 29 patients (19%) had significant new findings by prepump intraoperative echocardiography. These findings changed the operative plan in 14 patients (9%). The changes were more common in mitral than aortic operations. The most frequent additional finding in this study was an increase in the severity of the valvular regurgitation compared with preoperative studies.[24] Even in patients in whom no major change in plan occurred, the prepump echocardiogram provided an updated understanding of the specific valvular anatomy and the mechanism of dysfunction, which helped to refine the surgical technique. These changes result from the improvement in resolution of TEE over preoperative transthoracic echocardiography (TTE) or cardiac catheterization and from changes in hemodynamic conditions or ischemia between the time of preoperative testing and the time of surgery. A 1999 study of 1918 consecutive cases in which intraoperative echocardiography was used showed a very low prevalence (2.5%) of discordant findings by echocardiography compared with operative findings. In only 0.3% of patients were the discrepancies sufficiently severe to warrant a change in the operative procedure. [25]

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Technique of Intraoperative Echocardiography Intraoperative echocardiography may be performed from either the transesophageal or epicardial imaging windows (Table 19-2) . Transesophageal Echocardiography TEE is the most widely used technique for intraoperative echocardiography. Figure 19-1 illustrates the experience with intraoperative echocardiography at the Cleveland Clinic Foundation from 1984 through 1999. TEE became available in 1987 and progressively supplanted the epicardial route for most studies. Compared with epicardial echocardiography, TEE has the advantage of allowing image acquisition without interfering with the surgical field or procedure. Immediately after induction 419

TABLE 19-2 -- Relative Advantages of Epicardial and Transesophageal Approaches to Intraoperative Echocardiography INDICATIONS

TRANSDUCER ADVANTAGES

Epicardial LVOT gradients; HOCM; congenital, aortic atheroma; TEE impossible or nondiagnostic 3.5–7.5 MHz transthoracic (standard TTE) sector scan Excellent images, especially of LVOT and septum; rapid imaging in emergency

Transesophageal All others

3.5–7.5 MHz transesophageal Does not interfere with sterile field; continuous imaging possible

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DISADVANTAGES Requires plastic covers for May be difficult to sterile preparation of probe; intubate esophagus once patient is draped; interferes with operative field and procedure; imaging occasionally impossible to obtain images (e.g., due to of posterior structures hiatal hernia, air), imaging difficult with prosthetic of anterior structures shadowing; may interfere difficult with hemodynamics; requires >1 person HOCM, hypertrophic obstructive cardiomyopathy; LVOT, left ventricular outflow tract; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. of anesthesia and endotracheal intubation, the TEE probe is inserted and left in place throughout the operation. Although the technique of intraoperative TEE is similar to its use in the echocardiography laboratory, there are additional potential pitfalls. First, it is occasionally difficult to pass the probe, particularly if the patient has been draped and the ether screen has been positioned. Usually, Figure 19-1 Cleveland Clinic Foundation experience with intraoperative echocardiography from 1984 to 1999. The total number of intraoperative echocardiograms per year is shown (bars).

this problem can be overcome using a laryngoscope and direct vision. Inadequate imaging occurs with the transesophageal approach for a number of reasons. Anatomic causes include a hiatal hernia or the presence of an echodense structure such as a mechanical valve prosthesis can cause shadowing of other cardiac structures. With all TEE studies, there is a "blind spot" approximately 2 to 4 cm in size in the middle portion of the ascending aorta caused by interposition of the trachea between the esophagus and the ascending aorta. Interference from electrical apparatus such as electrocautery leads to distortion of two-dimensional imaging and renders spectral and color Doppler signals impossible to interpret. Fortunately, imaging may be resumed once the electrocautery is discontinued. Another potential cause of ultrasonic probe dysfunction in the operating room is the thermistor in the transesophageal probe, which can sense an elevated esophageal temperature and cause the probe to stop

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functioning. This safety feature, designed to minimize the risk of esophageal damage from excess heat buildup in a malfunctioning probe, may deactivate the TEE transducer while the heart is being rewarmed after surgery. Newer probes have a mechanism whereby the probe temperature can be reset to take into account the patient's temperature. Finally, while the heart is on cardiopulmonary bypass, the absence of cardiac motion causes suboptimal images until the heart is filled with blood again and starts to eject during rewarming. Epicardial Echocardiography In epicardial imaging, images of the heart are acquired by placing a standard transthoracic transducer directly on the epicardium. Sterility is maintained using a double plastic sleeve. Intervening air is eliminated by using sterile acoustic gel inside the layers of plastic and by moistening the epicardial surface. An acoustic standoff such as a sterile bag or glove filled with saline is sometimes used if the structures of interest are superficial, in the first centimeter of depth below the probe. Epicardial echocardiography often provides better image quality than TEE of structures such as the ascending aorta, aortic arch, and left ventricular outflow tract, and it is especially accurate in measuring the outflow tract velocities. We use an epicardial approach when images obtained by TEE are inadequate during an open-chest procedure. Similarly, TTE can be used when needed during closed-chest procedures, including most types of noncardiac surgery. In addition, epicardial imaging is needed in infants who are too small for the available TEE probes. In the experience at the Cleveland Clinic Foundation, progressively fewer procedures are performed using an epicardial imaging window. The major current indication for an epicardial approach is in the evaluation of the ascending aorta of patients with suspected ascending atheroma, on the basis of clinical suspicion, calcification on chest x-ray study, or palpation by the surgeon. Identification of the severity and location of atheroma helps the surgical team optimize the location and methods of cannulation, 420

including the use of an alternative cannulation site such as the subclavian artery. In 1987 we described the following four standard imaging windows (Fig. 19-2) to be useful for epicardial imaging:[26]

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1. Parasternal equivalent. The transducer is placed on the most anterior portion of the heart, the right ventricular outflow tract. Image planes are similar to those for transthoracic imaging from the left parasternal imaging window. Both long-axis and short-axis views are obtained. The heart is scanned in the short axis from base to apex. By imaging more medially, the tricuspid valve and right ventricle also may be imaged. 2. Aorta-pulmonary sulcus. The transducer is placed in the sulcus between the pulmonary artery and ascending aorta, with the long side of the transducer against the left side of the ascending aorta. This view provides excellent images of the left ventricular outflow tract, aorta, aortic valve, mitral valve, and left atrium. 3. Subcostal equivalent. The transducer is at the most inferior portion of the thoracotomy incision against the most inferior portion of the right ventricular free wall. The four-chamber view is used to evaluate all four chambers, mitral and tricuspid valves, pulmonary artery, and the systemic veins. Angling medially allows imaging of the venae cavae, atria, and atrial septum. Angling superiorly visualizes the right ventricular outflow tract. Angling laterally brings in the left ventricular apex. 4. Aorta-superior vena cava position. The long side of the transducer is placed against the right side of the ascending aorta, pointing inferiorly and to the left, to image the left ventricular outflow tract and the aortic and mitral valves. This view is the best way to determine left ventricular outflow gradients with the continuous wave Doppler beam parallel to flow. The left atrium is also well seen from this view. Figure 19-2 The four standard positions for epicardial transducer placement. (From Cosgrove DM, Stewart WJ: Curr Probl Cardiol 1989;XIV:359–415.)

The epicardial window allows excellent imaging of intracardiac structures such as the cardiac valves and myocardium. High-velocity jets may be measured by continuous wave Doppler either with an imaging transducer or a stand-alone, nonimaging transducer. The epicardial window also has some disadvantages: 1. It enters the operative field and interrupts the operation itself. For this

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reason, a more limited time is available for imaging. 2. Imaging of structures in the near field may be difficult unless a good acoustic standoff is achieved. 3. Most surgeons and individuals that are accustomed to scrubbing for surgery are not adept at image acquisition with a hand-held transducer or echocardiographic anatomy, which requires a substantial learning curve. 4. If the probe is applied too heavily against the heart, it may cause arrhythmias or transiently interfere with cardiac filling. Equipment Ideally, an ultrasound machine devoted solely to intraoperative echocardiography should be available. In addition to interfacing with transesophageal and transthoracic transducers, the machine should be capable of recording M-mode and two-dimensional imaging and all Doppler modalities. A facility should be available near the operating room for cleaning and disinfecting the probes. Transthoracic probes from 3.0 to 7.5 MHz may be useful for different purposes, depending on the objectives of the study, using the lower frequency for general cardiac imaging and the higher frequency for infant congenital cases and aortic atheroma investigation. A stand-alone continuous wave Doppler probe should also be available. Sterile sleeves and acoustic gel should be available for epicardial imaging. The ultrasonic machine should have a capability for cineloop display and retrieval to compare prepump with postpump images. Videotapes or digital storage media should be available for archival of each study, an important consideration for medical-legal purposes. Cables should be available to input the electrocardiographic signal from the operating room monitoring system into the ultrasound machine. Many institutions have the capability of transmitting images from the operating room to a remote site such as the echocardiography laboratory in order to allow oversight or second opinions to be obtained in selected cases. Increasingly, digital storage of images is possible, which allows rapid retrieval to demonstrate findings to the surgical personnel and facilitates comparison of the preoperative and postoperative images.[27] Personnel Intraoperative echocardiography is a highly demanding technical field requiring specialized personnel skilled in transesophageal and epicardial imaging. This field requires

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421

familiarity with the phases of cardiac surgery and their effects on hemodynamics as manifested by echo and Doppler studies. The American Society of Echocardiography suggests that those learning TEE be in the phase of developing level 3 experience, which is equivalent to experience in performing at least 300 echocardiographic studies. In busy operating rooms in which a large volume of intraoperative studies are being undertaken, an echo technologist or other ancillary support person, working under the aegis of the echocardiographer, can facilitate and improve the efficiency of acquiring multiple studies, some of which may be needed simultaneously. Intraoperative Echocardiography Examination Intraoperative echocardiography should be performed in a standard comprehensive manner so that the acquisition of critical information is not omitted. It is important to do a complete TEE study, using imaging planes that allow good views of each intracardiac valve and chamber as well as the great vessels.[28] The entire prepump examination should be recorded on videotape or digitally to provide a durable record of the examination, especially as a reference for postpump studies and for medical-legal purposes. In cases in which comparison with postpump findings is likely, storing key images in a cineloop facilitates rapid comparison at the end of the operation. In diagnostic (as opposed to monitoring) studies, the structure of interest to the primary surgical mission should first be examined thoroughly in multiple planes, using imaging and Doppler modalities. If the echo study must thereafter be abbreviated because of pressing demands of the surgical agenda or the need to limit anesthetic and cross-clamp time, the primary concern, the raison d'être of the echo study, has at least been addressed. Other structures of interest should then be examined, including long- and short-axis views of all four chambers, all four valves, and the great vessels. The entire aorta should be examined in all cases. We also advocate a routine intravenous contrast injection to look for intracardiac shunting. The number of times the probe is passed through the gastroesophageal junction should be minimized, as should all unnecessary manipulation of the probe, to reduce the risk of mucosal trauma, esophageal tears, and pharyngeal trauma that are reported in a very small percentage of cases.[29] Once the prepump study is completed, a written report of the examination detailing significant findings should be made. Although ultrasound has not

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been demonstrated to cause any significant damage to cardiac structures during prolonged examinations,[29] it is advisable to put the machine on freeze so that no ultrasound energy is transmitted when imaging is not required. After cessation of cardiopulmonary bypass, a second comprehensive examination should be carried out and a second or updated report generated. The intraoperative examination has several aspects that are different from a TEE or TTE study in the outpatient echocardiography laboratory: 1. The echocardiogram is performed simultaneously with the operation; therefore, the room conditions, including the lighting and the space for the machine, may be suboptimal. For example, radiofrequency interference from other machines may mar the quality of images for long periods. 2. The hemodynamic milieu may change quickly, and the echocardiographic appearance may differ from images acquired outside the operating room. Changes in hemodynamics, such as intravascular volume, preload, and afterload, substantially affect the severity of valvular lesions. If necessary, the hemodynamic situation may be manipulated to match "street conditions" in order to determine the true or potential severity of a valvular lesion. 3. The surgeon who requests the intraoperative study may request online interpretation. Care must be maintained to make only diagnoses and conclusions that have been verified by examination from multiple imaging planes under appropriate imaging and hemodynamic conditions.

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Prepump Intraoperative Echocardiography in Patients Undergoing Valve Repair for Mitral Regurgitation The prepump echocardiogram assessment of mitral regurgitation (Table 193) usually merely confirms findings made previously by preoperative echocardiography or cardiac catheterization. TEE, however, often can improve on the accuracy and resolution of preoperative TTE because of improved resolution of the component structures, the mitral valve and the regurgitant jet. There are four main goals of intraoperative echocardiography in mitral valve disease: 1. To assess the severity of mitral regurgitation and determine the need for mitral valve surgery. 2. To assess the mechanism of mitral regurgitation and determine if a repair rather than prosthetic replacement is feasible and to determine the technique of repair. 3. To determine the presence of other significant valvular 422

disease that may require surgical attention, such as tricuspid regurgitation or aortic valve disease. 4. To assess left and right ventricular function in order to be able to compare with the postpump study. TABLE 19-3 -- Intraoperative Assessment of Repair and Reconstructive Valve Operations Prepump Assess severity of stenosis/regurgitation. Assess mechanism of regurgitation and potential reparability of valve.

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Measure dimensions of annulus, chambers, valves. Assess whether lesions other than the primary lesion require surgery. Determine biventricular function. Postpump Assess severity and mechanism of residual regurgitation/stenosis. Detect systolic anterior motion of the mitral valve and left ventricular outflow obstruction. Determine change in severity of other valve lesions. Assess biventricular function. Detect iatrogenic complications. Severity of Mitral Regurgitation The severity of mitral regurgitation is assessed by intraoperative echocardiography in the same manner as the use of echocardiography for other applications in other parts of the hospital (see Chapter 1) .[30] [31] [32] [33] [34] Several have indicated that the intraoperative assessment of mitral regurgitation agrees with the preoperative assessment by contrast ventriculography or TTE.[35] [36] In patients with ischemic mitral regurgitation, agreement between preoperative studies and the intraoperative assessment is less, possibly because of changes in hemodynamics or the degree of ischemia. One study of patients with ischemic mitral regurgitation showed that in 11% of patients the preoperative and intraoperative assessments of mitral regurgitation severity differed by more than one grade, with discordance occurring in both directions.[37] Discordance was more common in patients with clinical instability or those who received thrombolysis. It is important to remember that mitral regurgitation is dynamic and is affected by loading conditions. Reduction of afterload or intravascular volume at the time of the operation may reduce the true severity of the regurgitation. When less mitral regurgitation is found than expected, the intravascular blood volume should be expanded and systemic vascular resistance increased transiently using repeated boluses of IV phenylephrine. The velocity of mitral regurgitation, and therefore display of its jet by color Doppler, depends on the pressure difference between the left atrium and left ventricle, which is higher with hypertension. The size of the jet in the left atrium is also very sensitive to changes in color gain (directly proportional) and pulse repetition frequency (inversely proportional) (see Chapter 17) .

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The transesophageal imaging window has advantages over epicardial imaging in the assessment of mitral regurgitation. A mitral prosthesis or severe mitral calcification causes acoustic shadowing of the regurgitant jet when the transducer is placed anteriorly, such as in epicardial imaging or TTE. Excellent agreement, however, has been reported between the epicardial and transesophageal approaches in assessing mitral regurgitation. [38]

Semiquantitation of mitral regurgitation on a scale from 0 to 4+[30] [31] is determined based on a weighted average of several criteria: 1. The size of the left atrial flow disturbance, based on the depth of penetration and area of the regurgitant jet in the left atrial cavity assessed in multiple imaging planes; a multiplane probe facilitates this process, especially in eccentric jets. 2. The geometry of the jet; eccentric jets tends to have a higher regurgitant volume than free jets of the same area.[32] 3. The size of the proximal convergence zone, also called the proximal isovelocity surface area (PISA) technique. More severe regurgitation is associated with a larger radius of the proximal flow convergence.[33] Flow convergence can be used to calculate regurgitant flow, orifice area, and volume (see later). 4. The width of the proximal portion of the regurgitant jet on the left atrial side of the orifice is also useful and may be less load sensitive than mapping of the regurgitant jet in the atrium.[39] 5. The pulmonary venous pulsed Doppler tracing. Severe mitral regurgitation often leads to systolic reversal of flow in the pulmonary veins,[34] which is 69% sensitive and 98% specific in predicting a regurgitant orifice area of greater than 0.3 cm2 .[40] Blunting of pulmonary vein flow is somewhat reliable in predicting severe mitral regurgitation for patients in normal rhythm with normal left ventricular function but is unreliable in patients with severe left ventricular dysfunction or atrial fibrillation. A normal pulmonary vein flow pattern is useful in excluding severe mitral regurgitation and predicting a regurgitant orifice area of less than 0.3 cm2 . Importantly, in patients in which the right and left pulmonary vein flow pattern is discordant (23% of patients), the more abnormal pattern is most predictive of mitral regurgitation severity. 6. Quantification of mitral regurgitant volume (RV) from the difference between Doppler echocardiography measurements of antegrade flow through the mitral and the aortic valves. Regurgitant fraction (RF) is

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the proportion of total mitral flow (MF) that is regurgitant: RF (%) = RV/MF Mitral and aortic valve flow can be assessed by the product of annular cross-sectional area derived from echo and velocity derived from pulsed Doppler measurements at the same site. Mitral cross-sectional area is derived from two orthogonal diameters of the annulus, which is elliptic in shape.[41] This method has not been used routinely because of the timeconsuming nature of the measurements required and the ease and general reliability of semiquantitative techniques (see Chapter 17) . Other methods of assessing the severity of mitral regurgitation in the operating room include surgical palpation of the left atrium for the thrill of a mitral regurgitant jet, evaluation of the size of v waves on the left atrial pressure tracing, fluid filling of the arrested left ventricle, and contrast echocardiography. These methods lack sensitivity and are not as reliable or as convenient as color flow Doppler techniques.[36] [42] [43] The size of the regurgitant orifice area can be derived from Doppler echocardiography techniques in the operating room,[44] using either the antegrade flow difference method or the flow convergence method. The maximum regurgitant orifice area is calculated by dividing regurgitant flow rate by the maximum mitral regurgitant flow velocity (Vmax ) obtained from continuous wave Doppler. The regurgitant orifice area is greater than 0.4 cm2 in severe mitral regurgitation and greater than 0.25 cm2 in moderately severe mitral regurgitation. The flow convergence, or PISA, technique analyzes flow proximal (on the left ventricular side) to the regurgitant orifice, assuming a hemispheric shape.[44] [45] In this area, blood accelerates predictably as it moves toward the 423

regurgitant orifice and forms a series of concentric shells of decreasing area and increasing velocity that are depicted clearly as easily measured hemispheres on the color image because of the color aliasing of the accelerating flow. Because the surface area of a hemiellipse can be calculated from 2πr2 for blood flow moving at velocity v and at a radius r from the regurgitant orifice (Fig. 19-3) , flow rate Q can be calculated as

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follows: Q = 2πr2 v The PISA method provides excellent estimation of regurgitant flow when the flow convergence is centrally located, well away from the walls; however, this method overestimates regurgitant flow when the proximal flow is constrained by the left ventricular wall. Use of appropriate correction factors can compensate for this problem.[46] Automated analysis of digital velocity maps in the echocardiographic machine is feasible and has the potential to further simplify this technique.[47] The PISA method of determining the regurgitant orifice area (ROA) may be simplified without significant loss of accuracy. If the aliasing velocity of the color Doppler is set to approximately 40 cm per second and the mitral regurgitation by continuous wave Doppler (Vmax ) is assumed to be 5 m per second (500 cm per second), then the formula becomes

ROA = (2πr2 v)/Vmax ROA

[2(3.14)(r2 )(40 cm/s)]/(500 cm/s)

ROA

250 r2 /500

ROA

r2 /2

This method has particular merit in the operating room where rapid quantification is often helpful. Mechanism of Mitral Regurgitation Assessment of the cause (Fig. 19-4) and mechanism (Fig. 19-5) of mitral regurgitation is of great importance Figure 19-3 (color plate.) Proximal convergence zone of a patient with severe mitral regurgitation. The hemisphere produced by flow at an aliasing velocity of 51 cm per second is shown (arrow). The radius of the hemisphere is 1 cm.

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Figure 19-4 Feasibility of mitral repair by etiology of valve disease at the Cleveland Clinic Foundation. (From Stewart WJ: ACC Heart House Learning Center Highlights 1995;10:2–7.)

in determining the suitability of the mitral valve for repair. Mitral valve repair is most likely in patients with mitral regurgitation due to myxomatous degeneration and is least likely in patients with regurgitation due to endocarditis. Repair is now successful in greater than 90% of all patients with myxomatous disease. The probability of repair, however, is affected by the mechanism of regurgitation, especially whether the posterior leaflet, the anterior leaflet, or both leaflets are involved. Repair is most likely with posterior prolapse or flail, whereas bileaflet involvement and isolated anterior leaflet prolapse reduce the likelihood of successful repair substantially.[48] An Organized Approach to Imaging the Mitral Valve

To adequately assess the pathophysiologic mechanism responsible for mitral regurgitation, it is essential to perform Figure 19-5 Feasibility of mitral valve repair by mechanism of regurgitation in myxomatous mitral valve disease. (From Stewart WJ: ACC Heart House Learning Center Highlights 1995;10:2–7.)

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a thorough examination of the mitral valve and mitral apparatus and to determine the origin and geometry of the regurgitant jet. The long-axis imaging planes are best for determining which mitral leaflet is involved. Long-axis views of the mitral valve are obtained by imaging from midesophageal TEE planes. Figure 19-6 shows the "multiplane protractor" with all of the multiplane angles superimposed on the mitral valve. Most basilar long-axis views around the entire multiplane sweep allow portions of both leaflets to be examined individually. At approximately 50 to 60 degrees in most patients, the imaging plane parallel to a line between the commissures, is very useful for determining which portion of the anterior or posterior leaflet is involved. Imaging at a multiplane angle of about 135 degrees cuts perpendicular to this intercommissural line.

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The short-axis views also are useful for determining which portion of the anterior or posterior leaflet is involved. These views may be obtained from either the transgastric short-axis view or the epicardial parasternal shortaxis equivalent view.[49] The posterior leaflet has three divisions or scallops: the medial, middle, and lateral. The anterior leaflet is not segmented but has a central portion known as the bare area between the insertions of the chordae from the anterolateral and posteromedial papillary muscles. In a similar way the posterior leaflet is also supported, about half each by chordae from the anterolateral and posteromedial papillary muscles. The papillary muscles lie below each mitral commissure. The papillary muscles and chordae usually are well visualized from the transgastric long-axis views of the left ventricle using biplane or multiplane probes.[50] In assessing the mitral valve and in providing the results to the surgeon, giving an accurate localization of the abnormality is important. A prospective study of 50 patients used a segmental approach to the mitral valve, breaking each leaflet into three segments, and found that TEE was 96% accurate for localization compared with surgical findings.[51] Other Figure 19-6 The short-axis view of the mitral valve in systole from a transverse transgastric view. The medial and lateral commissures (COMM) and the positions of the medial (MED), middle (MID), and lateral (LAT) scallops of the posterior leaflet are shown. ANT, anterior. (From Stewart WJ; Griffin B, Thomas JD: Am J Cardiol Imaging 1995;9:121–128.) Figure 19-7 Transgastric short-axis view of the mitral valve in a patient with severe prolapse of the middle scallop of the posterior leaflet (arrow). ANT, anterior leaflet.

researchers have shown that localization of the defect to the posterior leaflet by TEE is 78% sensitive and 92% specific in myxomatous disease, with accuracy being least when the medial rather than the lateral or middle scallop is involved.[52] Assessment of the mechanism of mitral regurgitation is performed by analyzing the motion of the valve leaflets with twodimensional echocardiography (Fig. 19-7) and the direction of the regurgitant jet with color flow imaging [53] (Table 19-4) . Three types of leaflet motion (Fig. 19-8) may be associated with mitral regurgitation: (1) excessive motion, as seen with prolapse or flail valve caused by chordal rupture or elongation, (2) restricted motion, as seen in rheumatic disease and papillary muscle infarction, and (3) normal motion, as seen with leaflet perforation and ventricular-annular dilation.

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Intraoperative echocardiography has been shown to be highly sensitive and specific in determining the mechanism of mitral regurgitation in patients undergoing mitral TABLE 19-4 -- Determination of the Mechanism of Mitral Regurgitation from Analysis of Jet Direction and Leaflet Mobility Jet Direction Anterior Posterior

Leaflet Motion RESTRICTIVE NORMAL

EXCESSIVE Prolapse/flail of posterior leaflet Prolapse/flail of anterior leaflet

Restriction of posterior > anterior leaflet Equal restriction of both leaflets

Central

Prolapse/flail of both leaflets

Commissural

Rupture of commissural chordae or papillary muscle

Eccentric origin

Apical tethering from LV dilation Apical tethering from LV dilation, annular dilation

Leaflet perforation or cleft

LV, left ventricular.

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Figure 19-8 Morphology and echocardiographic appearance of normal, excessive, and restricted motion of the mitral valve, each of which can cause mitral regurgitation. (From Cosgrove DM, Stewart WJ: Curr Probl Cardiol 1989;XIV:359–415.)

valve surgery. In a study of 286 patients undergoing mitral valve surgery in whom the echocardiography mechanism was correlated with the surgical findings, echocardiography was highly accurate (86%) in determining the mechanism of mitral regurgitation.[53] Echocardiography was least accurate in ascertaining the mechanism of mitral regurgitation in patients with

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leaflet perforation, bileaflet prolapse, or ventricular-annular dilation. Excessive Leaflet Motion.

Excessive leaflet motion occurs with elongation or disruption of any portion of the mitral valve or of the mitral apparatus, including the papillary muscles and chordae. Myxomatous disease, endocarditis, and papillary muscle infarction all can lead to this abnormality. With excessive leaflet motion, the regurgitant jet is directed away from the affected leaflet. Thus, prolapse or flail of the posterior leaflet leads to an anteriorly directed jet (Fig. 19-9) . In bileaflet prolapse, the excessive motion is often asymmetric, and the jet direction is away from the more severely affected leaflet. When the amount of prolapse or flail is completely balanced between both leaflets, a central jet direction occurs. If the chordae to the commissures are ruptured, then a jet originating at the commissures is seen in the transgastric short-axis view. Jets originating at the commissure also are seen in infarction of a papillary muscle, most commonly the posteromedial one.[54] Excess motion with overwhelming mitral regurgitation results when the head of a papillary muscle ruptures in an acute myocardial infarct. This type of rupture may be differentiated from acute chordal rupture by detecting a mass attached to the flail leaflet that is a portion of the muscle and by the appropriate clinical setting (Fig. 19-10) . Precise delineation of which portion of the valve has excess motion is important in planning the surgical repair. Rupture of the posterior chordae is the most common abnormality and is repaired by quadrilateral resection of the posterior leaflet (Fig. 19-11) . Elongation of the chordae is repaired by chordal transfer or by implantation of artificial chordae. Papillary muscle elongation or disruption may be repaired by reimplantation, supporting, or shortening the affected muscle.[48] Postoperative prognosis is best in those with excessive leaflet motion. Restricted Leaflet Motion.

This pattern is seen most commonly in rheumatic disease, but it also can occur in regurgitation from ischemic heart disease, the chronic phase of lupus, or acquired valvular disease caused by certain drugs such as ergot derivatives and anorexigenic drugs such as the fen-phen combination (fenfluramine and phentermine). In rheumatic, lupus, and drug-induced diseases, the leaflets are thickened. If both leaflets are equally affected by the pathologic process, the jet direction is central. More commonly in rheumatic disease, the posterior leaflet is more severely affected than the

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anterior leaflet, and the relatively normal anterior leaflet "over-rides" the restricted posterior leaflet. The direction of the regurgitant jet in this situation is posterior, toward the affected leaflet. The surgical approach to this condition includes débridement of the valve tissue and chordae, commissurotomy, and annuloplasty. This type of repair is more technically demanding and is less often successful. In ischemic heart disease, the posterior leaflet is typically restricted in motion owing to apical displacement of the posteromedial papillary muscle. The displacement results from ischemia or infarction of this papillary muscle or the muscle to which it is attached and which is usually in the perfusion territory of the right or circumflex coronary artery. The leaflets themselves are normal and are not thickened but fail to coapt adequately (Fig. 19-12) . In extreme cases the leaflets may not touch at all. The surgical approach to this problem usually involves placement of an annuloplasty ring to reduce the size of the mitral annulus and coronary revascularization. Use of a figureof-eight or Alfieri stitch either alone or in combination with annuloplasty ring also has been used. The Alfieri 426

Figure 19-9 (color plate.) Posterior leaflet prolapse (A) with severe mitral regurgitation (B) before mitral valve repair and no mitral regurgitation after successful mitral valve repair (C).

stitch effectively converts the mitral valve into a doubleorifice valve by attaching the leaflets at their midpoint. Surgical treatment of ischemic regurgitation with restricted leaflet motion is less successful in that residual regurgitation is often more significant than after myxomatous valve repair. Figure 19-10 Papillary muscle rupture with resulting severe mitral regurgitation. The rupture portion of muscle is seen prolapsing into the left atrium (arrow). Normal Leaflet Motion.

Perforation of the valve leaflet causing mitral regurgitation occurs most commonly because of endocarditis or because of a congenital cleft in the valve. Occasionally it is iatrogenic, after attempted repair. The jet origin is eccentric, arising from the midportion of the leaflets rather than from the coaptation line. The

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Figure 19-11 Quadrilateral resection of the posterior leaflet of the mitral valve with annular ring implantation. (From Cosgrove DM, Stewart WJ: Curr Probl Cardiol 1989;XIV:359–415.)

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Figure 19-12 Ischemic mitral regurgitation with restricted posterior leaflet motion and posteriorly directed jet of mitral regurgitation.

prejet flow acceleration also may be seen away from the coaptation line, along the affected leaflet. Leaflet perforation may be repaired in some instances by suture closure or with pericardial patch.[55] Normal leaflet motion is commonly seen in patients with mitral regurgitation secondary to left ventricular dilation of any cause, such as disease of other valves, dilated cardiomyopathy, or severe ischemic cardiomyopathy. We have previously termed this category ventricularannular dilation. Ventricular enlargement causes displacement of the mitral coaptation point toward the apex with resultant impaired coaptation. Annular dilation is seen in these patients, but it occurs in proportion to left ventricular dilation, in contrast to myxomatous or rheumatic mitral regurgitation patients whose annulus size is often abnormally large. Annuloplasty with ring insertion is commonly used in the surgical management of these patients. An Alfieri stitch to support the valve also has been used instead of or in addition to the annuloplasty. There has been an upsurge in interest in the surgical management of severe mitral regurgitation in patients with dilated cardiomyopathy. Excellent functional improvement with a relatively low operative mortality has been reported even in selected patients with severe mitral regurgitation and severe left ventricular dysfunction. One study of 248 patients undergoing mitral valve surgery showed that TEE was greater than 90% accurate for definition of the mechanism of regurgitation, localizing the origin of regurgitation, and in detecting a flail segment. TEE was 88% accurate in detecting ruptured chordae. The TEE findings of valve function were highly predictive not only of valve reparability but also of long-term survival, which were independent of age,

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gender, ejection fraction, and coronary artery disease. [56] Other Valve Disease and Biventricular Function During Mitral Repair The severity of aortic and tricuspid valvular disease is assessed by intraoperative TEE using color flow mapping to determine the severity of the dysfunction and the necessity of valve surgery. These decisions should be made preoperatively, but diagnostic information should be refined intraoperatively, as mentioned earlier. Intraoperative diagnosis is particularly important in patients with active endocarditis. Significant tricuspid or aortic regurgitation usually requires operative intervention; however, intraoperative echocardiography tends to underestimate the degree of tricuspid regurgitation because of optimization of the hemodynamics that usually results in a reduction of right-sided pressures and volume. Because the preoperative echocardiogram is generally performed under ambulatory conditions, it is a better guide to decision making with regard to tricuspid valve repair, as opposed to the intraoperative findings alone. Regional and global left ventricular function is best assessed using TEE from long- and short-axis transgastric views and various midesophageal long-axis views. The long- and short-axis views from any epicardial imaging window also show the left and right ventricle well. Right ventricular function is assessed by TEE in the midesophageal 45-degree view at the level of the short axis of the aortic valve, from the midesophageal transverse four-chamber view, or from a longitudinal transgastric view rotated clockwise to obtain a long-axis image of the right ventricle.

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Determining the Need for Mitral Valve Surgery in Patients Undergoing Cardiac Surgery for Other Reasons Intraoperative echocardiography increasingly is used to determine the need for a mitral valve operation in patients undergoing aortic valve surgery or revascularization procedures; this is especially true in the assessment of patients in whom the severity of the mitral regurgitation preoperatively is significantly different by cardiac catheterization and echocardiography, when the severity of mitral regurgitation over time is variable (such as in ischemic heart disease), and when the mitral regurgitation is of moderate severity. The following questions must be considered when determining the need for mitral valve surgery in addition to the primary surgery: 1. How severe is the mitral regurgitation? 2. Is there a primary abnormality of the mitral valve (such as a torn chord or prolapse)? 3. Will the mitral regurgitation change as a consequence of the primary operation? 4. Is the valve repairable or is prosthetic replacement necessary? 5. What is the additional risk imposed by the additional mitral valve procedure? The final decision on surgery is made by the surgeon; however, when the surgical objectives are changed in the operating room, telephone consultation with the referring cardiologist is advisable. In many patients, especially those in whom the regurgitation is secondary to ischemia or left ventricular dilation, 428

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the severity of the regurgitation may be variable. Sometimes, the severity of regurgitation detected at the time of operation is different from that recorded preoperatively. Frequently the difference in severity is due to a true physiologic change. Compared with ambulatory conditions, the loading conditions during surgery often entail a lower intravascular volume and less peripheral vasoconstriction, both of which may reduce the severity of valvular regurgitation and reduce stenotic valve gradients. On other occasions this discrepancy reflects the superior ability of esophageal and epicardial echocardiography to visualize mitral regurgitation. When approaching patients whose regurgitation is 2+ or less, we often purposely increase the afterload with multiple boluses of 100 µg of phenylephrine to determine the severity of regurgitation at a mean arterial pressure that is transiently as high as 120 mm Hg. Patients with 3+ or more mitral regurgitation at rest, or during this afterload stress test, are generally considered candidates for a mitral valve operation. The threshold for surgery on the mitral valve also is affected by other factors, including whether there is a primary structural abnormality of the valve. If the valve appears to be repairable, the threshold for surgery is lower, given the relatively low morbidity and mortality associated with repair as compared with valve replacement, whereas the threshold for surgery is higher in patients with valves that are not reparable. In patients undergoing surgery for aortic stenosis, improvement in the severity of the mitral regurgitation can be expected postoperatively. Therefore, the threshold for concomitant mitral surgery is higher.[57] [58] A postpump assessment of the mitral regurgitation is made regardless of whether a surgical intervention on the mitral valve has been performed.

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Postpump Intraoperative Echocardiography in Mitral Repair The most significant indication for intraoperative echocardiography in mitral valve repair (see Table 19-3) is to determine the competency of the repair immediately after cardiopulmonary bypass. If the repair is inadequate, further repair or replacement can be performed immediately during the same thoracotomy. Timing Return of the patient to normal loading conditions is necessary to make valid assessments of valvular performance. It is also best to make valvular assessments after ventricular function has reached its postoperative plateau. The most appropriate time to image after repair is when the patient is off cardiopulmonary bypass, the intravascular volume is replete, and the loading conditions are similar to those in the ambulatory state. Imaging can be initiated after the aortic cross clamp is off and when the left ventricle is at least partially filled, but abnormal findings at this time may result from abnormal left ventricle geometry. The surgeon should not act on these findings unless they are subsequently confirmed by further imaging after the cessation of cardiopulmonary bypass. Intraoperative Findings In most cases, with an experienced surgeon, mitral valve repair leads to a competent mitral valve with mild or no residual mitral regurgitation; however, there are potential complications of mitral valve repair that are readily recognized by postpump intraoperative echocardiography. Many of these complications may not be apparent clinically or may take longer to accurately diagnose without echocardiography. If left untreated, these complications may interfere with the long-term success of the procedure and require early reoperation. Complications seen after mitral valve repair by intraoperative echocardiography are shown in Table 19-5 .

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Incomplete Mitral Repair Significant residual mitral regurgitation is the most common postpump problem detected by intraoperative echocardiography. The incidence of this complication varies with the cause of the valvular regurgitation, the complexity of the repair, the experience of the surgeon, and the threshold of the operative team to accept a suboptimal result. Frequently, if the echocardiographer can define the mechanism of the residual regurgitation, further repair of the valve leads to an improved result with reduction or elimination of mitral regurgitation. In some patients, TABLE 19-5 -- Management of Abnormal Findings on Doppler Echocardiography after Mitral Valve Repair Complication Residual mitral regurgitation

Management Define mechanism. If ≤1 +, accept. If 2 +, give phenylephrine to recheck MR with increased afterload; if >2 +, further surgery is required. Systolic anterior motion with Assess LVOT gradient and MR. LVOT obstruction Increase ventricular volume, stop positive inotropes, and increase afterload. If these measures are not successful, further surgery is needed to revise repair. Dehisced ring or leaflet perforation Another pump run is needed to fix annuloplasty. Residual mitral stenosis Quantify severity. If mean gradient >5 mm Hg or area < 1.5 cm2 , consider further surgery. Significant tricuspid regurgitation If 3 + or more, consider further repair. Regional left ventricular Assess intracardiac air; if not resolved dysfunction after further time on pump, consider coronary bypass. Global (right or left) ventricular Assess volume status, afterload, and dysfunction response to medications. LVOT, left ventricular outflow tract; MR, mitral regurgitation.

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further repair is impossible or fails, and the patient requires another pump run to implant a prosthesis. Moderate (2+) or more mitral regurgitation, either at rest or following afterload challenge with phenylephrine as previously described, is generally considered excessive after mitral repair and is an indication for a further surgical procedure. If the regurgitation is mild (1+) or less, then the result is usually accepted, though individual surgeons vary in their willingness to accept even mild grades of regurgitation. The severity of mitral regurgitation detected by immediate postpump intraoperative echocardiography correlates well with angiographic or TTE and TEE estimates of severity obtained later.[59] [60] Rarely, changes in the early postoperative period such as chordal rupture, suture dehiscence, or early postoperative endocarditis may cause acute worsening of the mitral regurgitation. Thus, intraoperative echocardiography is a reliable measure of the severity of mitral regurgitation and the need for further intervention. Other considerations in deciding whether residual mitral regurgitation should be accepted or subjected to another surgical procedure include the mechanism of the mitral regurgitation, the overall condition of the patient, and left ventricular function. Postpump determination of the mechanism of the residual mitral regurgitation helps the surgeon to determine whether a further reparative procedure could lessen the regurgitation and yet conserve the valve. More mitral regurgitation than is usually desirable might be accepted when other surgical procedures such as aortic valve replacement or coronary artery bypass grafting also have been accomplished, particularly in elderly patients or those with significant left ventricular dysfunction. For example, in patients with extensive mitral annular calcification, mitral prosthetic insertion may be technically more difficult and more hazardous for the patient than accepting a 2+ or even 3+ mitral regurgitation.[61] In one study of 100 patients undergoing mitral valve repair, 8% needed a second pump run, and 3% had persistent mitral regurgitation that was greater than 2+. Further repair in all three patients led to an improvement in regurgitation. [35] In another study of 309 patients undergoing mitral valve repair, 26 (8%) had immediate failure and required further cardiopulmonary bypass. Ten of those patients (3.2%) had excessive residual regurgitation. Two of the 10 patients subsequently had mitral prosthetic implantation, and eight had further repair. The further repair

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included chordal shortening in three patients, annuloplasty in four patients, and both procedures in one patient. Residual mitral regurgitation after the second repair was mild or absent in all patients. In this study, inadequate repair was associated with a degenerative cause of the mitral regurgitation and with the absence of an annuloplasty ring implantation at the time of initial repair.[62] In another study, residual mitral regurgitation caused by inadequate repair was seen in 4% of patients immediately postpump. In this study, need for reoperation because of inadequate repair or systolic anterior motion of the mitral valve was more common in patients with anterior mitral leaflet or bileaflet prolapse, as opposed to those with posterior prolapse.[63] Impact on Clinical Outcome The severity of residual mitral regurgitation after mitral valve repair is important for prognosis, as shown by several studies. In one of these studies, moderate or greater mitral regurgitation was associated with a higher incidence of congestive heart failure, repeat valve surgery, or postoperative death.[37] In a study of ischemic mitral regurgitation, residual regurgitation by postpump intraoperative echocardiography was a strong predictor of survival after mitral valve repair.[24] Residual mitral regurgitation in ischemic heart disease, however, correlates more with the degree of permanent contractile impairment rather than the technical success of the repair procedure. In another study, two patients with 3+ mitral regurgitation as determined by postpump intraoperative echocardiography who did not undergo a further pump run at the time of initial surgery required reoperation within 5 days because of hemodynamic instability and the inability to wean off mechanical ventilation.[35] Patients who undergo a second pump run for an initially inadequate repair have an in-hospital complication rate that is similar to that of patients who require a single pump run.[64] In one study, residual mitral regurgitation of 1+ or 2+ did not increase hospital complications when compared with trivial or no regurgitation postoperatively. There was a trend for patients with 1+ or 2+ mitral regurgitation, however, to need more reoperations in late follow-up than those with trivial or no mitral regurgitation.[65]

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Other Complications of Mitral Valve Repair Systolic Anterior Motion of the Mitral Valve Significant left ventricular outflow obstruction caused by systolic anterior movement of the mitral valve (SAM) has long been recognized as a complication of mitral valve repair.[66] [67] This abnormality simulates that seen in hypertrophic cardiomyopathy, even though septal hypertrophy is absent. Similar to outflow obstruction in hypertrophic cardiomyopathy, SAM after mitral repair is dynamic and exacerbated by reducing the size of the ventricular chamber or augmenting the contractile state. SAM may cause pressure gradients of 100 mm Hg or more, severe hypotension, severe mitral regurgitation, and inability to wean the patient from cardiopulmonary bypass. Fortunately, this series of complications is readily recognized and quantified by an experienced echocardiographer on the postpump echocardiogram study (Fig. 19-13) . SAM has been reported in 2% to 9% of patients undergoing mitral valve repair.[35] [63] [68] Several mechanisms have been proposed to explain SAM following mitral valve repair. These mechanisms include anterior displacement of the posterior ventricular wall, anterior displacement of the posterior mitral leaflet, and narrowing of the angle between the mitral and aortic valves.[69] It is clear that SAM occurs primarily in patients 430

Figure 19-13 (color plate.) Series of images indicating the presence of systolic anterior motion at the end of the first pump run (A, arrow) leading to severe mitral regurgitation (B) and outflow obstruction (C). The maximal velocity measured in the outflow tract was 4.6 m per second, giving a pressure gradient of 85 mm Hg.

with degenerative mitral valve disease, those with large mitral leaflets, and

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in the presence of a hyperdynamic small ventricle.[63] SAM is usually seen only after annuloplasty ring insertion, but it has been reported after a suture annuloplasty.[63] It is seen more commonly with stiff than flexible annuloplasty rings.[63] [68] One quantitative study has shown that SAM is associated with anterior displacement of the mitral coaptation line. The anterior displacement is reduced or disappears after successful revision of the repair and elimination of SAM.[69] More recently, the ratio of the length of the anterior and posterior leaflet in the coapted state and the distance from the coaptation point to the septum were shown to be predictors of systolic anterior motion on preoperative TEE. The smaller the ratio between anterior and posterior leaflet and the narrower the distance between the coaptation point and the septum, the greater the likelihood of SAM.[70] When severe, SAM is easily recognized and may involve both leaflets. The left ventricular outflow gradient and the severity of mitral regurgitation are important indicators of the hemodynamic severity. The deep transgastric imaging window with the heart in an orientation similar to a transthoracic apical five-chamber image provides the best transesophageal window for assessing the left ventricular outflow tract gradient with continuous wave Doppler. When this examination cannot be reliably performed with the transesophageal approach, an epicardial study may be needed. The initial management of this condition should be to increase intracardiac volume by fluid repletion and to stop any positive inotropic agents that are being administered.[63] Systemic afterload can be supported by a pure alpha agonist (phenylephrine), avoiding any beta agonists. If these measures are inadequate to reduce the severity of SAM, another pump run to improve the SAM is indicated. Further procedures to improve SAM include (1) a sliding posterior leaflet advancement (sliding plasty), which reduces the anteriorposterior height of the posterior leaflet; (2) insertion of an annuloplasty of larger size; and (3) removal of the annuloplasty ring. Sliding annuloplasty is currently used as a component of the primary operative procedure on patients who are considered at risk for developing SAM and has significantly reduced the incidence of this complication in those patients in whom it has been used.[71] [72] If SAM persist despite these maneuvers, the final recourse is mitral prosthetic implantation. Patients in whom SAM is discovered by TTE days or longer after mitral valve repair, obviously a subset selected to have milder obstruction by successful weaning from bypass and extubation, may be treated medically with

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negative inotropic agents. Some patients show a late reduction in the left ventricular outflow gradient, but this may remain inducible by amyl nitrite. [73]

Suture Dehiscence

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Occasionally, suture dehiscence leads to significant mitral regurgitation immediately after mitral valve repair. This complication occurred in 2% of operations in one series.[62] Dehiscence of a suture at the site of the leaflet resection in the posterior leaflet simulates a posterior leaflet perforation and is easily repaired on a second pump run. Another rare complication of mitral valve repair that can be detected by intraoperative echocardiography is partial dehiscence of the annuloplasty ring. The annuloplasty ring shows increased mobility and regurgitation originates outside the ring (Fig. 1914) . Left Ventricular Systolic Dysfunction Some reduction in left ventricular function often is detected after mitral valve repair.[74] [75] When dysfunction occurs, it is most often global and may reflect the unmasking of left ventricular dysfunction present preoperatively that had been concealed by the effects of increased ventricular preload and decreased afterload. In a minority of instances, a regional wall motion abnormality is detected, despite normal coronary vasculature preoperatively. This abnormality is usually caused by passage of air into a coronary vessel, and it can cause transient wall motion abnormalities and occasionally permanent infarction.[18] Because of its anterior position, air is more likely to travel to the right coronary artery in a supine patient, causing inferior wall motion abnormalities. Air within the left ventricular cavity is readily detected by echocardiography because it is echodense. The presence of large amounts of air on echocardiography is an indication for increased surgical venting of the left ventricle to prevent coronary embolization. In minimally invasive operations in which small hemisternotomy incisions are used, surgical venting may be difficult or impossible. In this situation, resumption of cardiopulmonary bypass may be necessary for a period of time in order to allow slow resolution of the air. Fortunately, most instances of air embolization of the coronary vessels resolve without significant long-term

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ventricular dysfunction. A rare complication of mitral valve repair or of any mitral operation is the inadvertent entrapment of the circumflex artery in the annulus sutures, which causes a wall motion abnormality in the Figure 19-14 (color plate.) Ring dehiscence leading to severe mitral regurgitation. The dehisced portion of the ring is shown (arrow).

basilar posterolateral wall that may also be detected echocardiographically. Tricuspid Regurgitation Generally, tricuspid regurgitation that is treated with a ring annuloplasty at the time of mitral surgery should be rechecked on the postpump intraoperative echocardiogram.[76] The success of the tricuspid surgery should be checked only after the intravascular volume status has been normalized. [77] Occasionally, tricuspid regurgitation that did not appear to be significant preoperatively may appear to be more severe on the postpump study and require a further pump run for tricuspid repair. Mitral Stenosis In performing a mitral valve repair in a nonrheumatic valve, the surgeon may remove a significant portion of the leaflet or perform an annuloplasty that reduces the size of the mitral annular orifice. Despite these anatomic derangements, it is unusual to have any significant stenosis in degenerative or ischemic mitral valve repair. The annulus area is 5 to 10 cm2 , varying with the size of the annuloplasty ring inserted. In contrast, residual stenosis of mild degree is common after rheumatic mitral valve repair because of the thickened leaflets and fusion of subvalvular chordae and commissures. The mitral valve gradient should be measured using continuous wave Doppler after every mitral valve repair. A mean gradient in excess of 5 mm Hg should arouse suspicion of some degree of stenosis of the valve.

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Mitral Valve Repair Involving Commissurotomy Although balloon valvuloplasty is a common method of treating selected patients with mitral stenosis, mitral repair with open commissurotomy still has a place, especially in patients with moderate amounts of valve calcification or thickening, those with multivalvular disease, or those with combined stenosis and significant regurgitation. Before surgery, intraoperative echocardiography is used to determine the severity of stenosis as a reference to assess the success of surgery. The severity of mitral stenosis is determined by measuring the transmitral pressure gradient and the pressure half-time with continuous wave Doppler.[78] [79] An epicardial approach using a para-sternal short-axis equivalent view may be used to obtain views suitable for planimetry of the mitral orifice if needed, but most TEE short-axis views of the mitral valve from the transgastric short-axis view are not of sufficient quality. The mechanism of the stenosis, whether valvular or subvalvular, should also be determined. A splitability score generated in a manner similar to the transthoracic method used for percutaneous mitral valvuloplasty may help to determine the degree of valvular fibrosis and calcification and whether a valve-sparing procedure is feasible.[80] Because 432

the surgeon can débride the valve under direct vision, open commissurotomy is sometimes possible even with a moderately high splitability score of 9 to 11, when a balloon valvuloplasty is not as likely to be effective or durable (see Chapter 20) . The presence of mitral regurgitation is also determined, and its mechanism, usually restricted leaflet motion, is determined. It is important also to detect left atrial and appendage thrombus preoperatively so that the surgeon can remove it. Postpump mitral valve gradient and area and mitral regurgitation are assessed. The presence of residual mitral regurgitation of 2+ or greater, or a

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mitral valve area of less than 1.5 cm2 is an indication for a further pump run, either to improve the repair or to implant a prosthesis. Frequently, when the patient has a large atrium or atrial fibrillation, the surgeon attempts to ligate the left atrial appendage in an effort to reduce the embolic risk. One study with TEE Doppler has demonstrated that these ligation attempts may be incomplete in up to one third of patients and in these instances blood still may enter and leave the appendage.[81] Patients with incomplete ligation remain susceptible to left atrial appendage thrombus formation and even thromboembolism. It has not been demonstrated that TEE evaluation of the competency of the ligation at the time of surgery improves the outcome.

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Future Directions The acquisition and storage of digital images is available on many of the current echocardiographic machines and opens up new vistas for intraoperative echocardiography. This storage method preserves image quality better than does videotape. Retrieval of digital images also is more facile, but it depends on how and where the data is stored. Comparing previously performed studies directly with the current study provides a more reliable detection of change. Digital storage and retrieval of previously performed studies may reduce the need for prepump intraoperative studies, or at least shorten their duration. Appropriate training of additional personnel is changing intraoperative echocardiography for the better. Cardiac anesthesiologists are quickly learning the requisite skills, which could reduce the need for dedicated cardiology support to the cardiac operating rooms except to consult when specific problems arise. Online consultation is increasingly feasible with the availability of digital archival and retrieval of images on a common server. Additionally, training of cardiac surgeons in epivascular imaging of the aorta has the potential to reduce the involvement of other echocardiographers directly in image acquisition. New technology is constantly becoming available both in terms of the echocardiographic machines themselves and in terms of the available transducers. Image quality has improved remarkably, from faster computers and parallel processing circuitry. New technology including Doppler myocardial imaging, harmonic imaging, and contrast analysis software provides improved physiologic analysis. On the other end of the spectrum, smaller hand-held machines having many of the capabilities of bigger machines will soon become available in cardiac operating rooms, although they likely will need to be supplemented by more sophisticated technology for cases with significant diagnostic needs. As yet, these smaller machines have not had transesophageal capability, nor has their use in the operating

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room been reported. Newer transducers that are currently being evaluated include transnasal probes.[82] These smaller transducers, inserted through the nasopharynx, lessen the risk to teeth and the interference with the endotracheal tube. Currently, these probes are not available with multiplane capabilities. They are therefore at a disadvantage compared with standard multiplane TEE probes. Three-dimensional echocardiography has tremendous potential in any analysis of complex cardiac morphology, including the assessment of lesions in which repair or reconstruction is being considered[83] (see Chapter 10) . The complex three-dimensional geometry of some valvular and congenital lesions is easier to display and understand using three-dimensional echocardiography.[84] , [85] Threedimensional reconstruction may allow more appropriate selection of patients, help determine the most appropriate surgical procedure, and potentially allow the surgeon to map out the reconstruction ahead of time in three-dimensional computer space. Recently, the feasibility of intraoperative three-dimensional TEE has been shown, with acquisition time less than 3 minutes and reconstruction possible in greater than 90% of patients. Three-dimensional data yielded incremental information to TEE in up to 25% of patients but only led to a change in the operative plan in one of 60 patients studied.[86] Three-dimensional imaging for reconstruction of some structures has already been accomplished, including the regurgitant orifice area in patients with severe mitral valve prolapse.[87] Although realtime three-dimensional echocardiographic acquisition hardware is now a reality, transesophageal applications are not currently available and the exigencies imposed by the data acquisition render the image quality inferior to current two-dimensional echocardiographic images. Real-time acquisition of three-dimensional data has the potential to further expand echocardiographic abilities intraoperatively by allowing rapid changes in volume and structure to be quantified online and in allowing multiple slices of structure to be generated at a later time from one stored data set.

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Chapter 20 - Echocardiography in the Patient Undergoing Catheter Balloon Mitral Commissurotomy Patient Selection, Hemodynamic Results, Complications, and Long-term Outcome Cheryl L. Reid MD

Historical Background and Technique of Mitral Balloon Commissurotomy Mitral stenosis in the adult occurs most commonly as the late result of rheumatic fever. Rarely, mitral stenosis may be caused by congenital or mitral annular calcification, particularly in the elderly patient. The natural history of rheumatic mitral stenosis is progressive symptomatic deterioration owing to reduction in the mitral valve orifice area. In the 10 to 20 years following an initial bout of rheumatic fever, the effective mitral valve area decreases because of fusion of the commissures, thickening and calcification of the mitral leaflets, and fibrosis and retraction of the chordae tendineae. The normal mitral valve area of 4.0 to 5.0 cm2 gradually decreases to 2.0 cm2 or less, at which time symptoms begin to develop usually with moderate to severe exercise. When the mitral valve area is reduced to 1.5 cm2 or less, symptoms may become severe and complications may develop.

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Mechanical intervention for the treatment of mitral stenosis, either open or closed mitral commissurotomy, has evolved in the past 40 years. Surgery, which has been shown to be highly effective, is usually performed for the relief of symptoms. Surgical replacement of the mitral valve may be necessary in patients with rigid, calcified mitral valves or severe mitral regurgitation in whom results with commissurotomy are suboptimal. Early experience with surgical commissurotomy showed that M-mode echocardiography could be helpful in selecting patients who would have a successful surgical mitral commissurotomy. It is important to identify patients who will have a successful commissurotomy because of the wellrecognized complications of valve prostheses, including thromboembolism, endocarditis, and higher operative mortality. The percutaneous approach to dilate a stenotic mitral valve was first reported by Inoue et al[1] in 1984, with subsequent evolution of catheter design and technique since the initial description. Simply stated, the technique consists of the percutaneous insertion of a dilating balloon into the right atrium. Using a trans-septal approach, the balloon catheters are then positioned across the stenotic mitral orifice and inflated at high pressures (1 to 2 atm). The desired result from inflation of the balloons is splitting 436

Figure 20-1 Technique of double-balloon valvuloplasty of the mitral valve. Top left, Two trans-septal sheaths from the right femoral vein are advanced to the left atrium (LA). Top center, Two end-hole balloon wedge catheters are positioned in the apex of the left ventricle (LV). Top right, Two curved exchange guidewires are inserted through the balloon catheters, which are then withdrawn. Bottom left, Two dilation balloon catheters are placed across the mitral valve orifice and into the LV apex. Bottom center, Two dilating balloon catheters are then fully inflated. Bottom right, Valve dilation balloons are removed. AO, aorta; IVC, inferior vena cava; RA, right atrium. (From McKay CR, Kawanishi DT, Rahimtoola SH: JAMA 1987;257:1753–1761, with permission. Copyright © 1987 American Medical Association.)

of the fused mitral commissures with resultant increases in the mitral valve orifice area. The procedure can be performed using either the doubleballoon or Inoue technique (Fig. 20-1) . In the double-balloon technique, two balloons are positioned side by side across the mitral valve orifice and then simultaneously inflated to achieve the desired result. The Inoue technique uses a unique self-seating single balloon that sequentially inflates

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from the distal to proximal end of the balloon. In recent years, the technical complexity and potential for serious complications (specifically, cardiac rupture inherent with the double-balloon technique) have largely lead to the abandonment of the double-balloon technique in favor of the Inoue technique. Early results of the procedure showed that the increase in mitral valve area is comparable to that obtained with surgical mitral commissurotomy.[2] [3] [4] Mitral balloon commissurotomy is now considered the procedure of choice for the treatment of symptomatic mitral stenosis in selected patients. Twodimensional Doppler echocardiography has played a major role in the evolution of mitral balloon commissurotomy, guiding our understanding of the mechanism by which the mitral valve area is increased. It is essential for the evaluation and selection of patients before the procedure and for the assessment of complications following the procedure. Hemodynamic measurement of the severity of the mitral stenosis and associated valve disease before the procedure, immediate hemodynamic changes during the procedure, and long-term follow-up can be reliably estimated with Doppler echocardiography (Table 20-1) .

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Evaluation of the Patient Before Mitral Balloon Commissurotomy Mechanisms of Increase in Mitral Valve Area Studies performed by two-dimensional echocardiography have shown that the primary mechanism for the increase in mitral valve area following mitral balloon commissurotomy is splitting of the fused commissures (Fig. 20-2) .[5] Tears of either the anterior or posterior mitral valve leaflet rarely occur and usually result in moderate to severe mitral regurgitation. In contrast to open, surgical commissurotomy in which the fused and retracted chordae can be manually separated, it is unclear that mitral balloon commissurotomy has a significant effect in dilating the subvalvular apparatus. Fortunately, the subvalvular region is rarely the primary orifice in patients with mitral stenosis.

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TABLE 20-1 -- Role of Two-Dimensional Doppler Echocardiography in the Evaluation of Patients Undergoing Mitral Balloon Commissurotomy Initial studies Severity of valve disease Mitral valve gradient Mitral valve area Mitral regurgitation Initial valve morphology Left atrial thrombus During mitral balloon commissurotomy

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Balloon position or trans-septal catheterization Changes in valve area or gradient Changes in mitral regurgitation Complications (rupture, atrial septal defect, etc.) Immediate results Changes in valve function Complications Long-term results Restenosis Mitral regurgitation Atrial septal defects Pulmonary artery pressure Ventricular size and function Other valve disease Mitral Valve Morphology The pathologic processes of rheumatic heart disease include (1) fusion of the commissures, (2) thickening and calcification of the valve leaflets, and (3) fusion and shortening of the chordae tendineae. These processes result in varying degrees of involvement of the mitral apparatus. Given that the mechanism of the increase in mitral valve area by surgical or percutaneous techniques is splitting of the commissures, it is expected that the morphology of the mitral valve apparatus will influence the results of the procedure. Experience with both surgical mitral commissurotomy and mitral balloon commissurotomy has confirmed this expectation. The characteristic feature of rheumatic mitral stenosis on two-dimensional echocardiography is doming of the body of the mitral valve leaflets during diastole caused by the fused commissures. As blood flows from the left Figure 20-2 Two-dimensional echocardiogram in the parasternal shortaxis view at the level of the mitral valve during early diastole. A, Before double-balloon catheter balloon valvuloplasty the transverse diameter was 20 mm. Calcification of the posterior commissure was present. B, After catheter balloon valvuloplasty the transverse diameter increased to 27 mm. The increase in

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transverse diameter suggests that the split occurred at the commissures. Figure 20-3 Left, Transthoracic two-dimensional echocardiogram from a patient with mitral stenosis. The mitral valve is mobile with doming of the anterior leaflet. Minimal valve thickening and no subvalvular disease is noted. Right, Transesophageal echocardiogram in the midesophagus fourchamber transverse view from the same patient. The mitral valve morphology in this patient is ideal for mitral balloon commissurotomy and excellent results would be expected. LA, left atrium.

atrium to the left ventricle through the narrowed mitral orifice, the body of the leaflets balloon apically. The mobility of the leaflets (amplitude of doming) reflects the degree of calcification of the leaflets and commissural fusion. Both qualitative and semiquantitative criteria have been proposed for evaluation of leaflet morphology. [6] [7] In patients in whom the transthoracic echocardiogram is inadequate, transesophageal echocardiography can provide a similar analysis of the mitral valve morphology, although nonstandard image planes may complicate interpretation ( Fig. 20-3 and Fig. 20-4 ). [8] [9] In addition, subvalvular thickening and calcification may be underestimated on transesophageal imaging because of masking of the subvalvular region from thickening and calcification in the mitral valve leaflets. To some extent, these limitations can be avoided by use of biplane or multiplane transesophageal echocardiography with imaging of the subvalvular region in the transgastric longitudinal imaging plane. Total echocardiographic scoring systems based on leaflet morphology have been proposed as a guide to the selection of patients for mitral balloon commissurotomy. Although studies using these methods have been shown Figure 20-4 Left, Transthoracic two-dimensional echocardiogram from a patient with mitral stenosis undergoing evaluation for mitral balloon commissurotomy. The mitral valve is heavily calcified with decreased excursion of the mitral leaflets during diastole. Right, Transesophageal echocardiogram in the midesophagus transverse view, which again shows a heavily calcified immobile mitral valve. The assessment of the morphologic features of the mitral valve are similar between the transthoracic and transesophageal echocardiographic examinations. The increase in mitral valve area from mitral balloon commissurotomy in this patient would be expected to be minimal. LA, left atrium.

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Figure 20-5 The anatomic features of the mitral valve in relationship to the resultant mean mitral valve area immediately after catheter balloon valvuloplasty are shown for the presence or absence of calcification, subvalvular disease, and pliable or rigid mitral valves. The mean mitral valve area was greater in the groups with pliable mitral valves without calcification or subvalvular disease.

to correlate with the immediate results, the wide scatter of the data makes their value questionable in an individual patient for predicting the hemodynamic results of the procedure ( Fig. 20-5 and Fig. 20-6 ). These criteria should be used, therefore, only as a guide to the severity of the individual morphologic variables of the mitral valve. Table 20-2 is a summary from the literature of the morphologic features of the mitral valve and the criteria used in assessment before mitral balloon commissurotomy. The single best echocardiographic morphologic variable that predicts the results of mitral balloon commissurotomy is leaflet mobility, which reflects the extent of commissural fusion and calcification of the mitral leaflets.[10] In the studies of the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry and Reid et al,[6] [10] leaflet mobility was the only independent echocardiographic variable to predict the results of mitral balloon commissurotomy (Table 20-3) . The presence of calcification and the involvement of one or both commissures assessed in the twodimensional echocardiography parasternal short-axis view may also be helpful in predicting the success of commissural Figure 20-6 Total morphology score by echocardiography versus mitral valve area (MVA) measured by cardiac catheterization after mitral balloon commissurotomy (MBC). There is significant (P < .001) but weak negative correlation (r = -0.24).

splitting by the balloon dilation (see Fig. 20-2) .[11] In asymmetric involvement of the commissures, in which one commissure is heavily fibrosed or calcified, splitting occurs in the opposite commissure. If both commissures are equally fused without marked calcification, both commissures are expected to split. In one study, if at least one commissure split, 89% of patients had a good hemodynamic result.[11] The presence of severe subvalvular fibrosis and calcification may also result in suboptimal results from mitral balloon commissurotomy because it is unclear that balloon dilation is able to split chordal fusion. Isolated subvalvular disease,

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however, rarely occurs and is usually associated with extensive fibrosis and calcification of the commissures and valve leaflets. The best hemodynamic result based on echocardiographic evaluation is expected in a patient with a highly mobile mitral valve without evidence of calcification or severe subvalvular disease (see Fig. 20-3) . In this group of patients, a mean resultant mitral valve area greater than 2.0 cm2 is predicted.[6] Mitral valve morphology, however, should not be used alone in the selection of patients to undergo mitral balloon commissurotomy. In occasional patients, satisfactory hemodynamic and clinical improvement can occur with more severe mitral valve disease. Other variables that have been shown to influence the results of the procedure and should be considered in the selection of patients include evidence of long-standing disease such as a low cardiac output, baseline mitral valve area, and left atrial size and technical factors such as the balloon diameter used in the dilation. Assessment of Left Atrial Size and Left Atrial Thrombi As a result of chronic pressure overload, the response of the left atrium is progressive enlargement. With long-standing mitral stenosis, an extremely large or "giant" left atrium (>6.5 cm anteroposterior diameter) may result. The 439

TABLE 20-2 -- Two-Dimensional Echocardiographic Assessment of Mitral Valve Morphology Predicted Results SUBOPTIMAL Variable OPTIMAL Leaflet Highly mobile with restriction Minimal forward motion of motion of only leaflet tips and H/L leaflets in diastole or H/L ratio ≥ 0.45 ratio ≤ 0.25 Leaflet Leaflets < 4–5 mm or Leaflets > 8.0 mm thick or a thickening MV/PWAo ratio of 1.5–2.0 MV/PWAo ratio ≥ 5.0 Subvalvular Thin, faintly visible chordae Thickening and shortening disease tendineae with only minimal of chordae to papillary thickening below valve muscle; areas with echo

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density greater than endocardium Commissural hom*ogeneous density of both Both commissures heavily calcium commissures calcified H, height of doming of mitral valve; L, length of dome of mitral valve; MV, mitral valve; PWAo, posterior wall of aorta. Data from Reid CL, Chandraratna PAN, Kawanishi DT, et al: Circulation 1989;80:515–524; and Abascal VM, Wilkins GT, Choong CY, et al: J Am Coll Cardiol 1988;2:257–263. enlarged left atrium can compress the inferior vena cava, resulting in increased Doppler flow velocities and an increased incidence of hepatomegaly.[12] Other well-recognized complications associated with an enlarged left atrium include the development of atrial fibrillation and blood stasis within the enlarged left atrium with thrombus formation. Left atrial thrombi occur in approximately 25% of patients with mitral stenosis and are seen even in patients in normal sinus rhythm. [13] In the majority of cases, the thrombi are confined to the body of the left atrial appendage, but they may also protrude into the body of the left atrium or attach to the left atrial wall or interatrial septum (Fig. 20-7) . In patients undergoing mitral balloon commissurotomy, the size of the left atrium has been noted to have a significant influence on outcome.[14] In patients with large left atria (>6 cm), technical difficulties may be encountered in performing the trans-septal puncture and crossing the mitral valve orifice. Enlarged left atria also are more frequently associated with a suboptimal increase in the resultant mitral valve area, perhaps because of technical difficulties or as an index of more severe and chronic disease. Conversely, smaller left atria are more frequently associated with the development of an atrial septal defect after mitral balloon commissurotomy. In such patients, shorter balloon sizes should be used or care taken during the procedure to prevent slippage of the balloon catheter against the interatrial septum. Systemic embolization has been reported in 0 to 4% TABLE 20-3 -- Predictors of Mitral Valve Area Variable NHLBI-BVR[10]

R2 0.31

P value 6 cm) or low cardiac output, although results vary in individual patients. The presence of significant other valvular disease such as critical aortic stenosis or severe aortic or tricuspid regurgitation and coronary artery disease may warrant consideration for surgical referral. The decision to perform mitral balloon commissurotomy in patients considered to be high risk for surgery because of other medical diseases, suboptimal mitral valve morphology, or a left atrial thrombus must be based on consideration of the risk-to-benefit ratio and the patient's desire. During Mitral Balloon Commissurotomy Doppler echocardiography plays a major role not only in the selection and evaluation of patients before mitral balloon commissurotomy but also is a useful adjunct during the procedure (see Table 20-1) . Doppler echocardiography equipment should therefore be available during the procedure to assess the immediate results and potential complications.

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Imaging by two-dimensional echocardiography of the interatrial septum can be performed to confirm and aid in the proper location of the transseptal catheter in difficult circ*mstances. Variability in the location of the interatrial septum may occur because of aortic root dilation, right atrial dilation, or cardiac deformity owing to scoliosis, 445

and in these settings, fluoroscopy may be misleading. Echocardiography can be useful in this setting by visualization of the interatrial septum and confirming by contrast saline injection the location of the needle within the left atrium once the trans-septal puncture is performed.[15] The identification of the needle tip may be difficult if it is out of the imaging plane, but it can be assessed indirectly by the "tenting" of the interatrial septum. Following the trans-septal puncture, two-dimensional echocardiography can aid in positioning the catheters across the stenotic mitral orifice. This positioning is important if the double-balloon technique is used. The Inoue balloon technique involves a unique self-seating design, which makes positioning of the balloon catheter easier. Echocardiography is helpful to prevent inadvertent inflation within the left atrium, which may result in an atrial septal defect if it butts against the interatrial septum. In patients with left atrial thrombi considered high risk for surgical commissurotomy, transesophageal echocardiography may be beneficial in preventing inadvertent migration of the catheter into the left atrial appendage. Two-dimensional echocardiography can also be used during the procedure to assess the affects of sequential balloon dilation. The transmitral gradient and changes in mitral regurgitation can be rapidly assessed to determine the need for further inflations. If the mitral regurgitation increases by one or more grades the procedure should be terminated. The success of mitral balloon commissurotomy has been shown to be related to the mitral anulus–to–balloon diameter ratio.[47] The mitral anulus by two-dimensional echocardiography can be measured to aid in selecting the appropriate balloon sizes. The increase in mitral valve is directly related to the mitral anulus–to–balloon diameter ratio. If the balloon diameter is too large, however, excessive tearing of the commissures or mitral leaflets may occur resulting in significant mitral regurgitation. In patients undergoing doubleballoon dilation, a ratio of the sum of diameters of the two dilating balloons to mitral anulus of ≥1.1 is associated with a significant increase in mitral regurgitation without further increase in mitral valve area.

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Complications of Mitral Balloon Commissurotomy Complications that may occur with mitral balloon commissurotomy are those known to be associated with invasive procedures, including death, myocardial infarction, stroke, bleeding, and heart failure. In the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry, the incidence of serious complications was 12% and inhospital deaths 1%.[48] The reported complications of mitral balloon commissurotomy that can be detected by Doppler echocardiography are shown in Table 20-5 . Doppler echocardiography provides a rapid method for the early detection of complications and a noninvasive technique for serial evaluation. Atrial Septal Defects

The creation of an atrial septal defect in patients undergoing mitral balloon commissurotomy results from the TABLE 20-5 -- Complications of Mitral Balloon Commissurotomy Detected by 2D Doppler Echocardiography Event Thrombus (systemic embolization) Cardiac perforation (tamponade) Left-to-right shunt (atrial level) Valve related Acute mitral regurgitation (requiring early surgery) Increase in MR

Incidence (%) 2 4 10 3 12 36

Inadequate result (MVA < 1.5 cm2 ; ≥ 2 + increase MR) Restenosis ? MR, mitral regurgitation; MVA, mitral valve area. Data from National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry Participants: Circulation 1992;85:448–461, 2014– 2024. trans-septal approach. The reported incidence of atrial septal defects depends on the method of detection. By oximetry immediately following mitral balloon commissurotomy, the reported incidence ranges from 7% to 33% depending on the type of balloons used and diagnostic criteria.[3] [49] [50]

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Transesophageal echocardiography is the most sensitive method for detection of left-to-right shunting after mitral balloon commissurotomy and defects have been reported in 87% of patients examined within 24 hours of the procedure.[52] Transthoracic echocardiography detects left-to-right shunting in about half of the patients immediately following mitral balloon commissurotomy.[53] [51]

The detection of left-to-right shunting after mitral balloon commissurotomy requires a thorough evaluation of the interatrial septum in any patient who has undergone mitral balloon commissurotomy. The optimal view of detecting defects of the interatrial septum is obtained from the subcostal approach (Fig. 20-12) . In this position, the cardiac flow is parallel to the ultrasound beam, which is optimal for detection by color Doppler. The characteristic Doppler flow pattern is a continuous or late systolicholodiastolic left-to-right flow caused by the high pressure gradient between the right and left atrium in patients with mitral stenosis. The size of the defects range from 0.3 to 1.5 cm in diameter. By color Doppler, a jet width less than 0.5 cm is not likely to be detected by oximetry. Atrial septal defects greater than 1.0 cm are associated with significant right heart oxygen stop-ups. Shunt flow volumes calculated by Doppler echocardiographic methods range from 0.08 to 4.87 L per minute. The highest incidence of atrial septal defects is reported immediately after mitral balloon commissurotomy. Defects that are less than 0.7 cm in diameter usually close within 6 months.[54] Factors that have been associated with the development of atrial septal defects after mitral balloon commissurotomy include smaller increases in mitral valve area, the presence of mitral valve calcification, and smaller left atria. Atrial septal defects have also been reported to be initially detected during follow-up. Persistence of an atrial septal defect during follow-up is associated with larger sizes, a decrease in mitral valve area, and an increase in the mitral valve gradient. Clinically, significant problems are not associated with small atrial 446

Figure 20-12 (color plate.) Two-dimensional echocardiogram in the subcostal view from a patient after mitral balloon commissurotomy. Color Doppler flow mapping shows flow from the left to right atrium through a large atrial septal defect. The defect created by the dilating balloons measured 0.9 cm in diameter. RA, right atrium; LA, left atrium.

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septal defects. The effect on the right heart hemodynamics of large atrial septal defects with or without restenosis of the mitral valve remains to be determined. Mitral Regurgitation

Mitral regurgitation is a frequent complication of mitral balloon commissurotomy (Fig. 20-13) . The presence and severity of the mitral regurgitation should be carefully Figure 20-13 (color plate.) Transthoracic and transesophageal echocardiograms from a patient who had undergone mitral balloon commissurotomy (MBC). A, Transthoracic apical four-chamber view before MBC, which by color Doppler flow mapping shows a small blue jet in the left atrium during systole (arrow) consistent with mild mitral regurgitation. B, Same echocardiographic view obtained during the procedure following the first balloon inflation. The Doppler flow mapping shows turbulent flow into the left atrium. The mitral regurgitant jet is directed along the lateral wall and wraps around, almost completely filling the left atrium. C, Transesophageal echocardiogram from the midesophagus longitudinal view, which shows both the anterior and posterior leaflets of the mitral valve are flail with ruptured chordal attachments. LA, left atrium; LV, left ventricle.

evaluated by Doppler echocardiography using standard techniques before mitral balloon commissurotomy so that any change in severity can be recognized and evaluated immediately. Creation of new or an increase in pre-existing mitral regurgitation has been reported in 19% to 85% of patients undergoing mitral balloon commissurotomy.[5] [55] [56] [57] [58] [59] In most patients, however, the increase in mitral regurgitation is mild. An increase of greater than 2 grades in mitral regurgitation occurs in only 3% to 10% of patients. [48] [55] [56] [57] [58] [59] In the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry early surgery for mitral valve replacement owing to severe mitral regurgitation occurred in 2% of patients.[55] This rate is comparable to results of surgical mitral commissurotomy. Although some patients who develop severe mitral regurgitation require urgent surgery for mitral valve replacement, others may tolerate the mitral regurgitation acutely. The mechanisms in the development of mild increases in mitral regurgitation differs significantly compared with the mechanisms of severe mitral regurgitation.[58] [59] [60] [61] [62] Echocardiographic studies of patients who develop mild increases in mitral regurgitation have shown that the

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regurgitant jet originates from the split commissures. Severe mitral regurgitation following mitral balloon commissurotomy, however, results from tearing of the valve leaflets or rupture of the chordal attachments. In one study of patients having balloon commissurotomy with the Inoue technique, the incidence of severe mitral regurgitation was 7.5%.[59] The most common cause was rupture of the chordae tendinae to the anterior or posterior leaflet in 43% of cases. A heavily calcified posterior leaflet resulted in tearing of the leaflet in 30%. Other variables that have been associated with the development of severe mitral regurgitation include severe calcification of both commissures and extensive subvalvular disease. [60] Splitting of the commissures, which most commonly is associated with mild increases in mitral regurgitation, can, if "excessive," result in severe regurgitation owing to incomplete coaptation of the valve leaflets during systole.

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Unfortunately, the development of severe mitral regurgitation in patients undergoing mitral balloon commissurotomy cannot be reliably predicted from baseline characteristics, valve morphology, or technical factors during the mitral balloon commissurotomy procedure. The incidence of severe mitral regurgitation is not significantly different between patients undergoing double-balloon or Inoue techniques.[48] [56] [57] [58] [59] [60] [61] [62] [63] Similarly, stepwise inflation with the Inoue balloon technique has not reduced the frequency of severe mitral regurgitation. Indeed, inadvertent inflation of the Inoue balloon within the subvalvular apparatus, which may occur because of the unique design of the balloon catheter, can result in rupture of the chordal attachments or tear of the leaflets. Care must be taken in the positioning of the catheter before inflation. In one study, calcification of the posterior leaflet of the mitral valve resulted in a tear of the leaflet in the region of the calcification.[62] After each sequential balloon inflation, Doppler echocardiography should be performed to evaluate changes in mitral regurgitation. Two-dimensional echocardiography in the parasternal short-axis view permits evaluation of commissural splitting to assess the need for subsequent balloon inflations. Cardiac Perforation

Perforation of a cardiac chamber can occur during mitral balloon commissurotomy and is a major cause of death in these patients (see Table 20-5) . Atrial perforation can occur during the trans-septal catheterization

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and left ventricular perforation during the balloon inflations. The incidence of cardiac perforation is directly related, in part, to the dilation technique. In the Balloon Valvuloplasty Registry of patients undergoing mitral balloon commissurotomy with either a single- or double-balloon technique, the incidence of perforation was 4%. Perforation was the most common cause of death during the procedure, usually left ventricular perforation, and the most frequent indication for emergency cardiac surgery.[48] Cardiac perforation with the Inoue technique is much less common ( 2.0 cm2 , < 2 + mitral regurgitation) have an event-free survival rate of 79% at 5 years.[67] Noninvasive testing with Doppler echocardiography eliminates the need for repeat cardiac catheterization in the hemodynamic evaluation of these patients during long-term follow-up. In the limited reported studies, the mitral valve area by Doppler echocardiography has shown a small decrease in valve area but remains significantly greater than that measured before the procedure (Table 20-6) . Restenosis (loss of 50% of the initial increase and a valve area of < 1.5 cm2 ) occurs in 6% to 21% at a mean follow-up of 19 to 22 months depending on the type of valve anatomy.[64] [66] Clinical and echocardiographic variables that have been shown to predict a poor long-term result are shown in Table 20-7 . The strongest predictor of the long-term 448

TABLE 20-7 -- Baseline Variables Associated with Poor Long-term Results Following Mitral Balloon Commissurotomy Clinical

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Advanced Age Higher NYHA Previous commissurotomy Hemodynamics Lower initial valve area Presence of MR Poor valve morphology or calcification Severe tricuspid regurgitation Higher pulmonary artery pressure Immediate Hemodynamic Results

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64, 67, 69 43, 67, 69 43, 63 63 43, 64, 68 43, 64, 65, 66, 67, 69, 70, 71 43 67 67, 69

Poor initial result (MVA ≤ 1.5 cm2 ) 43, 63, 65, 67, 70 Severe MR (> 2T) 63, 70, 71 Procedural EBDA 67, 68 EBDA, effective balloon dilating area; MR, mitral regurgitation; NYHA, New York Heart Association functional class. results, as with the immediate results of mitral balloon commissurotomy, is the degree of valve deformity. Patients with severe calcification of the mitral valve have both a poorer immediate result and long-term outcome than patients with more favorable valve anatomy. Other predictors of an adverse outcome include a lower initial valve area, the presence of mitral regurgitation or severe tricuspid regurgitation, and a higher pulmonary artery pressure. Increases in mitral regurgitation, which are common following mitral balloon commissurotomy, are generally well tolerated during follow-up. Although patients who develop severe mitral regurgitation usually require valve replacement during short-term follow-up, the changes in the mild to moderate mitral regurgitation are variable. The degree of mitral regurgitation by color Doppler echocardiography in reported series remains unchanged in 46% to 60%, decreases in 30%, and increases in 20% to 10% of patients.[64] [66] Multivariate analyses, however, have shown that the

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presence of mitral regurgitation both before and after mitral balloon commissurotomy is associated with a lower event-free survival.[65] [68] Thus, patients with either pre-existing or new mitral regurgitation should be followed closely after mitral balloon commissurotomy with clinical and echocardiographic evaluation for the development of symptoms or changes in valve function. The long-term effects of atrial septal defects is yet undetermined. Small defects close in about two thirds of patients during follow-up, and small defects that persist are generally well tolerated. Factors that are associated with the persistence of an atrial septal defect are a pulmonary-to-systemic shunt ratio of greater than 1.5, elevated right and left atrial pressures, smaller mitral valve area following mitral balloon commissurotomy, and evidence of restenosis.[66] These findings are not unexpected because elevation of left atrial pressures either caused by a poor initial result or restenosis would favor shunting through the atrial septal defect and perhaps prevent healing of the atrial septum. The long-term effects of the right ventricular volume overload is unknown. If the patient requires mitral valve surgery during follow-up, the atrial septum should be carefully examined and any defect surgically closed. Difficult management problems, however, occur in patients who have a successful mitral valve dilation but in whom a significant atrial septal defect results. Unfortunately, the hemodynamic burden of mitral stenosis in these patients is exchanged for an iatrogenic Lutembacher's syndrome. Importantly, these patients should be closely evaluated by Doppler echocardiography during follow-up to evaluate the atrial septal defect and evidence of developing right ventricular volume overload or restenosis.

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Technical Limitations and Alternate Approaches The technique of mitral balloon commissurotomy has proved that sustained clinical and hemodynamic improvement occurs in most patients treated for symptomatic mitral stenosis. The immediate results are equal to those obtained with surgical commissurotomy. The technique is not, however, without its limitations. Suboptimal results and complications occur in a number of patients regardless of whether the double-balloon or Inoue technique is used. Doppler echocardiography has been invaluable in the evaluation of patients and the technique as mitral balloon commissurotomy has evolved. Patients with mitral stenosis who require intervention can be identified and the results predicted by careful Doppler echocardiographic evaluation. Before intervention, patients with mitral stenosis can be evaluated reliably by the pressure gradient, valve area, severity of valvular regurgitation, and indirect evidence such as chamber size and intracardiac pressures. Thus, the majority of patients with isolated mitral stenosis do not require more invasive testing with cardiac catheterization. In older patients, in whom the presence of coronary artery disease is a consideration, coronary angiography should be performed. Furthermore, cardiac catheterization, either as the initial evaluation or in patients in whom restenosis is suspected, should be reserved for those patients in whom there is a discrepancy between the physical or clinical signs and the Doppler echocardiographic examination. The choice of mitral balloon commissurotomy or surgical commissurotomy in patients identified who require intervention depends on a number of factors. Presently, mitral balloon commissurotomy should be considered the procedure of choice in patients with isolated mitral stenosis with favorable mitral valve anatomy because it is cost-effective and safe. In other patients, mitral balloon commissurotomy may be required if the patient refuses surgery or the medical condition makes surgery high risk. In

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patients with less favorable valve anatomy, the decision for mitral balloon commissurotomy or surgical commissurotomy must be made based on the consideration of risks and benefit of each procedure. Mitral balloon commissurotomy, however, should only be considered a palliative procedure, which may delay the time in which surgical 449

intervention may be required for mitral valve replacement.

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Future Directions Although the immediate and current follow-up of patients undergoing mitral balloon commissurotomy is favorable and comparable to surgical commissurotomy, several issues remain. Potential long-term questions remain unresolved. For example, does the presence of persistent small atrial defects significantly alter the clinical course of patients? In order to answer this question and others, continued follow-up of patients who have undergone mitral balloon commissurotomy is required. Further refinements in the technique and in the development of balloon catheters also may be expected; however, whether these changes will result in significant improvement in the expected outcome depends on careful patient selection. The development of intracardiac echocardiography also may be of benefit in the guidance of the procedure.[73] Regardless of these considerations, mitral balloon commissurotomy has become a proven technique and will continue to play a major role in the treatment of patients with symptomatic mitral stenosis.

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451

Chapter 21 - Clinical Decision Making in Endocarditis Nelson B. Schiller MD

Infection of the endocardium walls or lining layer of the heart—whether on valve leaflets or chordae, congenital defects, chamber walls, paraprosthetic tissue, or the attachment of implanted shunts or conduits—is known as infective endocarditis. The major milestones in our understanding of infective endocarditis include availability of diagnostic blood culture techniques in the first decades of the 20th century; reversal of its invariably fatal course with antibiotics; palliation of potentially fatal valvular complications with surgery; and, most recently, immediate and accurate diagnosis of its anatomic and hemodynamic manifestations with echocardiography. Although no technique in isolation can always establish this diagnosis, echocardiography has a very high sensitivity for detection of valvular vegetations and complications of infective endocarditis. Thus, echocardiography is the only imaging modality that has a significant role in the clinical diagnosis and treatment of infective endocarditis. The American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the clinical application of echocardiography (Table 21-1) indicate that echocardiography is an essential technique in the diagnosis and treatment of endocarditis and is mandatory in nearly all patients with this disease. [1] This chapter discusses the use of echocardiography in infective endocarditis

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with emphasis on both clinical applications and utility in research studies. The weaknesses and pitfalls of the technique are discussed, particularly how these factors might cause the performance of echocardiography in practice to fall short of published data.

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Basic Principles Underlying a discussion of the use of echocardiography in patients with suspected infective endocarditis must be an attempt to come to terms with a clinical definition of the diagnostic criteria of the syndrome. First, should the diagnostic criteria include echocardiography? The studies that initially evaluated the role of echocardiography in the diagnosis of infective endocarditis could not, of course, use an echocardiographic definition of this disease. Instead, TABLE 21-1 -- ACC/AHA Guidelines for Use of Echocardiography in Patients with Infective Endocarditis CLASS I (Evidence or general agreement that echocardiography is definitely indicated) Detection and characterization of valvular lesions, their hemodynamic severity, and/or ventricular compensation * Detection of vegetations and characterizations of lesions in patients with congenital heart disease suspected of having infective endocarditis Detection of associated abnormalities (e.g., abscesses, shunts) * Re-evaluation studies in complex endocarditis (e.g., virulent organism, severe hemodynamic lesion, aortic valve involvement, persistent fever or bacteremia, clinical change, or symptomatic deterioration) Evaluation of patients with high clinical suspicion of culture-negative endocarditis * CLASS IIA (Conflicting data, but the weight of evidence/opinion is in favor of the usefulness of echocardiography) Evaluation of bacteremia without a known source * Risk stratification in established endocarditis * CLASS IIB (Conflicting data, but efficacy is less well established) Routine re-evaluation in uncomplicated endocarditis during antibiotic

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therapy CLASS III (Not indicated) Evaluation of fever and nonpathologic murmur without evidence of bacteremia Modified from Cheitlin MD, Alpert JS, Armstrong WF, et al: J Am Coll Cardiol 1997;29:862–879. *Transesophageal echocardiography (TEE) may provide incremental value in addition to information obtained by transthoracic echocardiography. The role of TEE in firstline examination awaits further study.

452

TABLE 21-2 -- Clinical Definition of Infective Endocarditis Definite Direct evidence based on histology from surgery or autopsy or bacteriology by Gram stain or culture of valvular vegetation or arterial embolus Probable A. Persistently positive blood cultures plus one of the following: 1. New regurgitant murmur or 2. Predisposing heart disease and vascular/immunologic phenomena (e.g., splinter hemorrhages, Osler's nodes, glomerulonephritis) B. Negative or intermittently positive blood cultures ( 2 y ± 0.1 cm2 /m2

76% symptomatic

42 22– AVA 0.7 5.4 y 77 ± 0.3 (0.2–1.1) cm2

Severe aortic Symptomatic stenosis, no AVR, age ≥ 60

50 77 Vmax 4.5 1.7 y

Turina et Cardiac cath, al[91] no AVR

Symptomatic

Asymptomatic

m/sec, AVA 0.6 (0.3–8) cm2

(60– 89) 125 43 Mean ∆P 6.6 y 69 mm Hg AVA 0.56 cm2 (16– 73) 65 Mean ∆P 57 mm Hg AVA 0.76 cm2

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Horstkotte Catheterization Asymptomatic et al[89] for other reasons Catheterization Asymptomatic for other reasons

Refused surgery

Kelly et al Vmax ≥ 3.6 [131]

Symptomatic

Asymptomatic

m/sec

Symptomatic Pellikka et al[132]

Doppler Vmax Asymptomatic ≥ 4 m/sec

142

Mild AS (AVA > 1.5 cm2 ) 236 Moderate AS (AVA 0.8–1.5 cm2 ) 35 Severe AS (AVA < 0.8 cm2 ) 51 63 ± ∆P 68 ± 15 ± 19 19 mos 39 72 ± ∆P 68 ± 11 19 143 72 Vmax 4.4 20 m (4–6.4) m/sec

(40– 94)

18% Kennedy Moderate [135] aortic stenosis asymptomatic et al at cath, no AVR Otto et al Abnormal Asymptomatic [128] valve with Vmax > 2.6

66 67 ± AVA 35 m 10 0.92 ± 0.13 (0.7–1.2) 2.5 y 123 63 ± Vmax < 16 3.0 m/sec

m/sec

Vmax 3–4

m/sec Vmax >

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Rosenhek Abnormal et al[61] valve with Vmax > 4.0

Asymptomatic

4.0 m/sec 128 60 ± Vmax 5.0 27 ± mos 18 ± 0.6 m/sec

m/sec

AS, aortic stenosis; AVA, aortic valve area; AVI, aortic valve index, AVR valve replacement; cath, catheterization; ∆P, pressure gradient; Vmax , maxim jet velocity.

* Event-free survival.

obstruction. Continuity equation valve areas will reflect accurately the degree of impairment of valve opening. In the past, "severe" or "critical" aortic stenosis has been defined in terms of a specific valve area or valve area index. More recent studies[89] [91] [115] have shown marked overlap in hemodynamic severity between symptomatic and asymptomatic patients, indicating that the "critical" degree of valve narrowing varies from patient to patient (Fig. 22-18) . This observation has been confirmed in prospective studies showing that symptom onset occurs with a jet velocity as low as 3.0 m per second or may be delayed until the jet velocity is over 5.0 m second. Similarly, some patients remain asymptomatic with a valve area less than 0.7 cm2 , whereas others have definite symptoms with a valve area greater than 1.0 cm2 . Hemodynamic Progression Until recently, data on the hemodynamic progression of valvular aortic stenosis was limited to studies of patients in whom two cardiac catheterizations had been performed (Table 22-4) . [116] [117] [118] [119] [120] [121] The impact of selection bias on these data is difficult to assess, since only patients who did not die or undergo valve replacement after the first catheterization,

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487

Figure 22-18 Hemodynamically severe aortic stenosis: mean aortic pressure gradient, valve orifice area, cardiac index, and left ventricular end-diastolic pressure in severely symptomatic (open circles) and asymptomatic or mildly symptomatic (closed circles) patients. Mean value (horizontal line) and statistical difference between both groups are indicated. NS, not significant. (From Turina J, Hess O, Sepulcri F, Krayenbuehl HP: Eur Heart J 1987;8:471–473.)

yet required a second catheterization for clinical indications, are included in these series. In general, these studies showed an average rate of increase in mean pressure gradient between 0 and 12 mm Hg per year and a decrease in valve area between 0.02 and 0.3 cm2 per year. Marked individual variability in the rate of progression was noted, however, and no clear factors were identified that predicted the rate of progression. The availability of an accurate, noninvasive method to evaluate hemodynamic severity has allowed larger and more detailed studies on the rate of hemodynamic progression.[58] [60] , [61] [90] , [115] [122] [123] [124] [125] [126] [127] In these studies, the average rate of increase in aortic jet maximum velocity ranges from 0.2 to 0.4 m per second per year, with an increase in mean gradient of 6 to 7 mm Hg per year and a decrease in valve area of 0 to 0.3 cm2 per year. Again, marked individual variability in the rate of hemodynamic progression Figure 22-19 Change in maximal aortic jet velocity (Vmax ) and pressure gradient during follow-up in 45 patients. (From fa*ggiano P, Ghizzoni G, Sorgato A, et al: Am J Cardiol 1992;70:229–233.)

was observed ( Fig. 22-19 and Fig. 22-20 ). Although Dopplerechocardiographic studies have the advantage of larger patient numbers and potentially less selection bias (a repeat echocardiographic study is likely to be requested more often than a repeat cardiac catheterization), many of these studies are retrospective, with the data extracted from ongoing clinical databases. Thus, patients with rapid progression, those developing symptoms, or those requiring surgical intervention may be overrepresented. Conversely, repeat studies may not have been performed in clinically stable patients. The results of more recent prospective studies may avoid some of these biases.[61] [128]

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It is important to remember that as the disease progresses, increasing obstruction to left ventricular outflow most often is reflected by both a decrease in valve area and an increase in jet velocity and pressure gradient. However, if there is a concurrent decrease in transaortic 488

TABLE 22-4 -- Hemodynamic Progression of Valvular A

Study Bogart et al[116]

Clinical Status at Entry 2 cardiac caths

Cheitlin et al[117] Wagner and Selzer

2 cardiac caths 2 cardiac caths

Mean Follow up Type of Measurement Patients, Interva Study Method N yr Retrospective Invasive 11 4.9

Retrospective Invasive

29 4

Retrospective Invasive

50 3.5

Retrospective Invasive

26 9

[120]

Jonasson et al[118] Nestico et al[119] Davies et al[121] Otto et al

Calcific AS

2 cardiac Retrospective Invasive caths 2 cardiac Retrospective Invasive caths Asymptomatic Prospective Doppler

29 5.9 47 42 1.7

[90]

Roger et al AS on echo

Retro cohort Doppler

112 2.1

Retrospective Doppler

25 4.8

[123]

Thoreau et AS on echo al[122]

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fa*ggiano et al[124]

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AS on echo

Peter et al AS on echo

Prospective

Doppler

45 1.5

Retrospective Doppler

49 2.7

Retrospective Doppler

394 6.3

[126]

Brener et al[125] Otto et al

AS on echo

Asymptomatic Prospective

Doppler

123 2.5

Retrospective Doppler

91 1.8

Retrospective Doppler

170 1.9

Prospective

128 1.8

[128]

Bahler et AS on echo al[60] Palta et al AS on echo [127]

Roshenhek AS on echo et al[61] with Vmax

Doppler

>4.0 m/sec

AS, aortic stenosis; AVA, aortic valve area; ∆P, pressure gradient; Vmax , volume flow rate, a decrease in valve area alone may be seen with no change in jet velocity or transaortic gradient. A decrease in transaortic volume flow rate may occur secondary to comorbid disease, such as increasing mitral regurgitation or myocardial infarction, but also may occur late in the disease course of isolated aortic stenosis as left ventricular stoke volume decreases because of the onset of subtle systolic dysfunction (Fig. 22-21) . Conversely, some patients may have an interval increase in jet velocity and pressure gradient with no change in valve area if transaortic stroke volume is increased because of systemic factors (e.g., anemia, fever, pregnancy) or increasing aortic regurgitation. At this point, it is not clear whether the rate of hemodynamic progression in an individual patient is either predictable or "steady." In fact, it is most likely that the rate of progression is nonlinear; that is, a fairly slow rate of Figure 22-20 Maximal aortic jet velocity (Vmax ) is plotted for the initial

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and final Doppler echocardiographic studies in 42 asymptomatic patients. Group means are indicated by the symbol . (From Otto CM, Pearlman AS, Gardner CL: J Am Coll Cardiol 1989; 13:545–550.)

progression may change to a rapid increase in severity when the opposing forces of left ventricular ejection and leaflet stiffness can no longer be balanced. Predictors of Hemodynamic Progression Factors that predict the rate of hemodynamic progression in an individual patient have not been well defined. Clearly, valve anatomy is an important factor in disease progressive, since most patients with a bicuspid stenotic valve require surgical intervention at a younger age than patients with degenerative aortic stenosis.[114] Gender also is important, since the ratio of men to women with aortic stenosis is approximately 2:1. Other factors associated with the rate of disease progression are the severity of aortic stenosis when initially seen (more severe disease 489

Figure 22-21 A 32-year-old man had asymptomatic valvular aortic stenosis with a jet velocity of 5.0 m per second and a continuity equation valve area of 1.2 cm2 (A and B). Over the next year, he developed the onset of exercise intolerance and early symptoms of aortic stenosis. Repeat examination showed a decrease in aortic jet velocity to 4.5 m per second (C) in association with a decreased transaortic volume flow rate (D). Aortic valve area had decreased to 1.0 cm2 . Two-dimensional echocardiography showed normal left ventricular systolic function, but ejection fraction had decreased from 72% to 60%.

leads to symptoms more rapidly than milder disease) and age (older patients have more rapid disease progression than younger patients). Clinical factors such as elevated serum lipid levels, hypertension, smoking, and diabetes have been found to be associated with aortic stenosis.[129] In addition, a recent study found that smoking, hypercholesterolemia, and elevated creatinine and calcium levels were associated with more rapid disease progression.[127] However, further studies are needed to confirm these results. Two recent studies suggested that the amount of aortic valve calcium is an important determinant of disease progression.[60] [61] Despite using different grading scales to evaluate valve calcium, both of these studies found that the rate of disease progression was more rapid when

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more valve calcium was present. These studies also confirmed previous observations that the rate of disease progression is highly variable for individual patients. Given the continued uncertainty regarding which factors predict progression in an individual patient, it is prudent to follow patients with aortic valve thickening closely, monitoring for early symptoms of valve obstruction. Periodic echocardiographic examinations also are warranted, particularly for any change in symptoms or functional status. Uncertainty as to the rate of hemodynamic progression in an individual patient complicates the decision as to whether concurrent aortic valve replacement should be performed in patients with only moderate aortic stenosis who are undergoing coronary artery bypass surgery. Some surgeons recommend "prophylactic" valve replacement, since otherwise reoperation may be needed in less than 5 years.[130] Symptomatic versus Asymptomatic Aortic Stenosis The clinical course of the patient with aortic stenosis changes dramatically once symptoms supervene. The 490

Figure 22-22 (Figure Not Available) A, Event-free survival in hemodynamically severe aortic stenosis (triangles) or aortic regurgitation (circle) in severely symptomatic (solid lines and solid symbols) and asymptomatic or mildly symptomatic (dashed lines and open symbols) patients. B, Effective survival in hemodynamically severe aortic stenosis (triangles) or aortic regurgitation (circles) in severely symptomatic (solid lines) and asymptomatic or mildly symptomatic (dashed line) patients. (From Turina J, Hess O, Sepulcri F, Krayenbuehl HP: Eur Heart J 1987;8:471–483.)

asymptomatic patient (regardless of hemodynamic severity) has a low risk of sudden death with an actuarial survival rate no different from that of agematched normal subjects[89] [91] [131] [132] (Fig. 22-22 (Figure Not Available) and Fig. 22-23 ). In contrast, the symptomatic patient has a grim prognosis, with a 5-year actuarial survival rate of only 12% to 50% without surgical intervention. These data were derived from studies of patients who refused surgical intervention.[89] [91] , [111] , [131] [133] [134] [135] In patients with severe, symptomatic aortic stenosis, predictors of survival include the transaortic gradient or velocity, left ventricular systolic function as assessed qualitatively on echocardiography, age, and gender.[136] Of note, patients with a higher transaortic gradient have a better prognosis, most likely

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because when severe stenosis is present, a low gradient indicates a low transaortic stoke volume. In any case, valve surgery for relief of stenosis remains the appropriate treatment for symptomatic patients, even the elderly.[137] [138] Only rarely does severe comorbid disease result in an unacceptably high operative morbidity and mortality.

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Role of Echocardiography in Clinical Decision Making Timing of Intervention in the Symptomatic Patient Calcific aortic valve disease is prevalent in the elderly.[139] [140] Most of these patients have a systolic murmur on auscultation, but not all are symptomatic. The first step in the clinical decision making process for the timing of intervention in a patient with valvular aortic stenosis is a careful history as to whether symptoms (angina, exertional dizziness, exercise intolerance, or heart failure) are present or absent ( Table 22-5 ; ; Fig. 2224 ). Most clinicians defer intervention until definite symptoms are present, since the risk of sudden death is very low in the asymptomatic patient.[89] [91] [131] [132] , The presence of moderate or severe valve calcification in combination with a rapid increase in jet velocity over time (i.e., rapid progressors) identifies a subgroup of asymptomatic patients with a very poor short-term prognosis who are likely to develop symptoms soon.[61] If the patient has symptoms that may be due to aortic stenosis, the next step is to confirm the anatomic diagnosis and quantitate the degree of valve obstruction by Doppler echocardiography. The most appropriate standard of reference for the diagnostic utility of echocardiography in the management of symptomatic aortic stenosis patients is survival and functional status (not catheterization results), as our goal is to predict clinical outcome correctly.[16] Based on this reference standard, aortic jet velocity alone is a simple and useful initial diagnostic test. When jet velocity is very high (>4.0 or 4.5 m per second), severe stenosis is confirmed.[140] [141] [142] Some patients with mixed moderate aortic stenosis and aortic regurgitation will have a jet velocity over 4 or 4.5 m per second even though valve area is in the range of 1.0 to 1.5 cm2 . Comparing Doppler data with subsequent clinical outcome suggests that these patients benefit from valve replacement if symptoms of valve disease are present.[40] Decision making in patients with mixed aortic stenosis and aortic regurgitation is confounded by the need to take the degree of left

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ventricular dilation and systolic dysfunction into account as well as the severity of valve obstruction (see Chapter 4) . When jet velocity is very low (4.5 1988 with cath data stenosis value [141] severity at cath Galan 510 Observational, Actual 4.5 1991 retrospective outcome [3] (AVR) Shah 93 Blinded Actual 4.0 1991 decision re: outcome [142] AVR (AVR) AR, aortic regurgitation; AVA, aortic valve area; AVR, aortic valve replacement; Vmax , maximum aortic jet velocity.

replacement is unlikely to be helpful. When the valve area is between 1.0 and 1.5 cm2 , valve replacement may be indicated if there is at least moderate coexisting aortic regurgitation. Again, clinical decision making is problematic in this patient group. One prudent approach in the mildly symptomatic patient is to repeat the Doppler echocardiographic study after a reasonably short time interval (3–12 months). Evidence of disease progression will tip the balance toward intervention, whereas a stable examination and the absence of worsening symptoms argues for further waiting with close clinical follow-up. In clinical practice, the basic echocardiographic examination of a patient with valvular aortic stenosis includes measurement of maximum aortic jet velocity (with optional gradient calculations); continuity equation valve area; assessment of the degree of coexisting aortic regurgitation; evaluation of left ventricular size, hypertrophy, and systolic function; evaluation of the degree of mitral regurgitation; and estimation of pulmonary artery pressures. All of these parameters are included in the clinical decisionmaking process, along with any other specific measurements needed in an individual patient. Aortic Stenosis with Decreased Left Ventricular Function In some patients it is unclear whether valve opening is restricted due to excessive leaflet stiffness or whether there is only mild leaflet sclerosis with limited motion due to low transaortic stroke volume (Fig. 22-25) .

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There have been two basic research approaches to resolving the problem of distinguishing severe aortic stenosis with consequent depressed left ventricular systolic function from only mild to moderate stenosis with reduced leaflet motion due to intrinsic left ventricular dysfunction: (1) a flow-independent measure of stenosis severity or (2) a load-independent measure of left ventricular systolic function. Although significant progress has been made with both of these approaches, as discussed earlier, neither approach has provided a clear answer. A pragmatic clinical approach to this patient group is to (1) look at the valve, (2) look at the patient, (3) look at the options, and (4) consider further diagnostic evaluation (Table 22-6) . Direct assessment of the degree of leaflet thickening and calcification by fluoroscopy, transthoracic or transesophageal echocardiography, or, if 492

Figure 22-24 Flow chart for clinical decision making in aortic stenosis. AR, aortic regurgitation; AVA, aortic valve area; AVR, aortic valve replacement; F/U, follow-up; Vmax , maximum velocity of aortic jet.

Figure 22-25 A 61-year-old man presented with heart failure symptoms. Echocardiographic examination showed a moderately calcified valve with reduced leaflet opening (A) and reduced systolic function (ejection fraction, 20%) in association with marked left ventricular dilation as seen in the apical four-chamber view (B). Transaortic stroke volume was reduced as shown by pulsed Doppler echocardiographic examination of left ventricular outflow velocity in an anteriorly angulated four-chamber view (C). The aortic jet velocity (D) was 3.0 m per second corresponding to a maximum gradient of 36 mm Hg and a mean of gradient of 22 mm Hg. Continuity equation valve area was 0.9 cm2 . After multiple readmissions for heart failure on medical therapy, the patient underwent aortic valve replacement. Postoperatively, there has been no change in left ventricular function and persistent symptoms of heart failure are present. Ao, aorta; AS-jet, aortic stenosis jet; LA, left atrium; LV, left ventricle; LVOT, left ventricular outflow tract; RA, right atrium; RV, right ventricle.

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TABLE 22-6 -- Clinical Decision Making: Aortic Stenosis with Decreased Left Ventricular Function 1. Look at the valve Severely calcified versus Flexible leaflets 2. Look at the patient LV dysfunction due to end-stage ischemic disease or cardiomyopathy versus LV dysfunction due to aortic stenosis 3. Look at the options Risk of surgery Comorbid disease Outcome without surgery 4. Evaluate stenosis severity at two different flow rates (dobutamine or exercise): Increased transaortic flow rate Increased AVA suggests flexible valve leaflets No change in AVA suggests stiff, rigid valve leaflets No change in transaortic volume flow rate Severe AS versus unresponsive myocardium? AS, aortic stenosis; AVA, aortic valve area; LV, left ventricular. necessary, direct inspection at the time of surgery often is very helpful. A heavily calcified valve suggests that valve replacement will be beneficial, whereas thin, flexible leaflets argue against valve surgery. Additional clinical information about the patient may clarify the problem. If left ventricular systolic dysfunction is due to aortic stenosis, improvement is expected after valve replacement. However, if left ventricular dysfunction is due to end-stage ischemic disease or a primary cardiomyopathy, little improvement is expected after aortic valve surgery. Next, the therapeutic options and expected outcomes can be estimated for the individual patient. If the risk of surgery is acceptable or if the patient is having surgery for coexisting coronary artery disease, the threshold for valve replacement is reasonably low. If the risk of valve replacement is excessively high because of comorbid disease, medical therapy may be

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appropriate. If the patient has failed aggressive medical therapy, surgical intervention may be indicated, even if the risk is high. If the clinical decision still remains unclear, evaluation of stenosis severity at two different flow rates may be helpful. With mild to moderate aortic stenosis, augmentation of transaortic volume flow rate with exercise or a positive inotropic agent (e.g., dobutamine) will result in a significant increase (>0.2 cm2 ) in valve area as the flexible leaflets open to a greater extent. Conversely, with critical aortic stenosis, valve area will change little despite increased transaortic volume flow due to stiff, rigid valve leaflets. However, an increase in aortic valve area can be seen in some patients with surgically confirmed severe aortic stenosis, which therefore does not exclude fixed valve disease.[143] If the ventricle fails to respond to inotropic stimulation (i.e., no increase in cardiac output), interpretation is more difficult.[50] [144] [145] The failure of volume flow rate to increase may be due to limitation of flow by a severely stenotic valve or may be due to an unresponsive myocardium. In some patients, it may be preferable to evaluate stenosis severity at baseline and after several weeks of therapy to optimize preload and afterload, rather than using maneuvers to acutely increase volume flow rate. Instead of assessing changes in valve area, another approach is to calculate the end-systolic wall stress to fractional shortening relationship and compare the patient's data with those of published series[101] to assess whether improvement after valve replacement is likely. Unfortunately, despite meticulous diagnostic evaluation, outcome is likely to be poor in patients with aortic stenosis and low output, regardless of the therapy chosen.[146] [147] [148] [149] [150] Patients with reduced systolic function and a history of a prior myocardial infarction experience a particularly poor outcome following valve replacement.[151] A recent study that included patients with a low transvalvular gradient in addition to impaired systolic function found that the ejection fraction improved in the majority of patients following surgery, but that the 30-day mortality rate was 21%.[152] Evaluation of the Asymptomatic Patient Undergoing Noncardiac Surgery In the asymptomatic patient with valvular aortic stenosis undergoing noncardiac surgery, echocardiography allows (1) assessment of disease severity, (2) monitoring of left ventricular function before, during, and after the procedure, and (3) alerting the clinician to the need for invasive

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hemodynamic monitoring. Many of these patients, even with severe obstruction, can be managed without valve replacement if loading conditions are optimized preoperatively and careful invasive monitoring is continued in the postoperative period.[153] [154] Common postoperative complications include pulmonary edema or congestive heart failure associated with tachycardia that usually resolves quickly with rate control and diuresis. Similar considerations apply to the management of the pregnant patient with aortic valve disease (see Chapter 31) . Optimizing the Surgical Approach Once the decision has been made to proceed with relief of stenosis, the echocardiographic examination plays a key role in choosing the optimal surgical approach. Valve replacement remains the standard therapy for relief of valvular aortic stenosis. The optimal valve size and type typically are selected in the operating room based on direct measurement of the annulus by the surgeon. Echocardiographic prediction of prosthetic valve size has been only fair because of the limited number of valve sizes and the goal of implanting a larger valve when possible to improve hemodynamics. [155] For hom*ograft valve replacements, an estimate of the optimal size is more important than for mechanical valves, so that the correct size will be available at the time of surgery.[156] For hom*ograft aortic valves, diastolic left ventricular outflow tract diameter correlates best with implanted valve size. Note that the diastolic outflow tract diameter measurement averages 2 mm smaller than the systolic measurement (which is used in valve area calculations). A dilated aortic root commonly is seen as a result of poststenotic dilation and, in some cases, may be large enough to merit root replacement. In patients with a 494

small aortic annulus, an enlarging procedure may be considered or a specific valve chosen to avoid suboptimal hemodynamics postoperatively. Recognition of a subvalvular membrane, which can be mistaken for valvular stenosis on echocardiography, will alter the surgical approach and may allow resection of the membrane without valve replacement. Coexisting hypertrophic cardiomyopathy, although rare, is important to recognize to avoid postoperative dynamic subaortic obstruction.

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Echocardiographic Evaluation after Valve Replacement for Aortic Stenosis Evaluation of the Valve Replacement Surgical procedures that preserve the native aortic valve have not yet been successful for treatment of valvular aortic stenosis,[157] nor has percutaneous balloon valvuloplasty shown long-term benefit in adult patients. [136] A mechanical or stented tissue prosthetic valve is most often implanted after removal of the stenotic valve leaflets. The fluid dynamics of prosthetic valves, evaluation of valve function, and other postoperative complications are discussed at length in Chapter 23 , Chapter 24 , and Chapter 25 . Newer surgical approaches to treatment of valvular aortic stenosis include the development of stentless tissue valves[158] [159] [160] [161] [162] [163] and the use of aortic valve hom*ografts.[157] [164] [165] Both these valves types offer the advantages of improved hemodynamics compared with conventional valves, the absence of the need for chronic anticoagulation, and the hope of increased durability. Some centers also have reported success with the pulmonic valve autograft procedure in young adults, as well as adolescent patients.[166] [167] [168] In this procedure, the patient's stenotic aortic valve is replaced with his or her own native pulmonic valve. A hom*ograft then is used in the pulmonic position. Potential advantages of this procedure include optimal hemodynamics and low thrombogenicity. In addition, tissue viability of the pulmonic autograft provides the possibility of tissue growth and repair, which are particularly important features in adolescent patients. In one series including patients up to age 35 years, event-free survival rate after the pulmonic autograft procedure was 90% at 7 years.[166] Events included reoperation for either aortic or pulmonic valve dysfunction, significant aortic regurgitation, and death. More recently, echocardiographic follow-up of 100 patients undergoing the pulmonic valve autograft procedure was reported.[169] The reintervention rate was 2% at a mean follow-up period of 33 months, with a range of 6 months to 7

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years. A unique complication of the pulmonic autograft procedure is the development of hom*ograft failure, either from stenosis or regurgitation. With hom*ograft stenosis, patients typically develop progressive dyspnea approximately 3 to 6 months following surgery, at a time when continued physical recovery from the surgical procedure would be expected. Tissue from these failed explanted hom*ografts show a prominent inflammatory cell infiltrate and therapy has thus focused on suppressing the heightened immune response with oral steroids. When a course of oral steroids fails to control the disease process, reoperation may be required. Since stentless tissue valve, hom*ografts, and pulmonic autografts appear similar to a native aortic valve on echocardiographic examination,[160] [165] it is important that details about the surgical procedure be available at the time of the echocardiographic examination. Doppler findings for these valves also are similar to findings in native valves except that antegrade velocities may be slightly higher. Pulmonic autografts tend to have some degree of regurgitation early postoperatively, which typically decreases over the next several months, presumably due to collagen synthesis and increased structural stability of the valve in response to the increased mechanical stress on the valve leaflets. Other Hemodynamic Changes Postoperatively If left ventricular end-diastolic pressure has been chronically elevated preoperatively, as the ventricle remodels and filling pressures normalize, there may be a corresponding decrease in pulmonary artery pressures. If pulmonary pressures are elevated because of coexisting lung disease, little change is expected postoperatively. Moderate pulmonary hypertension (pulmonary artery pressures of 31 to 50 mm Hg) occurs in approximatly 50% of patients evaluated preoperatively with right heart catheterization.[170] However, the presence and magnitude of pulmonary hypertension do not appear to be related to the severity of aortic stenosis. It remains unclear whether preoperative pulmonary hypertension is related to postoperative survival, because studies have yielded conflicting results. [171] The effect of aortic valve replacement on coexisting mitral regurgitation remains controversial. In theory, mitral regurgitant severity should decrease given the "afterload reducing effect" of aortic valve replacement.[172] However, the magnitude of this effect may be small, particularly if there is anatomic abnormality of the mitral valve apparatus.[173] When significant mitral regurgitation accompanies severe aortic stenosis, it is prudent to consider a surgical intervention to reducing mitral regurgitant severity at

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the time of aortic valve replacement. Intracavity gradients due to dynamic obstruction at the midventricular level are seen in one quarter to one half of aortic stenosis patients in the early postoperative period.[174] [175] The severity of obstruction varies from trivial to severe, and clinical evidence of hemodynamic compromise may be seen in some patients. Patients with small hypertrophied and hyperdynamic ventricles at baseline are more likely to have obstruction postoperatively. [176] Typically, obstruction is manifested as a late-peaking systolic velocity curve, which is similar to the pattern seen in hypertrophic obstructive cardiomyopathy. However, the level of obstruction is at the midventricular or papillary muscle level, rather than subaortic, and systolic anterior motion of the mitral valve is not seen. Obstruction is dynamic in that the presence and severity of obstruction varies from day to day (peaking at the third postoperative day) and in that obstruction can be provoked or increased 495

by maneuvers that decrease left ventricular preload or increase contractility. Echocardiographic recognition of midcavity ventricular obstruction in the postoperative period affects clinical management, since intravascular volume loading and avoidance of agents that increase contractility or reduce afterload can result in significant clinical improvement. The echocardiographic finding of dynamic obstruction after aortic valve replacement also has significant prognostic implications. Patients with obstruction have more frequent postoperative complications (hypotension, arrhythmias), a longer hospital stay, and a higher mortality rate than those without obstruction.[175] [176] [177] The Effect of Valve Replacement on the Left Ventricle When left ventricular systolic function is depressed because of valvular aortic stenosis, improvement is seen early in the postoperative period. Predictors of improvement in the ejection fraction include female gender and less severe coexisting coronary artery disease.[103] When measured by quantitative angiography, left ventricular mass and wall thickness decrease substantially in the postoperative period. By 10 months postoperatively, left ventricular mass has decreased by about 30% as compared with the preoperative left ventricular mass, with a further decrease in left ventricular mass observed at studies performed 8 years

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postoperatively. Left ventricular mass may remain elevated in some patients, particularly if the prosthetic valve has suboptimal hemodynamics. Despite the apparent improvement in left ventricular geometry and systolic function seen in most patients, irreversible (or only very slowly reversible) changes in myocardial structure persist late postoperatively, with a relative increase in myocardial interstitial fibrosis as compared with normal and persistent diastolic dysfunction.[178] These myocardial changes, in combination with the mild pressure overload of the prosthetic valve, can result in persistent systolic overload at the myofibrillar level.[93]

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Future Directions Echocardiographic evaluation of aortic stenosis is an established and effective clinical tool. However, to explain the relationship between hemodynamic severity and symptom onset, a flow-independent measure of stenosis severity still is needed. At this point, the most promising research approach to a flow-independent measure of stenosis severity is to determine the change in the degree of valve narrowing measured at two different volume flow rates rather than utilizing data obtained only at rest. Continuity equation valve area and the slope of the maximum velocity/maximum volume flow rate relationship both are potentially useful approaches to this problem. A plausible hypothesis is that early in the disease course of "degenerative" aortic stenosis, increases in volume flowrate result in increased opening of the valve leaflets. As leaflet stiffness increases, this increase in leaflet motion diminishes until, eventually, increases in left ventricular ejection force no longer result in increased leaflet motion. We propose that symptom onset correlates with a stiff and rigid valve that limits the patient's ability to increase cardiac output with exercise. Other investigators have proposed a similar approach measuring stenosis severity at different flow-rates using exercise or dobutamine.[50] [78] [87] Further studies are needed to assess the potential prognostic value of this approach. As studies using Doppler approaches provide additional insight into the natural history of this disease, these data will allow prediction of disease progression in individual patients. In addition, these data will allow sample size calculation and appropriate risk stratification for interventional trials. In the future, these techniques will be used as end points in clinical trials of interventions to prevent or delay progression of "degenerative" valvular aortic stenosis.

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Chapter 23 - Fluid Dynamics of Prosthetic Valves Ajit P. Yoganathan PhD Brandon R. Travis PhD

Doppler echocardiography has made noninvasive examination of prosthetic heart valve function a clinical reality. Unfortunately, there are still many imperfections in echocardiographic examinations, including acoustic shadowing, reflections caused by implanted valves, and limitations in ultrasound technology. Despite these limitations, a number of important parameters can be calculated or estimated to aid in the assessment of prosthetic heart valve function and performance. Once a valve has been implanted, its function is governed primarily by its hemodynamic characteristics. In order to understand the hemodynamic performance of prosthetic heart valves, it is necessary to have a solid background in the physical laws that govern their function; therefore, the purpose of this chapter is to introduce cardiologists to the governing principles of fluid dynamics, relevant formulations used in prosthetic valve assessment, and fluid mechanical characteristics of specific prosthetic heart valves.

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Fluid Dynamics With few exceptions, a material can be characterized as a fluid if it deforms continuously under the action of shear stress.[1] Shear stress is defined as a force per unit area applied tangentially to a surface. Viscosity is related to the amount of deformation that a fluid experiences when a shear stress is imposed on it. A constant viscosity fluid, called a Newtonian fluid, is one in which the relationship between viscous shear stress and strain rate is linear, as shown in Equation 1: where µ is the viscosity, usually defined in centipoise (grams/cm·s). The coefficient in this linear relationship is the dynamic viscosity. Equation 1 states the relationship between viscous shear stress (τ), viscosity (µ), and strain rate for flow in the x-direction with the derivative taken in the ydirection, perpendicular to the direction of flow. Blood behaves as a Newtonian fluid in regions of high strain rate. For flow in large arteries, 3.5 cp is often used as a viscosity estimate for blood.[2] Conservation of Mass Conservation of mass governs all materials, and it is the logical starting point for an introduction to fluid motion. Consider an imaginary volume, a control volume, enclosed by a surface through which fluid can flow, as shown in Figure 23-1 . It is not necessary for this control volume to coincide with any physical boundaries; it is purely a tool for the analysis of physical systems. Conservation of mass, or continuity, states that the change in mass within this control volume is equal to the mass of fluid that enters the volume, minus the mass that exits. [3] A very good assumption for cardiovascular applications is that 502

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Figure 23-1 Control volume for the conservation of mass. V1 and V2 are the inlet and outlet velocities flowing over areas A1 and A2 . ρ, fluid density.

blood is incompressible, meaning its density does not vary. Assuming that there are only two surfaces across which fluid flows, surfaces 1 and 2, the velocities (v) and areas (A) can be related by conservation of mass, as shown in Equation 2.

pρv1 (t)A1 = ρv2 (t)A2 (2) Conservation of Momentum The principle of conservation of momentum was initially formulated as Newton's second law of motion—mass times the acceleration of an object is equal to the sum of the forces acting on that object. For application to fluid mechanics, it is more convenient to define this in terms of the fluid momentum. The momentum of a fluid is a measure of the mechanical force it is able to transfer and is equal to the product of fluid mass and fluid velocity. A change in momentum of a fluid can only be accomplished by the application of a force. The general form of the principle of conservation of momentum for an incompressible Newtonian fluid is called the NavierStokes equations.[3] The forces that merit consideration within the cardiovascular system are pressure, gravity, viscous shear stresses, and turbulent stresses. Conservation of Energy Consider the conservation of energy statement, again using the control volume approach. The change in energy within a control volume is equal to the net rate of energy crossing the surface of the control volume plus the net rate of energy generated within the control volume. Energy loss occurs when the net rate of energy generated within the control volume is negative. In cardiovascular applications, energy loss usually occurs because the viscosity of the fluid converts its kinetic energy to heat. The general equation for energy conservation is difficult to apply to cardiac blood flow; however, with a number of simplifying assumptions a useful relation can be obtained. The Bernoulli equation,[4] as shown in Equation 3, is used

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extensively in noninvasive cardiology:

where p is the static pressure and v is the velocity, along the streamline, h is the vertical distance above some reference point, and s is the distance between points one and two along the streamline. This equation can be derived from either the conservation of energy or the conservation of momentum. Each term in Equation 3 has a physical definition that aids in comprehension and application of the Bernoulli equation. The left side of the equation represents the difference in pressure acting on the fluid between the positions one and two. The first term on the right side is called the inertial term and represents the change in fluid acceleration owing to temporal changes in the applied force. The second term on the right side is the kinetic energy associated with the fluid at each location. This term can also be considered the convective acceleration term, which is associated with a change in the velocity of a fluid as it travels from one location to another. The classic example of convective acceleration is the steady flow of fluid through a converging nozzle, such as a funnel. Because of continuity, the velocity is higher at the exit of the funnel than at the entrance, and acceleration occurs even though the flow is steady. The third term on the right side of the equation is the hydrostatic pressure difference, owing to the difference in elevation between the two points. The final term on the right side of the equation is the irreversible loss of mechanical energy or momentum owing to viscous effects. The limitations that arise when using Equation 3 are important to understand. Initially, Bernoulli's equation was derived for inviscid flow, in which there are no viscous effects. Because it is not physically possible to obtain such a flow, the term on the far right was added to account for losses caused by viscous effects. Equation 3 must also be applied between two points that lie along a streamline within a flow field. Streamlines are imaginary lines in a flow field to which the velocity vector is always parallel. In steady flow situations, streamlines can be traced by placing a particle or dye into the fluid and following their motion throughout the flow field. If the flow is unsteady, however, streamlines change from one time to another, and the particle paths no longer coincide with streamlines. Because of the difficulty in defining streamlines, rigorous application of Equation 3 is not possible in cardiovascular flows.

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Dimensionless Quantities The structures of cardiovascular flows are governed by chamber geometry and two dimensionless quantities. The first of these quantities, the Reynolds number, is defined as follows: where v is the velocity, µ is the viscosity, ρ is the fluid density, and d is a length representative of the flow regime 503

in question. For flow in a pipe, d is the pipe diameter, whereas for jet flows, it is the diameter of the orifice through which the jet exits. Physically, the Reynolds number represents the ratio of the fluid inertia to the viscous forces acting on a fluid. The other important dimensionless quantity in cardiovascular flows, the Womersley number (α), represents the ratio of the local acceleration a fluid experiences to the viscous forces acting on it. The Womersley number is defined as follows:

where ω is the frequency (heart rate) and all other variables are the same for those used in the definition of the Reynolds number. These dimensionless numbers can be used to define a transition regime to turbulence common to all cardiovascular flows occurring in a similar geometry. Turbulence Consider a car traversing a winding road. As long as the car stays below a certain speed, the frictional force between its tires and the road enable the car to follow the path in which its front wheels are aligned. When the car surpasses a certain speed and passes around a large curve, however, the inertia of the car overcomes the frictional force holding the tires to the road. Similarly, flows with large inertia relative to the frictional, or viscous, forces acting on them become turbulent. Under these conditions, a small instability in the flow field (e.g., surface roughness within a pipe) can initiate fluctuations in fluid motion. When these fluctuations propagate to the point where fluid motion can only be described as random fluctuations about a mean velocity, the flow is said to be turbulent.

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In steady flows, the tendency of a flow to be turbulent is governed only by the Reynolds number and the chamber geometry. Two geometries that have been studied extensively and have direct applications to cardiovascular fluid mechanics are flow through a straight pipe and flow through a small, circular orifice. Flow through a straight pipe transitions to turbulence at Reynolds numbers of approximately 2000.[5] Flow through small, circular orifices create a phenomenon known as a free jet. For steady free jet flows, which are inherently more unstable than pipe flows, the critical Reynolds number is approximately 1000, with fully turbulent flow occurring at Reynolds numbers greater than 3000.[6] [7] In pulsatile flow, the transition to turbulence depends on the Womersley number and the shape of the flow waveform as well as the Reynolds number and chamber geometry.[8] [9] The critical Reynolds numbers for the transition to turbulence in pulsatile flow is much higher than the corresponding numbers in steady flow. Estimates of transition to turbulence in the ascending aorta by Yoganathan et al[4] (based on work by Nerem and Seed[10] ) indicated that the critical Reynolds number for transition is approximately 8000. It is also important to note that in pulsatile flow, turbulence may not be present during the entire cycle. Because flow acceleration is inherently more stable than flow deceleration, turbulence is more often observed during the deceleration phase of pulsatile flow. [9] Shear Stress Both viscous and turbulent shear stresses, if large enough, can potentially lyse or activate cells of the blood[11] [12] [13] [14] however, the origin, and consequently the scale, of viscous and turbulent shear stresses is different. Viscous shear stresses act on a molecular scale; they arise from the tendency of one molecule to remain near its neighbors. This tendency is quantified in fluids by their viscosity. Because viscous stresses act on a scale much smaller than the diameter of a blood cell, blood cells always experience a viscous shear stress if such a stress is present. In contrast, turbulent shear stresses arise from the inertia contained within the fluctuations of turbulent flow. Turbulent shear stresses act on a scale comparable to the length of the smallest turbulent fluctuations, often much larger than the diameter of a blood cell. Even if a turbulent shear stress is present, a blood cell may not experience this stress if the cell diameter is much smaller than the length scale of the smallest turbulent fluctuations. Boundary Layer Separation

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Due to viscosity, when a flowing fluid contacts a solid body, because of viscosity, the fluid that is immediately adjacent to the body must be the same velocity as the body. For this reason, a boundary layer is formed. The boundary layer is a region in which the velocity changes from zero at the wall to that of the free stream value. Boundary layers are extremely thin but very important, for it is only in this region of the flow that viscous effects are significant. As a fluid moves downstream, viscous diffusion occurs and the viscous effects are felt farther from the wall, and the boundary layer grows. When a fluid flows over a solid body, it must change direction to pass around the body. A pressure gradient is required for this to occur. When an adverse pressure gradient (i.e., a pressure gradient against the flow direction, tending to decrease fluid velocity) is applied, if the magnitude of the pressure gradient is large enough, the fluid within the boundary layer reverses and boundary layer separation occurs. Downstream of the separation point, a region exists in which there may be reversed, turbulent, or disturbed flow. Recirculating or vortical flows are characteristic of this region; they can lead to high particle residence times and oscillatory shear stresses, both of which can have a wide variety of clinical implications, including atherosclerosis.[15] [16] In pulsatile flows, separation can be generated by a geometric adverse pressure gradient or by temporal changes in the driving pressure. Geometric adverse pressure gradients are present behind all prosthetic heart valves because of the small orifice area. As the area increases downstream of a prosthetic heart valve, the velocity decreases, in accordance with the continuity equation. The decrease in velocity is caused by an adverse pressure gradient. Because of the contractile nature of the heart, 504

the blood that flows through it also experiences both acceleration and deceleration during a cardiac cycle. It is during the deceleration phase of a particular flow, when an adverse pressure gradient is present, that boundary layer separation is most likely to occur. Thus, in regions in which there are both geometric and temporal adverse pressure gradients, separation is even more likely. Cavitation Cavitation is the formation of vaporous bubbles resulting from a sudden

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drop in local pressure below the vapor pressure of the fluid. The abrupt closure of a mechanical prosthesis has been shown to induce cavitation in in vitro flow circuits,[17] [18] [19] and a few works have linked cavitation with mechanical valve closure in vivo as well.[20] , [21] The formation and subsequent collapse of cavitation bubbles releases a tremendous amount of energy within a very localized area; cavitation has been known to crack steel turbomachinery. Cavitation during the mechanical valve closure event is thought by some to be responsible for pitting on mechanical prosthesis surfaces[22] and the blood damage induced by mechanical prostheses.[18] The sharp drops in local pressure created by mechanical prosthesis closure lasts less than 2 ms,[18] [19] [20] [21] so the resulting cavitation bubbles collapse soon after they are created. Vaporous cavitation bubbles could act as nucleation sites, however, drawing in blood gasses such as nitrogen and carbon dioxide. The resulting gaseous emboli could last much longer than the cavitation event. Indeed, gaseous emboli have been detected in the circulation of patients with mechanical prostheses by transcranial Doppler. [23] Such emboli have been dubbed with the acronym HITS (high intensity transient signals). Pressure Recovery Consider steady flow of fluid through a pipe with a restrictive orifice placed downstream of the pipe entrance. Because of continuity, as the fluid enters the restriction, it accelerates. Assuming that the flow is streamlined when the particle enters the restriction, the velocity increases and the static pressure decreases, according to the Bernoulli equation. Once it exits the restriction and the cross-sectional area increases, the particle's velocity decreases and the pressure increases. The increase in pressure distal to a restrictive orifice is called pressure recovery. If there are no viscous energy losses, the pressure recovers to the value it had at the entrance to the restriction; however, viscous losses always occur, pressure does not recover completely, and irreversible mechanical energy losses occur.[3] Consider two similar steady flow situations. The first geometry is that of a Venturi flow meter, as shown in Figure 23-2 . The second case involves flow through an orifice meter, in which a restrictive orifice is placed in the center of a straight pipe (see Fig. 23-2A) . In the first case, because of the smooth contraction before the Venturi throat and the gradual area expansion downstream, there is no separation and very little energy loss. Most of

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Figure 23-2 A, Orifice meter with pressure drop. B, Venturi meter with pressure drop.

the velocity at the Venturi throat is converted back to pressure. For the same flow through the orifice meter, the velocity at the orifice would be approximately the same as the velocity at the Venturi throat. Because of the very rapid area contraction and expansion surrounding the orifice, however, a large separation region forms downstream and energy is lost. Pressure measurements at the location of the greatest contraction within each model would yield approximately the same value, which could lead one to believe that the energy losses in both models are identical. If the pressure is measured further downstream, however, it is evident that the Venturi meter has a much smaller energy consumption than the orifice meter, owing to downstream recovery of pressure. The same concepts may hold true for stenoses within the cardiovascular system. In the Venturi model, the peak velocity and the smallest pressure occur at or very near to the throat of the model, whereas in the orifice meter, because fluids cannot turn sharp corners, the peak velocity occurs slightly downstream of the orifice. The location at which this occurs is called the vena contracta because the area that the fluid passes through is less than the orifice area. Therefore, according to the Bernoulli and continuity equations, the maximum pressure drop across a prosthetic valve occurs at the location of the vena contracta and not at the valve orifice.

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Application of Fluid Mechanics to Prosthetic Heart Valves Pressure Drop The pressure drop (∆P) across a prosthetic valve is related to the energy losses caused by its presence. Pressure 505

drops across natural valves can be measured with invasive catheter techniques; however, it is both difficult and dangerous to pass a catheter through a prosthetic valve. Fortunately, the Bernoulli equation can provide a noninvasive estimate of the pressure drop across prosthetic or natural valves. Neglecting the viscous effects and applying Equation 3 at mean conditions, so that the integral term vanishes, yields Equation 4: Point 1 is proximal to the valve and point 2 is at the orifice. If the velocity upstream of the valve is much smaller than at the valve, v1 can be neglected and Equation 5 is obtained:

If the velocity is measured with continuous wave Doppler ultrasound (in meters per second), the pressure drop can be obtained from this equation in millimeters of mercury. When measuring pressure distal to prosthetic valves, it is important to note whether or not the recovered pressure is measured. It is especially important when using continuous wave Doppler ultrasound to evaluate prosthetic heart valves. Continuous wave Doppler ultrasound measures the highest velocity, which occurs at the vena contracta. Consequently, the Doppler-derived pressure drops are always based on the pressure at the vena contracta, before pressure recovery occurs. Thus, one is likely to

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overestimate the transvalvular pressure drop because pressure recovery is not considered. Although Doppler ultrasound may overestimate transvalvular pressure drops, however, they are extremely useful in patient diagnosis. A study by Marcus et al[24] has shown that Doppler-derived pressure drops measured across small-diameter prosthetic mechanical valves (Medtronic-Hall and St. Jude) correlate just as strongly with fluid mechanical energy losses as the recovered pressure drops measured by catheterization. Pressure drop and recovery through prosthetic valves can be significant factors affecting the pressure within the left ventricle. A larger pressure drop across a prosthetic valve requires a larger systolic pressure in the left ventricle to drive flow through the circulation. Because it has been shown that left ventricular pressure is the primary determinant of myocardial oxygen consumption,[25] it is imperative that the pressure in the left ventricle is minimized when dealing with prosthetic valves. Numerous studies detailing the effects of recovery on pressure drop measurements for both natural and prosthetic heart valves have been published, and this topic continues to be an area of active research.[26] [27] [28] [29] [30] [31] [32] [33] [34] [35] Valve Area Cardiologists have used a variety of methods to determine the forward flow area of a valve. Because of acoustic anomalies caused by prosthetic valves and the limited spatial resolution of echocardiography, it is often impossible Figure 23-3 Control volume in the left ventricle for determining aortic valve area. V1 and V2 are the inlet and outlet velocities flowing over areas A1 and A2 .

to measure the valve area directly. Applying a control volume analysis to a prosthetic valve in the aortic position (Fig. 23-3) and rewriting Equation 1, however, allows for estimation of the mean area over which fluid flows, as shown in Equation 6: The integral is taken with respect to time over the systolic flow period, v1 is

the velocity upstream of the aortic valve, and v2 is the velocity at the vena

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contracta. A2 is the area of the vena contracta or the effective valve area and A1 is the area at the upstream face of the control volume, measured by

echocardiography. Inherent to Equation 6 is the assumption that the spatial velocity profile is uniform over the entire orifice area; however, because the velocity profile is nonuniform in mechanical prostheses, it is difficult to apply Equation 6 accurately. By extending the control volume from the left ventricular outflow tract to encompass the entire left ventricle (Fig. 23-4) , it is possible to use this technique to determine the mean mitral valve area. The time-velocity integral of both the mitral and the left ventricular outflow tract positions must be calculated over the entire cardiac cycle. It is only necessary to integrate the velocity at the mitral valve during diastole and that of the aortic valve during systole, because these are the only times in which there is flow through the valves. If regurgitation is not present in either valve, Equation 6 can be applied and the effective area of the mitral valve can be obtained. When aortic regurgitation is present, the velocity and area at the light ventricular outflow tract can be used instead for calculation of effective mitral orifice area. Another method for determining valve area can be 506

Figure 23-4 Control volume in the left ventricle for determining mitral valve area. V1 and V2 are the inlet and outlet velocities flowing over areas A1 and A2

derived using the Bernoulli equation and conservation of mass. A contraction coefficient (Cd ) can be defined as the area of the vena contracta

divided by the area of the valve orifice (Ao ).[3] The continuity equation for flow through an orifice, including the contraction coefficient, appears in Equation 7, where Q is the flow rate and v is the velocity at the vena contracta: Q = Ao vCd (7) Substituting Equation 5 into Equation 7 and solving for velocity yields an

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equation that can be used to determine the effective orifice area of a cardiac valve:

The constant was determined by using the density of blood (ρ = 1050 kg/m3 ) and converting the units to those convenient for biomedical use.

The effective area will be square centimeters, if the root mean square systolic or diastolic flow rate (Qrms ) is in cubic centimeters and the mean systolic or diastolic pressure drop (∆P) is measured in millimeters of mercury.

Another method that has been developed involves measuring the pressure half-time of an orifice to estimate the orifice area. The pressure half-time (Pt/2 ) is the time required for left ventricular pressure to decrease to half of its peak value. An empiric relation between the pressure half-time and the area of the mitral valve (Amv ) has also been established. It was based on observations that changes in the mitral pressure drop with time were constant for a particular orifice area[36] [37]

The constant 220 was empirically determined,[38] but this equation has been shown to be dependent on a number of factors other than the valve area, including the severity of aortic regurgitation and ventricular wall properties. This equation is ineffective for prosthetic heart valves, limiting its application.[39] [40] Regurgitant Flow Rate Because mechanical prosthetic valves are fairly rigid, they are unable to form tight seals when closed. Consequently, regurgitant jets are present in prosthetic valves under normal conditions, although the amount of regurgitation is usually small. Normal regurgitant flow is characterized by a closing volume during valve closure and leakage after closure (see Figure 23-11) . Regurgitant flow is often characterized by the regurgitant volume. The regurgitant volume is the total volume of fluid through the valve per beat owing to the retrograde flow. It is equal to the sum of the closing volume and the leakage volume. The closing volume is the volume of fluid flowing retrograde through the valve during valve closure. Any fluid volume accumulation after valve closure is caused by leakage and is

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referred to as the leakage volume. These quantities are dependent on valve size, increasing with increasing valve diameter. Typically, the regurgitant volume is higher for mechanical valves than for bioprosthetic valves; however, prosthetic valves can exhibit substantial regurgitation when they malfunction. To distinguish normal from abnormal valve function, it is important to differentiate between normal regurgitant volume and additional regurgitation owing to disease. Fluid mechanical analysis of this problem has provided two different techniques that at least partially fulfill this requirement. Turbulent Jet Theory

Using free turbulent jet theory, Cape et al[41] [42] [43] (and later Sugawara et al [44] ) were able to derive relations for the regurgitant flow rate based solely on Doppler ultrasound measurements. Turbulent jets have a number of unique characteristics. Upon entering a chamber they spread radially, pulling or entraining stationary fluid with them. Initially, though, the jet has a core of fluid that is not affected by the stationary fluid. This potential core has the same velocity as the jet at the orifice and persists for a few orifice diameters downstream, as shown in Figure 23-5 . Once the core vanishes, the jet reaches a state that is amenable to theoretical analysis. It is important to recognize, however, the assumptions inherent in this theoretical analysis. Unsteady flow effects are neglected, and the analysis assumes that the jet enters a stationary fluid and does not impinge on solid boundaries. In the heart, regurgitant jets are unsteady, often impinge on the walls of the heart, and always encounter incoming forward flow. Additional work has been performed that treats jets in confined and impinging geometries; these geometries more closely resemble the chambers of the left heart. Burleson et al [45] [46] constructed a dimensional analysis model of valvular regurgitation based on the center line velocity decay of the jet and the width and length of the receiving chamber. Their equation has been shown to 507

Figure 23-5 Free jet center line velocity decay showing jet velocity (v) plotted versus distance (x).

be accurate for a number of in vitro geometries and conditions.[45] [47]

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Proximal Flow Convergence

The principle of conservation of mass was also applied in the region proximal to the valvular orifice to measure regurgitant volume.[48] [49] [50] [51] When fluid enters a regurgitant orifice it must accelerate to reach a peak velocity at the throat of the orifice. If the orifice is circular, this acceleration region should be axisymmetric about the center of the orifice. Thus, upstream of the regurgitant orifice, a series of concentric isovelocity contours hemispherical in shape can be defined within the flow field. This physical argument is the basis for the proximal flow convergence method of quantifying regurgitant flow rate. If a control volume is constructed to coincide with a hemispherical contour and the regurgitant orifice, as shown in Figure 23-6 , the same amount of fluid that enters the volume from an isovelocity contour exits the control volume through the regurgitant orifice. The control volume statement is represented mathematically in Equation 9. Qo = (2πr2 )Vr (9) The term within parentheses is the surface area of the hemispherical control surface. Vr is the velocity measured with color Doppler echocardiography

and r is the distance at which the velocity is measured. Qo is the flow rate at the regurgitant orifice.

Because of its simplicity and ease of application, this technique has received a great deal of attention, especially for mitral regurgitation. The effects of regurgitant orifice motion,[52] orifice geometry variation,[53] [54] [55] [56] and ultrasound machine settings[53] have all been addressed with both in vitro and in vivo investigations. In addition, its application to prosthetic valve regurgitation has also been considered.[57] Studies in our laboratory have found that isovelocity contours from regurgitant orifices can be described better by a hemielliptical shape than by a hemispherical shape, yielding more accurate estimations of regurgitant flow rate in vitro.[58] [59] Unfortunately, rigorous in vivo validation of the proximal flow convergence technique is difficult.

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Hemodynamic Characteristics of Native Valves In order to effectively analyze flow through prosthetic heart valves in the mitral or aortic positions, it is important to understand the conditions under which natural valves function. Figure 23-7 illustrates typical pressure and flow waveforms for healthy individuals at both the aortic and the mitral valves. During systole, the pressure difference required to drive the blood through the aortic valve is on the order of a few millimeters of mercury. Diastolic pressure differences across the aortic valve are much larger than systolic, the pressure usually being about 80 mm Hg. The valve closes near the end of the deceleration phase of systole with very little reverse flow. The blood flow through the mitral valve is biphasic during diastole, as shown in Figure 23-4 . The first peak, the E wave, is due to ventricular relaxation, whereas the second peak, the A wave, is caused by contraction of the left atrium; therefore, all valves in the mitral position open and close twice during each cardiac cycle. It is also evident that all cardiac valves are closed during both isovolumic contraction and isovolumic relaxation. Measurements of the velocity profile just distal to the aortic valve have been performed with Doppler echocardiography in normal subjects.[60] The peak systolic velocity is Qo = (2πr2 )Vr . (12) Figure 23-6 Proximal isovelocity surface area schematic. Vr is the velocity on a hemispheric shell defined by the radius (r) with surface area A1 . A2 is the regurgitant orifice area and Vo is the peak regurgitant jet velocity.

508

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Figure 23-7 Pressure and flow waveforms for the left heart.

1.35 ± 0.35 m per second and the velocity profile at the level of the aortic valve annulus is relatively flat; however, there is usually a slight skew toward the septal wall (10 mm) are associated with increased embolic complications.[126] , [127] Figure 24-17 shows a TEE at the midesophageal level in a septic patient with a stented bioprosthesis in the aortic position. The large echodense mass seen within the left ventricular outflow tract is consistent with a vegetation. Differentiation of vegetation from thrombus may be difficult and often impossible. An important hint is that endocarditis more commonly is associated with regurgitant lesions, whereas thrombosis more commonly is associated with stenotic lesions. Either condition, however, can be seen as mobile echodense masses. Thus, such separation primarily should be based on the clinical presentation and bacteriologic results. Rarely, both complications 540

Figure 24-17 TEE at the midesophageal level from the transverse (T) and longitudinal (L) views in a septic patient with a stented bioprosthesis in the aortic position. A large echodense mass in the left ventricular outflow tract is clearly seen (arrows). LA, left atrium; LV, left ventricle; RA, right atrium, RVOT, right ventricular outflow tract.

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may be present in the same valve. Figure 24-18 corresponds to a midesophageal view in a septic patient with a St. Jude Medical valve in the mitral position and a bioprosthesis in the tricuspid position. A large vegetation and a thrombus can be seen on the atrial aspect of the mitral valve. Early and accurate identification of septic complications TABLE 24-8 -- Sensitivity (Sens) and Specificity (Spec) of TTE versus TEE for the Diagnosis of Vegetations and Associated Abscesses in Patients with Endocarditis TTE

Reference Mugge et al (1989)[127] * Taams et al (1990)

No. of Patients Studied 105

No. of Patients with PVE 25

SENS (%) 58

118

TEE

SPEC SENS SPEC (%) (%) (%) ‡ 90 ‡ 100 100 100

[128] *

Daniel et al (1991)

[129] †

PVE, prosthetic valve endocarditis; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. *Identification of vegetations. ‡Insufficient data available, but smaller studies have reported specificity of TEE at 100%. †Identification of abscesses.

Figure 24-18 TEE at the midesophageal level from the transverse view in a septic patient with a St. Jude Medical valve in the mitral position and a stented bioprosthesis in the tricuspid position. A large vegetation (veg) and a thrombus (th) are clearly identified within the left atrium. LV, left ventricle; RA, right atrium; RV, right ventricle.

in patients with prosthetic valves have a significant impact on the decisionmaking process. TEE has dramatically improved the diagnostic accuracy in detecting vegetations, abscesses, and other complications associated with

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prosthetic valve endocarditis. [127] [128] [129] [130] Studies comparing TTE and TEE have included both native and prosthetic valves in their analysis. Table 24-8 lists studies comparing the two modalities in which patients with prosthetic valves were included. Although prosthetic valves are not analyzed separately, the data clearly favors TEE as a superior imaging modality; therefore, TEE should be performed routinely in patients with suspected prosthetic valve endocarditis, most notably in patients who fail to improve on therapy. Development of a perivalvular abscess is associated with a grave prognosis and indicates the need for aggressive medical and surgical therapies.[131] [132] Clinical findings suggestive of an abscess include persistent sepsis despite appropriate antibiotics, new or worsening heart failure symptoms, and development of first-degree atrioventricular block or incomplete right bundle branch block. Figure 24-19 illustrates a range of possible outcomes of a prosthetic valve abscess. Rupture may occur into adjacent structures, including the pericardial sac creating cardiac 541

Figure 24-19 A to D, Clinical, electrocardiographic, and echocardiographic characteristics in septic complications of mechanical valves. AV, atrioventricular; CHF, congestive heart failure; RBBB, right bundle branch block.

tamponade; however, a rather common outcome is the development of perivalvular dehiscence with a tunnel communicating the aorta with the left ventricular outflow tract and consequently severe perivalvular regurgitation. Emergent surgical treatment may be a lifesaving procedure in these acutely ill patients. Echocardiographic findings of perivalvular abscess include valve rocking, periaortic root thickening, or perivalvular echolucency.[133] As noted in Table 24-8 , identification of an abscess is very difficult from TTE; therefore, TEE is mandatory when this complication is clinically suspected. In addition, fistulous tracts connecting the perivalvular space with adjacent structures can be imaged and tracked down with color flow. Figure 24-20 represents the mid- and upper esophageal images in a septic, critically ill patient with a St. Jude Medical aortic prosthesis who presented to the emergency room with acute aortic insufficiency and pulmonary edema; a large perivalvular abscess is clearly noted.

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Patient-Prosthesis Mismatch The term patient-prosthesis mismatch refers to the clinical setting in which the prosthesis is structurally normal but the hemodynamic data are consistent with a greater stenosis than expected for the valve type and size. [134] [135] The mismatch occurs because the valve area is relatively insufficient to fit the patient's body surface area. A given valve area perfectly acceptable for a small relatively inactive subject may be inadequate for a larger physically active individual. This problem is usually seen in patients with small aortic annulus sizes and in whom the valve replacement was performed because of native valve stenosis rather than regurgitation.[134] From the clinical point of view, the patient fails to improve or may even be symptomatically worse. The long-term implications of this condition are not known. After successful aortic valve replacement, regression of cardiac hypertrophy is commonly detected. Failure to regress 6 months after surgery may be a subtle indication that residual aortic stenosis is present and that the hemodynamic burden persists.[136] [137] In some patients inadequate hemodynamics may be apparent only at higher cardiac output stages (i.e., during exercise). For patients with exertional symptoms suggesting high valve resistances without evidence of a primary valve dysfunction, stress echocardiography (see later) should be considered. The diagnosis of patient-prosthesis mismatch requires exclusion of an intrinsic valve dysfunction, which further emphasizes the need for a baseline postoperative study. Prosthetic Aortic Stenosis The initial suspicion of prosthetic valve stenosis may be the incidental finding of abnormally high flow velocities detected during a routine examination. This finding should prompt careful inspection from the parasternal long- and short-axis views to determine possible causes. In addition to thrombus formation, obstruction also can occur from gradual ingrowth of fibrous tissue called pannus formation. An encapsulated perivalvular abscess may reduce the outflow tract area leading to stenosis. Figure 24-21 shows images from a patient with a hom*ograft and a sterile perivalvular cavity reducing the effective orifice area. In the absence of symptoms and if there is normal valve motion otherwise, close follow-up is probably appropriate. Alternatively, stress echocardiography may be necessary to unmask a truly symptomatic stenosis or to address the patient's or referral physician's concerns. If the valve area calculated from TTE data

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is markedly reduced, 542

Figure 24-20 TEE in a septic patient with a St. Jude Medical aortic valve. A, Partial dehiscence and a large abscess cavity (arrow). B, Cross-sectional view of the same pathology. The abscess cavity is composed of echodense and echolucent material (arrow). AO, aorta; LA, left atrium; LV, left ventricle; RA, right atrium.

we commonly reassess the aortic valve area (continuity equation) by combining the diameter of the left ventricular outflow tract accurately determined by TEE at the upper-midesophageal level with the transthoracic velocity time integrals obtained during the same setting. Prosthetic Mitral Stenosis Valve area should be routinely calculated from the pressure half-time or the continuity equation (or both) in patients with suspected prosthetic mitral stenosis. Although an E wave velocity greater than 2 m per second may be indicative of prosthesis stenosis, increased velocities in the absence of a prolonged pressure half-time may be a result of prosthetic regurgitation.[2] Color flow can aid in aligning the Doppler beam parallel to the mitral inflow in obtaining the most representative Doppler signal. Mean valve gradient should be combined with pressure half-time or flow volume determination to differentiate prosthesis stenosis from increased transvalvular volume. As noted earlier, TEE is a very useful tool for detecting thrombosed mitral prosthesis and guiding thrombolytic therapy; thus, TEE should always be performed in patients in whom stenosis is suspected. Prosthetic Aortic Regurgitation The approach to grading prosthetic regurgitation is similar to that of native valves and involves evaluation of several echo-Doppler indices. As with native valve regurgitation, ventricular size and function are important clues to the severity of regurgitation. Normal left ventricular internal dimensions is incompatible with severe chronic Figure 24-21 TTE of a patient with stenosis of an aortic hom*ograft. A, Parasternal long-axis view showing an encapsulated antibiotic-sterilized

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cavity (C), which reduces the outflow tract diameter (LVOT) in half (arrows). B, Continuous wave Doppler from the five-chamber view in the same patient with elevated velocities up to 4.0 m/sec, maximal gradient of 64 mm Hg, and a mean gradient of 34 mm Hg. The continuity equation valve area was estimated at 0.7 cm2 . LA, left atrium.

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aortic regurgitation. Jet height and area from the short-axis view have been compared with angiographic grading in native valve regurgitation with excellent correlations of 0.93 and 0.91, respectively.[138] [139] In our laboratory we have found the parasternal long-axis view a more useful view to assess the jet area in relation to the left ventricular outflow tract area. Eccentric valvular or perivalvular jets may overestimate the severity of prosthetic regurgitation because they may be directed perpendicular to the outflow tract, occupying a larger portion of the ventricular outflow tract area. The apical five-chamber view should also be used to determine jet characteristics. The pressure-half time can be helpful in differentiating chronic from acute regurgitation. In general, acute (commonly severe) aortic regurgitation has a rapid slope decay indicative of acute elevation of left ventricular pressures at end-diastole. Although highly specific, this finding is poorly sensitive because the decay slope may be altered by changes in diastolic function, particularly ventricular compliance, heart rate, and rhythm. Thus, patients with severe chronic aortic regurgitation and a compliant left ventricle may have an aortic-ventricular diastolic pressure slope similar to patients with milder degrees of aortic regurgitation. Consequently, in many patients the Doppler diastolic slope decay helps in differentiating acute from chronic regurgitation, but not severe from moderate regurgitation. The intensity of the continuous wave Doppler signal may help in assessing severity of regurgitation. In patients with severe regurgitation, the signal intensity of the forward and regurgitant flows are similar. Unfortunately, such estimation is subject to wide interobserver variations. In addition, signal intensity depends highly on the specific gain settings on different ultrasound systems and even in the same machine. Thus, in our laboratory an intense Doppler signal of aortic insufficiency is a hint that the severity of regurgitation is more than mild. The amount of flow reversal in the descending thoracic aorta also has been correlated with severity. Normal flow reversal in the ascending aorta is confined to the early part of diastole,

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whereas flow reversal that persists throughout diastole is seen in patients with severe regurgitation.[3] [81] TEE may provide important etiologic information such as primary mechanical failure (i.e., flail cusp), ring dehiscence, vegetations, or abscess formation with a paravalvular fistula (see Fig. 24-19D) . Additionally, TEE offers an excellent visualization of the ventricular outflow tract area for severity assessment based on the relation of jet area and ventricular outflow tract area. Finally, evaluation of the ascending aorta for aneurysmal dilation or dissection should be part of the TEE examination in these patients. Prosthetic Mitral Regurgitation Assessment of mitral regurgitation by TTE is problematic because reverberations from the metallic material of the prosthesis commonly obscure the left atrium. This problem is less noticeable with bioprostheses. Nevertheless, the common practice in our laboratory is to turn to TEE every time there is clinical or TTE suspicion of pathologic mitral regurgitation, regardless of the type of prosthesis. Color Doppler demonstrating flow convergence or a clearly visible proximal isovelocity surface area on the ventricular aspect of the valve is suggestive of severe regurgitation. The maximal area of the acceleration signal has been used to assess severity of mitral regurgitation.[140] Similar to aortic insufficiency, the intensity of the continuous wave Doppler signal is related to severity; the more intense the signal, the more severe the regurgitation.[71] Significant regurgitation has a density similar to the antegrade flow signal.[141] A recent evaluation of TTE for evaluating prosthetic mitral regurgitation compared proximal isovelocity surface area, intensity of the Doppler signal, and color Doppler jet within the left atrium.[142] Flow convergence was more sensitive but less specific for predicting significant prosthetic mitral regurgitation. Doppler indices used for severe native valve regurgitation also may be helpful in prosthesis regurgitation, such as increased E wave velocity (>2 m/sec), increased mean gradient (>5 to 7 mm Hg), short pressure half-time (40 cm).[6] [142] [143] Unexplained, worsening, or new pulmonary hypertension may be indicative of significant regurgitation. TEE has substantially improved the diagnostic accuracy of the jet characteristics for determining severity and etiology of prosthetic regurgitation. [4] [144] Remember that color Doppler is a measure of velocity and not of volume, and although the jet area may be relatively small,

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eccentric jets may result from severe regurgitation, particularly when they wrap around ("hug") the left atrial wall (Fig. 24-22) . An eccentric jet of severe mitral regurgitation loses momentum and velocity as it contacts the atrial wall despite a large volume, a phenomenon known as the Coanda effect.[145] In our laboratory, we use an eccentric jet as an evidence of severity. In fact, most cases of eccentric regurgitation hugging the lateral wall of the left atrium Figure 24-22 (color plate.) TEE from the transverse plane (0 degrees) illustrating a large, eccentric jet of severe mitral regurgitation.

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enter into one of the pulmonary veins or into the left atrial appendage, confirming severe mitral regurgitation. Prosthetic valve dehiscence, that is, a separation of the prosthetic sewing ring from the native fibrous ring, is caused by detachment of the retaining sutures. Careful TEE evaluation of the annulus at the midesophageal and transgastric levels can reveal a dropout of echoes; when color Doppler is applied, an eccentric jet may become obvious. Detection of valve dehiscence is important because it usually means severe regurgitation requiring surgical repair or replacement. Figure 24-23 is a set of TEE images illustrating a patient with a Hanco*ck bioprosthesis in the mitral position with dehiscence and severe eccentric regurgitation. The morphology of the pulmonary vein Doppler waveform is dependent on both volume of regurgitation and left atrial properties. Pulmonary vein flow characteristics have been useful in assessing severity of native mitral valve regurgitation. Typically, there is loss of the systolic wave amplitude and eventually reversal of systolic flow as the Figure 24-23 (color plate.) TEE showing dehiscence in a stented mitral bioprosthesis with perivalvular regurgitation. A and C, The dehiscent site (arrows) is seen as a dropout of echoes at the annular attachment. B and D, Eccentric severe paravalvular regurgitation is seen through the dehiscence. LA, left atrium; LAA, left atrial appendage; LV, left ventricle; RA, right atrium; RV, right ventricle.

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severity of regurgitation increases from moderate to severe. These changes should not be interpreted as an absolute measure of regurgitant severity, however. In vivo models suggest that pulmonary venous flow reversal is more likely in acute versus chronic mitral regurgitation because the atrium is less compliant and has a smaller initial volume.[146] In addition, characterization of the pulmonary vein flow in prosthetic mitral regurgitation is lacking, and extrapolation of the data from native to prosthetic valves has not been documented.

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Stress Echocardiography in Assessing Prosthetic Valve Function In patients with suspected prosthetic valve dysfunction, one may encounter symptomatic patients in whom the 2D and Doppler imaging indicates normal valve function at rest. Under these circ*mstances, exercise echocardiography may elicit abnormal hemodynamics indicating valve 545

TABLE 24-9 -- Prosthetic Valve Exercise Doppler Hemodynamics No. of Patients Aortic Position CarpentierEdwards MedtronicHall MedtronicHall St. Jude Medical Mitral Position Björk-Shiley

Valve Sizes (mm)

Mean Gradient (mm Hg) * EXERCISE INCREASE † REST (%)

4 21

15 ± 3

21 ± 3

14 21

15 ± 4

24 ± 6

14 21–27

9±4

15 ± 6

17 21–27

11 ± 4

18 ± 7

11 25–31

4.9 ± 1.8

10.3 ± 2.9

100

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6 28–32

4.6 ± 12.6 ± 130 1.2 4.1 St. Jude 17 26–32 2.5 ± 5.1 ± 3.5 102 Medical 1.4 Medtronic15 26–32 3.0 ± 7.0 ± 2.9 116 Hall 1.1 Data from Tatineni et al,[147] Wiseth et al,[148] and Halbe et al.[150]

*Mean ± SD. †Exercise protocols used were symptom-limited treadmill and upright or supine bicycle.

dysfunction or patient-prosthesis mismatch. In our laboratory, we prefer supine bicycle ergometry over treadmill because serial hemodynamic data can be obtained at different exercise stages. Normal hemodynamics with stress in these patients excludes valve dysfunction as the cause of the patient's symptoms. Valve gradient, valve area, degree of regurgitation, and systolic pulmonary artery pressure can all be calculated at rest and at peak stress (or immediately afterward). Despite its clinical potential, relatively few stress echocardiographic studies in patients with suspected prosthetic valve dysfunction have been published.[61] [147] [148] [149] [150] Table 24-9 summarizes data available regarding valve gradients at rest and with exercise. Dobutamine provides an excellent alternative for evaluating valve hemodynamics when the patient is unable or unwilling to undergo treadmill exercise or bicycle ergometry.[151] In our laboratory we use a protocol similar to that for ischemic heart disease; that is, we attempt to reach at least 85%, or ideally 90%, of the maximal predicted heart rate according to the patients' age and gender. We start with IV administration of dobutamine at 10 µg/kg per minute and increase sequentially every 3 minutes to 20, 30, and 40 µg/kg per minute. If the Doppler signal intensity of tricuspid regurgitation is weak because of trivial or mild regurgitation, we routinely add a small amount of diluted Optison to enhance signal intensity, allowing calculation of systolic pulmonary artery pressure. In patients with single tilting disc prostheses in the aortic position, peak and mean gradients are higher with the dobutamine stress echocardiography compared with symptom-limited treadmill exercise.[152]

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Evaluation of the patient with decreased left ventricular systolic function and possible prosthetic aortic stenosis is problematic. In 24 adults with native aortic valve stenosis (area ≤ 0.5 cm2 /m2 ), mean gradient less than 30 mm Hg, and ventricular dysfunction (ejection fraction ≤ 0.45), deFilippi et al[153] performed echocardiography at baseline and at peak dobutamine stress to distinguish severe fixed aortic stenosis from flow-dependent (relative) aortic stenosis. Three hemodynamic subsets were identified: (1) fixed aortic stenosis with increased cardiac output and transvalvular gradient and no change in valve area; (2) relative aortic stenosis with increased valve area but no change in gradient; and (3) lack of contractile reserve with indeterminate stenosis because of inability to increase cardiac output.[153] Theoretically, a similar study may be applicable, although not yet proved, in patients with severe ventricular dysfunction and prosthetic stenosis of undetermined severity.

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Three-Dimensional Echocardiography in Assessing Prosthetic Valve Function Current echocardiographic approaches to determination of effective orifice area are based on flow characteristics. Flow characteristics, however, also depend on several factors in addition to the actual orifice area, including ventricular compliance, systolic function, and loading conditions. A classic dilemma is the patient with a mechanical aortic valve with high flow velocities detected in a routine Doppler examination. Is this a normal finding? Is it consistent with pannus formation and therefore with some stenosis? Is this a patient-prosthesis mismatch? An echocardiographic technique that actually allows us to visualize the orifice size would likely improve our diagnostic abilities. Three-dimensional echocardiography involves the acquisition and display of cardiac structures in three spatial dimensions allowing their visualization and analysis as they move in time and space. Figure 24-24 illustrates a commonly used rotational scanning mechanism in which the transducer is rotated at 3-degree increments up to 180 degrees. Dynamic 3D imaging may provide a more realistic representation of prosthetic morphology than 2D images. Recent advances in ultrasound equipment, digital storage, and display techniques have made 3D clinically feasible; however, the clinical potential of 3D imaging has just begun to be recognized, and there are no published data on the use of 3D technology in assessing prosthetic valve function. Figure 24-25 depicts a 3D reconstruction of a St. Jude Medical valve performed in our laboratory. The two hemicircular lateral orifices and the central rectangular orifice are clearly indicated. Mitral annular rings have been reconstructed with 3D 546

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Figure 24-24 Left, The rotational mechanism for acquisition of two-dimensional images at 3-degree intervals from 0 to 180 degrees. Right, The twodimensional images are piled up one after another, gated by the electrocardiogram. Figure 24-25 Three-dimensional reconstruction of a St. Judge Medical valve in the mitral position as seen from the left atrium or "surgeon's view." The semicircular orifices (curved arrows) and the rectangular orifice (straight arrow) are seen.

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technology.[153] Dall'Agata et al[154] used TEE to analyze mitral valve rings in 19 consecutive patients who underwent annuloplasty because of severe regurgitation. Fifteen patients received a Cosgrove-Edwards (flexible) ring and four received a Carpentier (rigid) ring. Imaging acquisition used the rotational technique immediately after the operation and was considered to be adequate in 17 of 19 patients. The authors were able to differentiate values from end-systolic to end-diastolic orifice areas (4.2 ± 1.5 cm2 versus 4.8 ± 1.5 cm2 ; P < .0001) in the Cosgrove-Edwards ring, and no significant change in the Carpentier ring.[154]

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Chapter 25 - Echocardiographic Recognition of Unusual Complications After Surgery on the Great Vessels and Cardiac Valves William A. Zoghbi MD

The surgical approach to treating diseases of the aorta and cardiac valves has evolved dramatically over the past two decades. Concurrent with these developments, echocardiography and particularly Doppler techniques have been refined, allowing a better definition of cardiac structures and flow dynamics. Furthermore, transesophageal echocardiography (TEE) has improved the diagnostic capabilities of sonographic techniques by providing superior imaging of the aorta and cardiac structures, thus increasing the diagnostic impact of echocardiography in patients with diseases of the aorta and cardiac valves. A variety of complications, however, may occur in patients undergoing surgery on the great vessels and cardiac valves. These complications may occur early or late in the postoperative period and include infection, thrombosis, obstruction or dehiscence of prosthetic material, and progression of the underlying disease disorder, particularly in diseases of the aorta. Recognition of diseases of the aorta and of the infectious complications and dysfunction of prosthetic valves has been addressed elsewhere in detail ( see Chapter 23 and Chapter 24 ). This chapter focuses

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on unusual complications following surgery on the aorta and cardiac valves and the role of echocardiographic techniques in assessing these complications.

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Unusual Complications Following Surgery on the Aorta Pseudoaneurysms of Composite Aortic Grafts Clinical Setting

In patients with aortic aneurysm or those with dissection of the aortic root involving the aortic sinuses and aortic valve, which are not amenable to repair, replacement of the aortic root with a composite graft is now widely accepted. [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] First reported, in 1968, by Bentall and De Bono,[1] and more recently modified since then, [5] , [6] [10] [11] [12] [13] this surgical procedure has significantly prolonged the life expectancy of patients affected with annuloaortic ectasia.[5] [9] [14] Knowledge of this procedure, its variations, and complications is crucial for the echocardiographer, particularly because echocardiography with Doppler has emerged as a powerful diagnostic modality in assessing the function and complications of composite aortic grafts. The original Bentall procedure consists of replacing the aortic root and valve with a composite aortic graft 552

(ascending aortic graft and prosthetic aortic valve). The coronary arteries are reimplanted onto the graft, and the aorta is wrapped around the graft to improve hemostasis.[1] [2] [3] [4] [15] Among the complications of composite aortic grafts is the development of a pseudoaneurysm of the ascending aorta. This pseudoaneurysm occurs secondarily to dehiscence of the suture line at the aortic annulus, the coronary ostia, or the distal graft anastomosis. In patients with composite grafts who underwent the original Bentall procedure, this potentially lethal complication was reported to occur at a rate of 7% to 25%. [3] [16] [17] [18] [19] Modifications of the original method have since been proposed to decrease the incidence of pseudoaneurysm

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formation.[2] [5] [6] [11] [12] [13] In 1981, Cabrol et al[2] modified the operation by introducing a second tube graft connecting the coronary ostia and the main ascending aortic graft (Fig. 25-1) . In 1991, Kouchoukos and co-workers[5] showed that the "open," or "button," technique for reimplantation of the coronary arteries led to a lower incidence of pseudoaneurysms. With the present modifications, the incidence of pseudoaneurysm formation has decreased to less than 6%.[5] [7] [8] [9] [12] [19] [20] [21] [22] The clinical symptoms associated with pseudoaneurysm formation vary. Whereas some patients have nonspecific symptoms or may be completely asymptomatic, other patients may be severely limited by dyspnea and fatigue. Given the possibility of aortic rupture, early diagnosis of aortic pseudoaneurysm is therefore essential. Echocardiography with Doppler and, more recently, TEE have had a significant impact on the detection of pseudoaneurysms and the evaluation of patients with composite grafts.[18] [23] [24] [25] [26] [27] [28] [29] [30]

Figure 25-1 (color plate.) Diagram of the surgical reconstruction of the aortic root in a patient with ruptured aortic dissection, using a composite aortic graft (modified Cabrol technique). The native aortic root is excised and replaced with a composite graft. A tube graft connects the aortic graft to the left main coronary artery. A vein graft (dark blue) was used in this case to bypass a stenosed right coronary artery. (Courtesy of Dr. Hazim J. Safi.) Echocardiographic and Doppler Findings

A normal composite aortic graft is visualized with echocardiography as an echo-dense ascending aortic root, with a prosthetic valve in the aortic position. The maximal diameter of the composite graft depends on the size of the graft. In 27 patients with normal composite grafts evaluated in the author's institution, the diameter of the ascending aorta ranged from 3.2 to 5 cm (mean of 4.2 cm).[18] In patients whose native aorta wrapped the graft, a small echo-free space between the graft and the wall of the aorta was seen in most patients (80%) and usually was small, ranging from 0 to 1.4 cm (mean 0.6 cm).[18] In all cases of normal composite graft, Doppler examination showed no evidence of flow in this small echo-free space and the presence of only trivial aortic insufficiency. Echocardiography can provide important diagnostic information about the presence of the pseudoaneurysm and the site of dehiscence of the surgical anastomosis.[18] [31] [32] [33] The identification of an enlarged ascending aorta with an echo-free space around the aortic graft should prompt investigation

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for the presence of a pseudoaneurysm. Other considerations include a hematoma without pseudoaneurysm or, depending on the clinical setting, the presence of graft infection with abscess formation. The space around the graft may contain varying amounts of echo-dense debris or thrombus. A pseudoaneurysm is diagnosed as an enlarged ascending aorta with an echofree space between the aortic graft and the wall of the aorta, along with the demonstration of flow into the echo-free space (Fig. 25-2) .[18] [31] [32] In a series of patients with pseudoaneurysms diagnosed in the author's institution, [18] 553

Figure 25-2 (color plate.) Echocardiographic and Doppler findings using transthoracic echocardiography in a patient with a large pseudoaneurysm of the ascending aorta complicating a composite graft. The dehiscence was at the aortic annulus anastomosis. A and C show the extent of the pseudoaneurysm as delineated by the arrows in short-axis (A) and long-axis (C) views. The origin and extent of the systolic jet into the pseudoaneurysm are shown in B and D in the same image planes as in A and C. During diastole (E), blood converges from the pseudoaneurysm toward the aortic annulus and enters the left ventricle (arrow) through the dehiscence, mimicking aortic insufficiency. The corresponding angiographic findings are shown in Figure 25-9 . GR, aortic graft; LA, left atrium; LV, left ventricle; PSA, pseudoaneurysm. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

the maximal diameter of the ascending aorta ranged from 6 to 14 cm. The maximal echo-free space between the aortic graft and the wall of the ascending aorta ranged from 2 to 7 cm. This space may be eccentric or concentric around the graft. Although most cases of pseudoaneurysms report more than 2 cm of echo-free space surrounding the graft, the demonstration of flow into the space outside the graft is essential for the diagnosis, irrespective of the size of the echo-free space. Once a pseudoaneurysm is suspected, special attention is directed to imaging the ascending aorta, aortic root, the plane of the prosthetic valve, and the coronary ostia from the left and right parasternal and suprasternal windows. In cases of pseudoaneurysms, color-flow Doppler imaging frequently demonstrates evidence of a pulsatile flow jet into the echo-free space between the graft and the wall of the ascending aorta (see Fig. 2) . This finding confirms the entity of pseudoaneurysm, as opposed to the mere presence of blood or fluid collected around the graft (Fig. 25-3) . In

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the author's experience, however, transthoracic color-flow examination may not identify flow in the echo-free space in some patients. In these cases, transesophageal examination clearly demonstrates flow into the pseudoaneurysm (Fig. 25-4) . This limitation is the result of the lower resolution and sensitivity of surface echocardiography combined with posterior shadowing from the graft and aortic prosthesis. Transthoracic and transesophageal echocardiography do provide complementary information regarding the status of a composite aortic graft. If any suspicion arises about the presence of a pseudoaneurysm, a TEE is clearly indicated for further evaluation of the abnormality. Following is a description of Doppler echocardiographic findings observed with composite graft pseudoaneurysms.

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Figure 25-3 Transesophageal horizontal plane demonstrating a large hematoma (arrows) surrounding a composite aortic graft (G) in a patient early after operation. There was no flow detected around the graft by Doppler echocardiography at any level. Th, Thrombus. The hematoma was secondary to postoperative bleeding complications. Aortic Annulus Dehiscence

In cases of dehiscence at the aortic annulus anastomosis, with ensuing communication between the left ventricle and the pseudoaneurysm, colorflow Doppler identifies a systolic jet arising from the paraprosthetic valve area, directed cranially into the pseudoaneurysm ( see Fig. 25-2 and Fig. 25-4 ). Because the jet frequently is eccentric, the imaging plane showing the flow jet in the long axis of the aortic root usually is lateral or medial to the plane showing the aortic graft. Thus, the flow jet and aortic graft may not be seen in the same longitudinal plane (see Fig. 25-2) . The short-axis view at the level of the prosthetic aortic valve demonstrates the jet arising in the Figure 25-4 (color plate.) Transesophageal echocardiographic frames and corresponding color Doppler systolic frames in a patient with composite graft pseudoaneurysm. The transthoracic examination in this patient did not demonstrate flow in the pseudoaneurysm. The upper panels are at the level of the ascending aorta; the lower panels are at the prosthetic aortic valve level. The dehiscence at the aortic annulus is depicted by a

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straight arrow. Color flow Doppler demonstrates flow into the pseudoaneurysm. GR, aortic graft; LA, left atrium; LV, left ventricle; PrV, prosthetic valve; PSA, pseudoaneurysm. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

paravalvular area and oriented into the pseudoaneurysm. Short-axis views from a more cranial angle demonstrate the orientation of the jet in the pseudoaneurysm in relation to the aortic graft. These considerations apply for both transthoracic and TEE imaging ( see Fig. 25-2 and Fig. 25-4 ). Generally, detection of the dehiscence and flow into the pseudoaneurysm is much easier with TEE than with the transthoracic approach. In most cases of dehiscence at the aortic annulus, continuous-wave Doppler views from the apical window demonstrate two distinct systolic jets: one coursing through the prosthetic valve and another coursing through the left ventricular-pseudoaneurysm communication (Fig. 25-5) . In the author's experience, the maximal velocity and derived pressure gradient through the communication have been higher than those through the prosthesis.[18] The systolic jet through the dehiscence frequently starts before the opening click of the prosthetic valve, and its duration is usually longer than the ejection time through the valve (see Fig. 25-5) . In all cases of dehiscence of the aortic annulus, a diastolic jet is seen in the left ventricular outflow, simulating valvular aortic insufficiency. In these cases, concomitant aortic insufficiency arising from within the valve usually cannot be excluded with confidence; however, with TEE, the mechanism of regurgitation can be much better defined. Continuous-wave Doppler recording of these diastolic jets also shows a short pressure half-time, mimicking severe aortic insufficiency. In some cases, an abrupt termination of diastolic flow before the prosthetic aortic-valve click at the onset of early systolic flow through the communication supports the conclusion that this regurgitation is not occurring through the aortic valve (see Fig. 25-5) . Coronary Artery Dehiscence

Coronary artery dehiscence is diagnosed by color-flow Doppler as a jet arising from the level of the coronary ostia or coronary anastomosis and directed into the pseudoaneurysm. Dehiscence 555

Figure 25-5 Continuous wave Doppler from the apical window of the

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patient with aortic annulus dehiscence shown in Figure 25-2 . Recordings are obtained from the same position on the chest wall, with minor change in angulation. Compared with the systolic jet velocity through the prosthetic aortic valve, the systolic jet through the ventricular-pseudoaneurysm communication has a higher maximal velocity (Vmax), is of longer duration, and starts (oblique arrow) before the first click of the prosthetic valve (horizontal arrow). The diastolic regurgitant jet into the left ventricle has a steep deceleration slope and ends before the first systolic aortic valve click (upper panel, straight arrow) at the time of onset of systolic flow into the pseudoaneurysm. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

usually is easier to define in patients in whom the pseudoaneurysm is large because of the more defined spatial distribution of the jet. Various flow patterns may be recorded, as shown in Figure 25-6 . Whether the flow is predominantly systolic into the pseudoaneurysm or systolic and diastolic depends on factors such as the compliance of the pseudoaneurysm and whether a communication exists between the pseudoaneurysm and the left ventricle. Compression of the Composite Graft or Adjacent Structures

Compression of the graft may result from hematoma or pseudoaneurysm formation[27] and is most commonly observed with aortic annulus dehiscence. With two-dimensional echocardiography, pulsatile compression of the graft can be seen during systole (Fig. 25-7) , most likely because of the high pressure surrounding the graft and possibly a Venturi phenomenon occurring within the graft. Using continuous-wave Doppler, a high-velocity systolic jet can be recorded, a finding similar to that seen in an obstructed prosthetic aortic valve. Differentiation of the two entities may be difficult; however, visualization of the pulsatile compression of the graft provides a good assessment of the underlying condition. If the pseudoaneurysm is extensive, it may compress adjacent structures. Compression of the pulmonary artery with resultant pulmonary arterial stenosis was recently reported as a complication of a large pseudoaneurysm.[33] Role of Transesophageal Echocardiography

The use of TEE clearly is advantageous in the overall definition of complications of composite aortic grafts.[18] , [27] [30] [31] [32] [33] [34] For delineation of pseudoaneurysms, the aortic suture ring is clearly visualized with TEE, thereby enhancing the evaluation of dehiscence at this level with both echocardiography and Doppler techniques. Furthermore, the

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anastomosis of the coronary arteries to the aortic graft is better assessed. Evaluation of flow in the potential space between the graft and native wrapped aorta or fibrous tissue (in the case of excision of the native aorta) is improved. Dehiscence at the distal anastomosis of the aortic graft to the aortic arch remains difficult to assess because of limitations of imaging in this area; however, this type of dehiscence is the least frequent and rarely occurs alone. In cases of pseudoaneurysm formation secondary to endocarditis, TEE may detect vegetations that can further substantiate the diagnosis (Fig. 25-8) . In the absence of such a finding, however, exclusion of an infected graft based on echocardiographic examination, or based on any structural imaging alone, is difficult. Because of anterior 556

Figure 25-6 (color plate.) Examples of different velocity patterns observed by continuous wave Doppler in two patients with coronary artery dehiscence. In A, the color jet arising from the left main dehiscence is depicted in the parasternal long- (A1 ) and short- (A2 ) axes by a large arrow. In this patient with concomitant aortic annulus dehiscence, continuous wave Doppler (A3 ) shows increased systolic and diastolic velocities directed from the graft into the pseudoaneurysm. The patient in B has a sole dehiscence at the right coronary anastomosis depicted in short axis (B1 and B2 ). Continuous wave Doppler recording (B3 ) shows flow directed from the graft into the pseudoaneurysm in systole and flow reversal from the pseudoaneurysm into the graft in diastole (small arrows). GR, graft; LV, left ventricle; PA, pulmonary artery; PSA, pseudoaneurysm; RV, right ventricle. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

shadowing produced from the prosthetic valve and graft, an optimum assessment of the aortic root in composite grafts involves combined transthoracic and transesophageal studies. In cases of suspected pseudoaneurysm formation in which a collection of blood and thrombus is seen around the graft, and without demonstration of flow by transthoracic echocardiography or other imaging modalities, a transesophageal study is crucial in providing the diagnosis.[18] Other Imaging Modalities

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Several modalities have been suggested as diagnostic screens for the development of pseudoaneurysm after Figure 25-7 Right parasternal transthoracic echocardiographic images of composite graft pseudoaneurysm demonstrating systolic compression of the graft by the pseudoaneurysm. Gr, graft; PSA, pseudoaneurysm.

composite graft surgery, including chest radiography, computed tomography (CT), digital subtraction angiography, and more recently, magnetic resonance imaging (MRI).[3] [17] [35] , [36] Although chest radiography may warn of the possibility, its sensitivity and specificity for the diagnosis of pseudoaneurysm are poor. Computed tomography and MRI are currently recommended as diagnostic imaging modalities for the serial evaluation of composite grafts and progression of the underlying disease to other segments of the aorta. [10] As for diagnosing pseudoaneurysm, although CT scanning or MRI can provide the diagnosis of blood or fluid collection around the graft, whether this finding represents a mere collection of fluid around the graft or is the result of communication with the ventricle, coronary arteries, or aorta may not be adequately differentiated. Until recently, aortography was the most widely used method for diagnosis of pseudoaneurysms and was the primary diagnostic modality for further evaluation of fluid collection around the composite graft.[36] Aortography still is an excellent modality for diagnosing dehiscence of the composite graft at the coronary artery anastomosis and distal graft (Fig. 25-9) ; however, in cases of isolated dehiscence of the graft at the aortic annulus anastomosis, aortography has been found to completely miss the diagnosis of pseudoaneurysm.[18] [27] This is explained by the fact that in these cases, the pseudoaneurysm communicates only with the left ventricle; a contrast injection in the aortic root would therefore not opacify the left ventricle or the pseudoaneurysm. An example of such a case is 557

Figure 25-8 (color plate.) Transesophageal echocardiographic frames (left) and corresponding color Doppler systolic frames (right) in a patient with endocarditis and composite graft pseudoaneurysm secondary to aortic annulus dehiscence. The upper panels are at the level of the prosthetic valve; the lower panels are at the level of the left main coronary artery. Two large vegetations are depicted (top, arrows) near the site of dehiscence.

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Systolic flow into the pseudoaneurysm is shown, and the limits of the pseudoaneurysm are indicated (bottom, arrows). Gr, graft; LA, left atrium; LVO, left ventricular outflow; P, pseudoaneurysm; RV, right ventricle; Veg, vegetations. Figure 25-9 Aortograms of the thoracic aorta in two patients with pseudoaneurysm complicating composite aortic graft. A, The pseudoaneurysm around the ascending graft is opacified (arrows). B, Aortogram of the patient whose echocardiographic images are in Figure 252 . In this case with single aortic annulus dehiscence, the large pseudoaneurysm is not opacified. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

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presented in Figure 25-2 and Figure 25-9 . Echocardiography in these cases is superior to aortography in the detection of pseudoaneurysms. Because in most of these cases the prosthetic aortic valve is not crossed at catheterization, opacification of the pseudoaneurysm necessitates a left ventriculogram using the transseptal technique or the levo phase of a pulmonary angiogram. In cases with concomitant dehiscence at the coronary or distal graft anastomoses, or in those with coexisting aortic insufficiency, the pseudoaneurysm may be opacified with aortography. [18] Complications of Aortic Allografts for Replacement of the Aortic Valve and Aortic Root Clinical Setting

Allograft or hom*ograft replacement of the aortic root also has provided an effective therapy for diseases of the aortic root and the aortic valve. [37] [38] [39] [40] Three general techniques for insertion have been used: subcoronary valve implantation, a mini- or inclusion-root implantation, and an aorticroot replacement. Compared with composite graft replacement of the aortic root, the use of an allograft is particularly helpful in recurrent complications of the aortic root, especially in the presence of infection. Aortic allografts, therefore, have been performed predominantly in patients with destruction of the aortic root resulting from endocarditis, in patients with congenitally narrowed or hypoplastic aortic roots, in patients with complications involving previous root replacement such as heavy calcifications, and in those for whom anticoagulation is contraindicated.

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Among the most commonly reported complications of aortic allografts are calcifications of the root, aortic regurgitation, and infectious complications occurring primarily in patients whose underlying indication for aortic root replacement was endocarditis. Similar to composite aortic grafts, reports of unusual complications include problems with anastomotic sites (dehiscence with pseudoaneurysm formation), problems with coronary artery anastomosis, and possible compression of the graft. [38] [40] [41] [42] Figure 25-10 (color plate.) Transesophageal echocardiographic findings in a patient with systolic compression of aortic hom*ograft secondary to dehiscence at the aortic annulus anastomosis. The upper panels display the dynamic compression of the hom*ograft in short axis. Color M-mode echocardiography at the same level shows the systolic compression of the graft (white arrows) and systolic flow in both the pseudoaneurysm (above the arrows) and the hom*ograft. Continuous wave Doppler recording from the transgastric view depicts the high gradient through the obstruction. The aortic valve was normal. Gr, gradient; H, aortic hom*ograft; LA, left atrium; RV, right ventricle. (From Nagueh SF, Bozkurt B, Li GA, et al: Am Heart J 1996;132(5):1070–1073, with permission.) Echocardiographic and Doppler Findings

Data are scarce on the echocardiographic findings in aortic root allografts. [42] [43] A normal aortic root allograft, especially early after surgery, may be difficult to differentiate from a native aortic root. Late after surgery, however, calcifications of the hom*ograft are common and are detected by echocardiography as increased echogenicity in the aortic root. If leaflet degeneration occurs, varying degrees of aortic insufficiency, with or without aortic stenosis, may be present. In a recent study, paravalvular aortic insufficiency and eccentric jets were more common in patients with subcoronary aortic allograft implantation (41%) than in those with root replacement (11%).[43] Some unusual complications may affect the allograft, but these complications have occurred early in the postoperative period and can be detected with intraoperative TEE. Recently, cases have been reported with complications related to anastomosis of the coronary arteries with the allograft.[41] Aliasing by color flow was detected along with ischemia in the distribution of the involved anastomosis (left main or right coronary artery). Other reported complications included dehiscence of the hom*ograft with resultant pseudoaneurysm formation. Compression of the graft by the pseudoaneurysm may occur, simulating valve stenosis (Fig. 2510) .[42] With more extensive experience in cardiac imaging of these patients, the spectrum of complications and the role of echocardiography and other imaging modalities in patients undergoing aortic allograft surgery

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will be better defined. Replacement of the Aorta with an "Elephant-Trunk" Procedure In patients with extensive aortic aneurysmal disease or in dissection involving the ascending aorta, arch, and descending aorta, replacement of the aortic arch and varied lengths of the aorta can be a major undertaking. In 1983, Borst et al[44] described a dual-stage technique whereby the ascending aorta and arch are replaced first, leaving a segment of the distal tubular graft in the descending 559

Figure 25-11 (color plate.) Transesophageal imaging of the descending aorta (Desc Ao) (longitudinal plane) in a patient with aortic aneurysm involving the arch and descending aorta following a successful first stage of an "elephant trunk" procedure. The free distal end of the tubular graft is seen in the descending thoracic aneurysm. Color flow Doppler shows flow into the descending aorta arising from the distal end of the graft (Gr).

thoracic aorta. Borst coined the name "elephant-trunk" technique for this procedure. [44] At a second stage, the distal aorta is repaired beyond the subclavian artery. Since its original description, few modifications have been applied to the technique.[6] [45] [46] After the first stage of the operation, TEE imaging of the descending aorta shows the free position of the distal tubular graft in the descending aneurysm, with blood flow detected in the graft emptying into the aneurysm (Fig. 25-11) . This finding at this stage is normal and should not be mistaken for dehiscence of the graft. Following a successful first stage of the procedure, the most serious and usually fatal complication is rupture of the remaining descending thoracic aneurysm while awaiting the second stage of the surgery. The author has observed an unusual interim complication of severe hemolytic anemia following the first stage, which resolved after the second stage of the repair. The intravascular hemolysis was caused by insertion of the distal graft into the false lumen during the first operation. Because insertion of the graft into the descending aorta during the first stage is performed blind, some surgeons in the author's institution currently use intraoperative TEE to assess the position of the inserted graft in the descending aorta. Other Complications Progression of aortic disease with further aneurysm formation or dissection

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in additional segments of the aorta is the most common cause for reoperating on patients with diseases of the aorta.[19] [47] [48] [49] Monitoring the progression of aortic disease after the initial surgery affects prognosis and is crucial in the overall management of these patients. In addition to the complications mentioned earlier, rupture of the great vessels with fistula formation, although infrequent, can occur as a complication of aortic dissection or aneurysm. Communication between the aorta and pulmonary artery is clinically suspected by the findings of a continuous murmur, similar to patent ductus arteriosus or the presence of heart failure. Echocardiographic findings depend on the size of the shunt and may include volume overload of the left ventricle and elevated pulmonary pressures. Doppler echocardiographic findings are those of continuous flow into the pulmonary artery from the aorta.

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Unusual Complications Following Valve Surgery Left Ventricular Pseudoaneurysm After Mitral Valve Replacement Clinical Setting

Rupture of the left ventricle with pseudoaneurysm formation is a rare but serious complication following mitral valve replacement. Overall, the incidence appears to range from 0.5% to 2% in isolated or combined mitral valve procedures. [50] [51] [52] [53] [54] Rupture of the left ventricle may occur immediately after surgery, presenting with hemodynamic collapse, or may present in the delayed postoperative period as a false aneurysm of the left ventricle. Anatomic characteristics and other factors have been described as predisposing to rupture of the ventricle such as heavy mitral or annular calcifications, the operative procedure itself, the number of surgical procedures previously undergone, or other hemodynamic considerations; however, often no clear cause for the pseudoaneurysm formation can be found.[55] The clinical presentation of pseudoaneurysm formation is variable. In the early postoperative period, it can present as poor postoperative progress, chest pain, heart failure, or as the development of a new murmur.[51] [52] [56] Late postoperative presentation may be similar or may be totally asymptomatic. In unusual cases, the pseudoaneurysm can compress the coronary arteries, leading to ischemia or myocardial hibernation.[57] Echocardiographic and Doppler Findings

Echocardiographic techniques play a significant role in the diagnosis of left ventricular pseudoaneurysm.[58] [59] A pseudoaneurysm, in contrast to a true aneurysm, is visualized as a saccular or globular chamber communicating with the left ventricle through a narrow and abrupt discontinuity in the ventricular myocardium. Over the past few years, the important role of Doppler echocardiography in the diagnosis of pseudoaneurysms has been increasingly appreciated. The demonstration of flow into the

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pseudoaneurysm by pulsed- and color-flow Doppler substantiates the diagnosis and may at times be the only clue for its presence in cases where the origin of the pseudoaneurysm cannot be visualized.[60] [61] [62] Doppler echocardiography is crucial in differentiating a pseudoaneurysm from other entities such as pericardial cysts, loculated pericardial effusion, or hematoma, especially in cases in which communication of the cavity with the left ventricle is not seen. As with true left ventricular aneurysm, a pseudoaneurysm demonstrates akinesis or dyskinesis during ventricular systole. Characteristic Doppler patterns can be seen with systolic filling and diastolic emptying of the pseudoaneurysm.[63] In patients with sinus rhythm, filling of the pseudoaneurysm during atrial contraction 560

can also be seen. With the availability of intravenous contrast echo agents that can cross the pulmonary circulation,[64] the administration of contrast can be of important diagnostic value in these situations by identifying whether such a communication exists with the left ventricle and by localizing its site. The use of contrast is particularly helpful when the communication with the ventricle is rather large and blood velocity in the cavity is too low to be clearly detected with Doppler. The location of the pseudoaneurysm can vary in relation to the prosthetic valve. Transthoracic echocardiography can demonstrate its presence and characteristic features; however, because of technical difficulties and imaging in the far field, the pseudoaneurysm may be frequently missed with the transthoracic approach. TEE is currently the echocardiographic method of choice in evaluating patients with suspected left ventricular pseudoaneurysm complicating mitral valve replacement.[63] [65] [66] [67] An example of a pseudoaneurysm complicating mitral valve replacement demonstrated by TEE and missed by transthoracic imaging is shown in Figure 25-12 . Other Imaging Modalities

Nonsurgical detection of pseudoaneurysm previously has depended on left ventriculography. Angiography is still important in the diagnosis of pseudoaneurysms in patients in whom the transthoracic examination may be difficult and also provides a spatial distribution of the Figure 25-12 (color plate.) Transverse transesophageal

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echocardiography planes at four levels (A to D) are shown along with contrast left ventriculography in the right oblique view, demonstrating opacification of a left ventricular pseudoaneurysm complicating mitral valve replacement. The approximate locations of the transverse echo planes are schematically shown on the angiogram. A1 and A2 show the maximal extent of the pseudoaneurysm and respective color flow demonstrating flow in the cavity. B and C show the neck of the pseudoaneurysm by color Doppler and its proximity and impingement on the proximal circumflex artery (C, arrows). The most caudal plane (D) is at the level of the prosthetic valve (PrV), which is normal. Ao, aorta; LA, left atrium; LV, left ventricle; PsAN, pseudoaneurysm; RV, right ventricle. (From Baker WB, Klein MS, Zoghbi WA: J Am Soc Echocardiogr 1993;6:548–552.)

pseudoaneurysm (see Fig. 25-12) ; however, because of its tomographic nature, TEE can further add to left ventricular angiography in pinpointing the site of origin of the pseudoaneurysm and its relation to adjacent structures for later surgical correction. The intraoperative use of TEE in surgical repair of these lesions can also be crucial when the repair involves areas close to the coronaries, in the assessment of ventricular function immediately postoperatively, and to indirectly detect whether injury occurred in the area of the coronary vessels with the evaluation of regional myocardial function.[63] It is generally agreed that management of patients with pseudoaneurysm formation of the left ventricle necessitates surgical intervention because of the risk of rupture and potential sudden death. Although surgical correction has been carried out almost uniformly in highrisk patients, some authors have advocated continued TEE follow-up in asymptomatic patients.[67] Left Atrial Dissection after Mitral Valve Replacement Clinical Setting

Dissection of the left atrium with resultant pseudoaneurysm formation is a rare complication of mitral valve replacement.[68] [69] [70] [71] [72] Predisposing factors for this unusual complication are similar to those for left ventricular pseudoaneurysms and include mitral annulus calcifications, 561

Figure 25-13 Dissection of the left atrium demonstrated with intraoperative transesophageal echocardiography after mitral valve surgery. A, horizontal view; B, 73-degree view. Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle. (From Genoni M, Jenni R, Schmid ER, et al: Ann Thorac Surg 1999;68:1394–1396.)

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external cardiac massage, friable atrial wall tissue, preexisting pericardial adhesions, and technical considerations during surgery. Clinical presentation varies from detection in the operating room with TEE, to the presence of a systolic murmur of mitral regurgitation, heart failure, or an asymptomatic state. Surgical correction is recommended for symptomatic cases or those with severe left atrial compression. Spontaneous healing has been reported in only one case.[70] Internal drainage of the false lumen into the right atrium has been recently proposed in cases where the dehiscence at the mitral annulus is small.[71] Echocardiographic and Doppler Findings

On echocardiography, a cavity formation is seen within the left atrium, with a linear echo density consisting of the dissection of the atrial wall. This is best delineated with TEE (Fig. 25-13) .[71] [72] Paraprosthetic valve regurgitation is usually seen, with flow by Doppler entering into the false lumen through the communication.[72] Recording of the jet with continuouswave Doppler provides various degrees of velocity and duration of flow, depending on the size of the communication, and compliance of the false lumen. Pseudoaneurysm of the Ascending Aorta After Aortic Valve Replacement Clinical Setting

False aneurysm of the ascending aorta is a rare but serious complication of aortic valve replacement. Potential factors contributing to this complication include leaking aortotomy suture lines, needle punctures for air-evacuation procedures after surgery, postoperative endocarditis, or friability of the aortic wall.[73] [74] [75] [76] Clinical presentation is variable, including an asymptomatic, incidental finding on chest radiography or echocardiography, symptoms of atypical chest discomfort or dyspnea, and the finding of a continuous murmur because of fistula formation with adjacent cardiac chambers.[73] [74] [75] [76] Surgical repair generally is recommended because these pseudoaneurysms have a high propensity for rupture. Echocardiographic and Doppler Findings

Echocardiography shows a typical pseudoaneurysmal cavity arising from the ascending aorta in the vicinity of the prosthetic aortic valve. Usually the aorta is of normal size, and the neck of the pseudoaneurysm is small and

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may be difficult to appreciate on transthoracic echocardiography. TEE enhances imaging and definition of the pseudoaneurysm, which could be lined with thrombus. Color Doppler identifies flow into the cavity in systole, emptying in diastole (Fig. 25-14) . In a typical aortic pseudoaneurysm, there is no associated aortic insufficiency or flow in the cavity. In case of further complications of the pseudoaneurysm, however, continuous flow can be detected at the site of rupture into the right atrium or right ventricle.[75] [76] Similar to other pseudoaneurysms of the aorta, aortography, CT, or MRI also can delineate the pseudoaneurysm 562

Figure 25-14 (color plate.) Echocardiographic and Doppler images of an aortic pseudoaneurysm obtained with transesophageal echocardiography in the 30-degree and 90-degree planes. Flow is seen entering the pseudoaneurysm in systole and emptying in diastole. The corresponding aortogram delineates the extent of the pseudoaneurysm. Ao, aorta; An, pseudoaneurysm; LA, left atrium.

(see Fig. 25-14) . In these cases, Doppler echocardiography and aortography can aid surgical correction by more accurately pinpointing the site of rupture and flow into the pseudoaneurysm. Pseudoaneurysm of the Mitral-Aortic Intervalvular Fibrosa Clinical Setting

The region of the mitral-aortic continuity or mitral-aortic intervalvular fibrosa (MAIVF) contains mostly fibrous, relatively avascular tissue. Because of its composition, the MAIVF is the weakest segment of the aortic ring,[77] is prone to infection, and is more sensitive to trauma. The roof of the MAIVF is formed of pericardium, and its ventricular side is the posterior portion of the left ventricular outflow tract. Dehiscence in the MAIVF region, secondary to infection, trauma, or even surgical manipulation may result in the formation of an abscess or a pouch between the medial wall of the left atrium and the aorta. An intervalvular pseudoaneurysm ensues when the abscess or pouch communicates with the left ventricular outflow tract.[78] [79] [80] [81] An example of an MAIVF pseudoaneurysm is shown in Figure 25-15 . Most pseudoaneurysms in the MAIVF region occur secondarily to infection and are more common in

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patients with prosthetic valves.[82] Other causes include trauma, surgical trauma, and congenital pseudoaneurysms.[82] [83] [84] Detecting these pseudoaneurysms is important because of their potential complications, which may include rupture into the left atrium or aorta, resulting in mitral or aortic regurgitation, respectively, or even rupture into the pericardial space, with ensuing cardiac tamponade and death.[78] [81] [83] Determining the incidence of MAIVF pseudoaneurysms is difficult. Prior to the use of TEE, the few reports available surfaced at pathology or during angiography. With the advent of TEE, the most sensitive technique for evaluating these lesions, MAIVF pseudoaneurysms were detected in 9% of patients undergoing TEE for suspected aortic valve or ring disease.[82] The clinical presentation varies but is most commonly that of endocarditis, congestive heart failure, valvular regurgitation, or it may be asymptomatic, without a history of endocarditis. Because the pseudoaneurysm is located between the left atrium and aorta, and its origin is in the left ventricular outflow, it is not readily identified at surgery and may be missed. Thus, accurate detection, delineation, and differentiation of MAIVF pseudoaneurysms from ring abscesses is important in overall patient management and in the guidance of surgical correction. Echocardiographic and Doppler Findings

Transthoracic echocardiography has been used for the diagnosis of aortic root complications.[85] [86] Its sensitivity, however, recently has been shown to be limited in the evaluation of posterior lesions, particularly in the presence of prosthetic aortic valves; by contrast TEE substantially improves the diagnosis of such lesions.[87] [88] In a series from the author's institution, transthoracic echocardiography detected 43% of a total of 23 lesions affecting the aortic root, whereas TEE identified 90% of the lesions.[82] The importance of the transthoracic approach in detecting anterior ring abscesses cannot be ignored, however, particularly in the presence of prosthetic aortic valves, where TEE may have significant limitations because of shadowing of the prosthesis in the region of the anterior aortic ring. Combining transthoracic and transesophageal imaging, therefore, would allow a comprehensive evaluation of the aortic root and is strongly recommended. In contrast to aortic ring abscesses, intervalvular pseudoaneurysms exhibit a characteristic dynamic feature during the cardiac cycle. Marked pulsatility is observed in most MAIVF pseudoaneurysms, with expansion during early systole and collapse in diastole (see Fig. 25-15) . [82] This

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feature is explained by the fact that the pressure in the pseudoaneurysm reflects left ventricular pressure and 563

that a large portion of the pseudoaneurysm is surrounded by the left atrium. Thus, when left atrial pressure exceeds left ventricular pressure in diastole, the pseudoaneurysm collapses, whereas it expands in systole. This dynamic behavior during the echocardiographic examination is indeed the first clue to the presence of an MAIVF pseudoaneurysm. In contrast, aortic ring abscesses located anteriorly or posteriorly in the aortic root do not exhibit this marked pulsatility, which may be explained by several factors. In walled-off abscesses without detectable flow, pulsatility is not expected. In ring abscesses with systolic and diastolic flow owing to paraprosthetic aortic regurgitation, the pressure remains high throughout the cardiac cycle in these cavities compared with adjacent chambers so that pulsatility is not seen. Although collapsibility provides indirect evidence for the presence of an MAIVF pseudoaneurysm, confirmation of this diagnosis requires visualization of the neck of the pseudoaneurysm in the left ventricular outflow. This communication rarely can be seen by transthoracic echocardiography[82] however, it is usually well visualized with the transesophageal approach. In the author's experience, the size of the neck has ranged from 0.5 to 2.1 cm in diameter. In cases where there is still doubt about whether the cavity communicates with the aorta or left ventricle, the administration Figure 25-15 (See also color plate.) Echocardiographic and color Doppler frames from the transverse plane during transesophageal echocardiography showing a typical simple mitral-aortic intervalvular fibrosa pseudoaneurysm with its location, pulsatility, and flow patterns during the cardiac cycle. Top, Pseudoaneurysm (straight arrow) and communication with the left ventricular outflow (curved arrow) are shown. The pseudoaneurysm begins to expand during early systole, remains distended in late systole, and collapses during diastole. Bottom, Magnified color Doppler views of the area within the box seen in the top middle panel. During early systole, the pseudoaneurysm fills, showing high, aliased velocities. Low, nonaliased velocities are seen during the remainder of systole while the pseudoaneurysm remains expanded (middle). During diastole, the pseudoaneurysm empties and collapses. LA, left atrium; LV, left ventricle.

of intravenous contrast agents that cross the pulmonary circulation can help resolve this issue.

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Color Doppler imaging is crucial in the evaluation of MAIVF pseudoaneurysms. Its application helps to assess whether rupture of this cavity into adjacent chambers has occurred and define its communication. The following are characteristic Doppler features in unruptured and ruptured MAIVF pseudoaneurysms. In the case of unruptured pseudoaneurysms, Doppler evaluation usually is less impressive. Only a brief duration of flow into the pseudoaneurysm occurs during early systole (20–60 msec), at which time pressure between the pseudoaneurysm and left ventricle is equalized, and no further flow is detected by Doppler (see Fig. 25-15) .[82] During diastole, a brief period of flow exiting from the pseudoaneurysm may be seen but frequently can be missed because of its low velocity. In contrast, in pseudoaneurysms that have ruptured, into either the left atrium or aorta, an intense color-flow signal can be seen during the cardiac cycle. In cases of rupture into the left atrium, color Doppler shows holosystolic, intense flow signal in the pseudoaneurysm and eccentric "mitral" regurgitation through the perforation of the pseudoaneurysm, the latter acting as a conduit for blood flow from the left ventricle to the left atrium (Fig. 25-16) . The use of color Doppler actually facilitates 564

Figure 25-16 (See also color plate.) Two-dimensional and color flow transesophageal echocardiography images of a complicated mitralaortic intervalvular fibrosa pseudoaneurysm with rupture into the left atrium in the setting of endocarditis after mitral valve annuloplasty and aortic valve replacement. The pseudoaneurysm (slender arrow) and its neck (large arrow) are shown. The pseudoaneurysm is septate, has mobile vegetations, and expands significantly in systole. An intense color flow jet in systole is seen through the pseudoaneurysm with subsequent, eccentric regurgitation into the left atrium. Ao, aorta; LA, left atrium; LV, left ventricle.

the identification of the rupture site of the pseudoaneurysm by tracking the origin of the regurgitant jet. The ruptured site is rarely seen by transthoracic echocardiography but can be suspected by the presence of eccentric mitral regurgitation arising close to the aortic root. Similar to unruptured pseudoaneurysms, those pseudoaneurysms communicating with the left atrium show systolic expansion and diastolic collapse (see Fig. 25-16) . In cases where rupture of the pseudoaneurysm occurs into the aorta, with or without concomitant dehiscence of the prosthetic aortic valve, aortic insufficiency is detected (Fig. 25-17) . In systole, color Doppler shows

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antegrade flow from the ventricle through both the pseudoaneurysm and the prosthetic aortic valve. In diastole, retrograde flow of "aortic" insufficiency is seen, directed from the aortic root into the pseudoaneurysm and into the ventricle. Other Imaging Modalities

Until recently, cineangiography has been the standard for diagnosing aortic root lesions.[89] With the advent of echocardiography with Doppler, and more recently TEE, however, these techniques have rivaled the invasive diagnostic modality. Few cases of MAIVF pseudoaneurysms have been described with angiography.[80] [90] [91] The pulsatility described earlier is also seen on angiography (Fig. 25-18) . In a case series in which patients underwent both diagnostic modalities, MAIVF pseudoaneurysms were more frequently detected by TEE than by aortography.[82] Only 2 of 9 pseudoaneurysms were identified by aortography, both of which had associated aortic insufficiency (Fig. 25-19) . The direct communication between the left ventricular outflow tract and pseudoaneurysm explains the need for a ventricular injection of dye to detect this abnormality. This finding is similar to that described earlier for pseudoaneurysms of composite aortic grafts with a single dehiscence at the aortic annulus anastomosis. Thus, in patients without aortic insufficiency, demonstration of the pseudoaneurysm with angiography requires left ventriculography. Compared with angiography, TEE more clearly delineates the origin of the intervalvular pseudoaneurysms and their communication elucidating 565

Figure 25-17 (See also color plate.) Two-dimensional and color Doppler frames during omniplane transesophageal examination at an angulation of 120 degrees, showing a ruptured mitral-aortic intervalvular fibrosa pseudoaneurysm into the aorta. During systole, blood flows into the pseudoaneurysm and from the pseudoaneurysm into the aorta through small fenestrations (white arrow). Normal flow direction through the prosthesis (black arrow) is also shown. During diastole, blood regurgitates into the left ventricle through the pseudoaneurysm (black arrows). An, pseudoaneurysm; Ao, aorta; LA, left atrium; LV, left ventricle; PrV, prosthetic aortic valve. (From Afridi I, Apostolidou MA, Saad RM, et al: J Am Coll Cardiol 1995;25:137–145. Reproduced with permission from the American College of Cardiology.)

the origin of concomitant mitral regurgitation or aortic insufficiency and, therefore, assisting in planning surgical repair.[82]

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Patients with cavitary lesions complicating aortic valve disease, particularly prosthetic valves, require extensive surgical intervention, including in some cases aortic root replacement. Because of the risk of rupture into the pericardium, surgical correction of MAIVF pseudoaneurysm is warranted in most cases. Although the natural history of uncomplicated pseudoaneurysm is unclear, surgical repair was performed in the majority of cases reported. In patients who do not undergo an immediate operation, TEE may be useful in identifying serial changes in the pseudoaneurysm or the development of a rupture into adjacent chambers, which can help plan appropriate therapy. Intracardiac Fistula following Valve Replacement Clinical Setting

Intracardiac fistula formation is an uncommon complication following valve replacement surgery. Several types of fistulae may occur following mitral valve replacement, Figure 25-18 Left anterior oblique view during aortography in a patient with mitral-aortic intervalvular fibrosa (MAIVF) pseudoaneurysm and aortic insufficiency. The MAIVF pseudoaneurysm (arrows) shows pulsatility during the cardiac cycle. (From Afridi I, Apostolidou MA, Saad RM, et al: J Am Coll Cardiol 1995;25:137–145. Reproduced with permission from the American College of Cardiology.)

including left ventricular–to–right atrial communications and left ventricular–to–coronary sinus fistulae.[92] [93] [94] [95] These complications are attributed mainly to excessive débridement and injury to the mitral annulus during surgery. Concomitant endocarditis, however, may be an underlying mechanism in late postoperative cases. In the early postoperative period, the clinical presentation may include a new systolic murmur, findings of high cardiac output, or a high oxygen saturation in the pulmonary artery; however, this condition may be often misdiagnosed as remnant tricuspid regurgitation or periprosthetic valve regurgitation. Conversely, fistula formation following aortic valve replacement, between the aorta and cardiac chambers, such as left or right atrium or right ventricle, is usually secondary to infectious causes but could also occur in the setting of a ruptured pseudoaneurysm.[75] [76] Findings in these conditions are similar to those of rupture of sinus of Valsalva, including a continuous murmur. Echocardiographic and Doppler Findings

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A left ventricular-to-right atrial fistula mimics tricuspid insufficiency, and differentiating it from the latter may be difficult. A few direct and indirect clues may raise suspicion for this diagnosis. In contrast to most tricuspid insufficiency 566

Figure 25-19 Example of a patient with an unruptured mitral-aortic intervalvular fibrosa (MAIVF) pseudoaneurysm diagnosed with transesophageal echocardiography (TEE), missed at aortography. Top, TEE transverse planes show the MAIVF pseudoaneurysm expanding during systole (left) and collapsing during diastole (right). Communication between the pseudoaneurysm and left ventricular outflow region (arrow) is seen. Bottom, Aortogram during systole and diastole in the same patient appears normal. An, MAIVF pseudoaneurysm; LA, left atrium; LV, left ventricle; PrV, prosthetic aortic valve. (From Afridi I, Apostolidou MA, Saad RM, et al: J Am Coll Cardiol 1995;25:137–145. Reproduced with permission from the American College of Cardiology.)

jets, which are directed towards the interatrial septum, the jet from the fistula seen by color Doppler arises near the crux of the heart and is usually directed centrally or toward the free wall of the right atrium. Unconventional imaging planes used to assess the origin of the jet may provide visualization of proximal velocity acceleration on the left ventricular side, raising suspicion for the diagnosis. Recording of jet velocity by continuous-wave Doppler will invariably lead to registering a high-velocity jet, similar to mitral regurgitation. If there is concomitant mitral regurgitation, the jet velocities will be almost equal—this will lead to an overestimation of pulmonary artery pressure when using the modified Bernoulli equation. A close examination of right ventricular function, septal motion, pulmonary flow velocity contour, and pulmonary insufficiency jet, if available, may reveal a discordance between findings of normal pressure by these indices and that derived from the "tricuspid insufficiency" jet, raising suspicion for the diagnosis. Further confirmation may be carried out with TEE aiming at better definition of the origin of the jet. In the case of left ventricular–to–coronary sinus fistula, a high-velocity intense color jet is seen in the coronary sinus, which in these cases is usually dilated. The differential diagnosis includes a coronary artery–to– coronary sinus fistula, where, in contrast, a continuous flow occurs.[96] On the other hand, fistula formation between the aorta and cardiac chambers through a periprosthetic aortic valve abscess rupture is diagnosed as a

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continuous systolic and diastolic jet into the respective chamber, with a continuous and intense recording by continuous-wave Doppler of high velocity reflecting the high-pressure difference between aorta and the communicating chamber. In the above conditions, the most often used alternative diagnostic modality is contrast cineangiography for demonstrating the communications. Pulmonary Valve Autotransplantation: The Ross Operation In 1967, Ross described the use of an autologous pulmonary valve to replace the diseased aortic valve. The procedure, presently known as the Ross operation, consists of implanting the patient's own pulmonary valve within the aortic root and replacing the pulmonary valve with either an aortic or pulmonary allograft. This procedure is performed predominantly in young adult patients and children with aortic valve disease and offers the advantages of valve viability and potential for growth in young patients, and the elimination of the need for long-term anticoagulation, in addition to increased durability compared with aortic allografts and bioprosthetic valves in this age group.[97] [98] Complications of the Ross operation include the potential for aortic insufficiency because of malalignment of the pulmonic valve in the aortic position, and valve degeneration occurring late after surgery. More recently, replacement of the aortic root with a pulmonary root autograft has been proposed.[99] [100] [101] The potential advantage of this procedure, compared with simple pulmonary valve autograft, is the more optimal alignment and function of the valve leaflets, because the sinuses of Valsalva also are transplanted. Short-term follow-up data from these patients have not revealed significant dilatation of the wall of the pulmonary artery in the aortic position. Over the past few years, more experience with the procedure has been acquired.[40] [102] [103] [104] [105] [106] The incidence of progressive aortic insufficiency has been low and has improved with the root-replacement technique.[40] [107] Annular dilatation of the pulmonary autograft occurs after implantation in the aortic position (20% increase on average).[107] [108] Infrequently, however, aneurysmal or pseudoaneurysmal formation may develop at this site, complicating pulmonary autograft surgery and necessitating reoperation.[109] [110] Progressive stenosis of the allograft in the pulmonary position has been infrequently reported, usually at the distal anastomosis in the pulmonary artery[101] [111] however, reoperating on the pulmonary allograft may be necessary in up to 20% of patients, at 20 years.[40] Echocardiographic techniques are ideally suited for the follow-up and

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detection of complications in patients with pulmonary valve or pulmonary root autografts.[101] [107] [108] [109] [110] [111] [112] [113] In most cases, transthoracic echocardiography with Doppler is sufficient to evaluate the aortic root and the presence and severity of aortic insufficiency. In suspected complications, TEE improves the definition of aortic root pathology.[109] Similarly, echocardiography can provide serial assessment of allograft function in the pulmonary position. Stenosis at the distal anastomosis has been recently reported with Doppler echocardiography, requiring reoperation in few patients.[101] [111] The transesophageal approach may be needed to evaluate complex lesions or the mechanism of postoperative complications.

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Section 5 - Cardiomyopathies and Pericardial Disease

571

Chapter 26 - Doppler and Two-Dimensional Echocardiographic Evaluation in Acute and Long-term Management of the Heart Failure Patient Jannet F. Lewis MD

Background It is estimated that there are 2 million individuals in the United States with a diagnosis of congestive heart failure, and nearly 400,000 new patients are diagnosed each year. Among 652 members of the Framingham Heart Study who developed congestive heart failure between 1948 and 1988, median survival after onset of heart failure was 1.7 years in men and 3.2 years in women.[1] One-year and 5-year survival rates were 57% and 25% in men and 64% and 38% in women, respectively. No significant change in the prognosis of congestive heart failure was identified during the 40 years of observation. However, the course of the disease is not uniformly poor, and considerable variability exists among individual patients. [2] [3] [4] [5] [6] [7] [8] [9]

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Moreover, newer therapeutic interventions, both pharmacologic treatment [10] [11] [12] [13] and cardiac transplantation,[14] [15] [16] promise improved survival in patients with congestive heart failure. Improvement in survival depends in part on the ability to correctly characterize the disease and stratify patients with regard to prognosis to make the most appropriate therapeutic plan. Two-dimensional and Doppler echocardiography have markedly improved our understanding of the pathophysiology of congestive heart failure and have also provided noninvasive techniques for accurate diagnosis of underlying causes, hemodynamic evaluation at baseline and during medical intervention, and important prognostic information to guide further management. This chapter is devoted primarily to the use of twodimensional and Doppler echocardiography in the evaluation and management of congestive heart failure due to dilated cardiomyopathy. Other diseases associated with heart failure (coronary artery disease, valvular heart disease, other cardiomyopathies) are the subjects of separate chapters.

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Echocardiography in the Diagnosis of Cardiomyopathy 572

The widespread use of echocardiography in the management of patients with suspected or known cardiac disease has facilitated our appreciation of the spectrum of diseases that present with the constellation of signs and symptoms of congestive heart failure. Thus, while many patients with manifestations of decompensated congestive heart failure have reduced left ventricular ejection fraction, congestive symptoms and signs may be present in other conditions.[17] [18] Previous observations in patients undergoing noninvasive assessment of systolic function have shown that as many as 50% of patients with clinically diagnosed congestive heart failure have a normal left ventricular ejection fraction. Most of these patients have systemic hypertension alone or in combination with ischemic heart disease. A substantial minority have nondilated cardiomyopathies, such as hypertrophic or restrictive cardiomyopathy, with heart failure occurring primarily as a consequence of diastolic dysfunction. Echocardiography provides excellent visualization of the left ventricle in most patients and readily distinguishes the three major forms of cardiomyopathy. Dilated cardiomyopathy is characterized by dilated cardiac chambers, most prominently the left ventricle, and reduced ejection fraction[3] [8] [19] , [20] (Fig. 26-1) . Echocardiographic diagnosis of hypertrophic cardiomyopathy is based on identification of severe asymmetric hypertrophy of the left ventricle, usually most marked in the ventricular septum with sparing of the posterior wall, and normal or increased ejection fraction[21] [22] [23] [24] [25] (see Chapter 27) . The disease shows considerable morphologic diversity, however, and recognition of this diversity is essential for diagnosis. Thus, while septal hypertrophy is the most prominent and best-recognized feature of the

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disease, hypertrophy may be confined to the apical segments of the left ventricle[26] [27] or most marked in the posterior free wall.[28] Also, there appear to be definite age-related morphologic differences among patients with hypertrophic cardiomyopathy[29] [30] [31] (Fig. 26-2) . Elderly patients with this disease, compared with younger patients, generally show less severe hypertrophy that is more often localized to the ventricular septum. Restrictive cardiomyopathy, most commonly due to cardiac amyloidosis, may also present with signs and symptoms of congestive heart failure (see Chapter 28) . The disease is characterized by a symmetrically thickened left ventricular wall with a "ground-glass" appearance of the myocardium, and normal left ventricular chamber size and systolic function until the very advanced stages of the disease (Fig. 26-3) . Doppler echocardiographic studies in patients with amyloid heart disease have identified a spectrum of transmitral filling patterns that correlate with the severity of disease and prognosis.[32] [33] Echocardiographic diagnosis of ischemic heart disease is based on identification of segmental wall motion abnormalities ( see Chapter 11 Chapter 12 Chapter 13 Chapter 14 ). In most patients, the distinction between ischemic heart disease and dilated cardiomyopathy is readily apparent. However, in some Figure 26-1 Diastolic (A) and systolic (B) frames in an apical four-chamber echocardiographic view from a 23-year-old man with dilated cardiomyopathy. The left ventricle is dilated and the ejection fraction is markedly depressed. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

patients with severe ischemic heart disease, there may be substantial left ventricular dilation and global systolic dysfunction.[34] Alternatively, patients with nonischemic dilated cardiomyopathy may demonstrate segmental areas of akinesis as well as regions with apparently preserved contractility, usually the basal segments of the inferior and posterior walls. [35] Consequently, in patients with severely depressed left ventricular systolic function, the distinction between nonischemic and ischemic disease may present an important diagnostic problem. Although coronary arteriography provides definitive diagnosis in such cases, other noninvasive modalities such as dobutamine stress echocardiography also give important diagnostic and therapeutic information.

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Figure 26-2 Echocardiographic images in a parasternal long-axis view from a 23-year-old woman (A) and a 66-year-old woman (B) with hypertrophic cardiomyopathy. In the younger patient, the ventricular septum (VS) is markedly and diffusely thickened and bulges into the left ventricular chamber. In the older patient, the septum is more modestly thickened (arrowheads), and the ventricular chamber shape appears normal. Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/220.html/top

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Assessment of Dilated Cardiomyopathy by Echocardiography Morphologic Description Cardiac enlargement is a central feature in dilated cardiomyopathy. [3] [19] , [36] However, echocardiographic assessment has demonstrated a spectrum of findings with regard to the degree of chamber enlargement, magnitude of left ventricular dysfunction, myocardial thickness, and size and systolic function of the right ventricle.[8] [20] [37] , [38] For example, although most patients show a marked increase in the size of the left ventricular chamber, Keren et al[38] described a group of patients with "minimally dilated cardiopathy." The cause of lack of dilation is not entirely clear, but pathologic examination shows less myofibrillar loss in these subjects than in patients with more dilation. The prognosis for these patients appears to be similar to the prognosis for those with the more classic form of the disease. The morphologic variability in dilated cardiomyopathy has also been demonstrated at postmortem examination. Benjamin et al[39] found variability in the degree of left ventricular wall thickness and relation of wall thickness to chamber size. A review of clinical records revealed greater wall thickness in long-term survivors than in short-term Figure 26-3 Echocardiographic images from a 62-year-old man with cardiac amyloidosis. The ventricular wall thickness is markedly increased, and the ventricular septum has a typical "ground-glass" appearance. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

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Figure 26-4 Two-dimensional echocardiographic images in an apical four-chamber view from two patients with dilated cardiomyopathy. A, Predominant and disproportionate dilation of the left ventricular chamber can be seen. The right ventricle in this patient appears relatively small. B, More pronounced right ventricular chamber dilation can be seen. Right ventricular systolic function is also depressed in this patient. Pacemaker leads (arrowheads) are present in the right cardiac chambers. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

survivors, and a smaller radius-to-thickness ratio appeared to confer a somewhat protective effect. Similarly, Gaasch and Zile[40] found wall stress to be an important predictor of outcome in patients with dilated cardiomyopathy. Investigations of patients with dilated cardiomyopathy have focused largely on description of the left ventricle. However, right ventricular size and systolic function also vary among patients with dilated cardiomyopathy and have important implications for prognosis and treatment.[9] [41] In a clinical and echocardiographic study of patients with dilated cardiomyopathy, two morphologic subsets were identified: patients with relatively equal degrees of ventricular enlargement, and patients with predominant and disproportionate dilation of the left ventricle but relative sparing of the right [9] (Fig. 26-4) . Severe mitral and tricuspid regurgitation were more common among patients with pronounced right ventricular enlargement. Survival over a mean follow-up period of 28 months was better among patients with primarily left ventricular dilation. Pinamonti et al [42] subsequently reported right ventricular systolic function as a strong predictor of death or cardiac transplantation in 79 consecutive patients with dilated cardiomyopathy followed for a mean of 22 months. Noninvasive Hemodynamic Assessment The hemodynamic parameters assessable by two-dimensional and Doppler echocardiography are listed in Table 26-1 . Assessment of Left Ventricular Systolic Function

Left ventricular systolic function in the setting of congestive heart failure has important diagnostic and prognostic implications. In addition, parameters of systolic function may be useful in evaluating the response to therapeutic intervention. The most widely used clinical index of systolic function is ejection fraction (calculated as [end-diastolic volume − end-

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systolic volume]/end-diastolic volume). Left ventricular volume has been assessed by echocardiography on the basis of a number of geometric assumptions (see Chapter 4) . Because the left ventricle commonly loses its normal elliptical geometry in TABLE 26-1 -- Noninvasive Hemodynamic Data Obtainable by TwoDimensional (2D) and Doppler Echocardiography 2D Alone X X X

Hemodynamic Parameter LV diastolic volume LV stroke volume/cardiac output LV ejection fraction LA/LV diastolic pressure Pulmonary artery pressure RA pressure X Valvular regurgitation severity X LA, left atrial; LV, left ventricular; RA, right atrial.

Doppler Alone

Both

X X X X

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TABLE 26-2 -- Measurement of Stroke Volume/Cardiac Output by Doppler Echocardiography Study Fisher et al[46] † Dubin et al[49] Lewis et al[47]

Subjects, n 15 18 39

Huntsman et al

r Value * (SEE) Variability, % 0.97 (0.23 L/m) 0.87 (11 mL) 0.91 (0.63 L/m) inter: 6.8 ± 1.5 0.87 (0.59 L/m) inter: 16.4 ± 13.8 0.94 (0.58 L/m)

Method Mitral LV outflow Mitral inflow Aorta

[45]

Nicolosi et al[48] ‡

—

inter: 6.8

Six methods

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intra: 5.9 methods 16.0 Inter, interobserver variability; intra, intraobserver variability; method, variability of the method; LV, left ventricular; SEE, standard error of estimate. * Correlation with stroke volume/cardiac output measured by roller pump and thermodilution cardiac output. † Canine studies. ‡ Healthy volunteers without thermodilution measurements.

the setting of heart failure, however, the biplane "method of discs" is less dependent on geometric assumptions and provides a more accurate determination of ventricular volume.[43] The major limitation to this method is the requirement for apical four- and two-chamber views with endocardial definition of sufficient technical quality to permit manual tracing during freeze-frame analysis. Developments in automated border detection may resolve this problem (see Chapter 7) . Aside from these technical considerations, ejection fraction is largely dependent on the loading conditions of the left ventricle, and therefore may not serve as an accurate surrogate of myocardial contractility. For example, in the setting of mitral regurgitation, ejection fraction poorly reflects myocardial contractility. Determination of stroke volume and cardiac output provides more accurate assessment of ventricular performance. Stroke volume can be calculated from diastolic and systolic left ventricular volumes by echocardiography.[43] [44] However, as with calculation of ejection fraction, significant error may occur because of suboptimal visualization of endocardial borders during freeze-frame analysis. Studies by several investigators in different laboratories have demonstrated excellent correlation between cardiac outputs obtained by Doppler echocardiography and flow measured by invasive techniques[45] [46] [47] [48] [49] (Table 26-2) . Doppler echocardiographic assessment of stroke volume is based on the principle that flow (Q) across an orifice can be calculated as the product of the cross-sectional area of the orifice (CSA) and the time velocity integral (TVI) across the orifice: Q = CSA × TVI

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Stroke volume = CSA × TVI Cardiac output = stroke volume × heart rate Theoretically, flow can be assessed across any vessel or cardiac valve. Thus, stroke volume has been calculated using Doppler sampling of left ventricular outflow, ascending aorta, and mitral, tricuspid, and pulmonic valves.[45] [46] [47] [48] [49] [50] Each method is limited by the ability to measure orifice size accurately. Calculation of stroke volume and cardiac output from the flow velocity in the left ventricular outflow tract (Fig. 26-5) utilizes cross-sectional area calculated from diameter measurement of the left ventricular outflow tract, assuming a circular geometry: Area = π(diameter / 2)2 As is apparent, small differences in diameter measurement result in relatively larger differences in calculation of cross-sectional area and stroke volume. Nonetheless, the overall correlation of cardiac output determined from the left ventricular outflow Doppler method and output measured by thermodilution is excellent, and reproducibility of this method is approximately 16%.[47] Use of ascending aortic flow velocity for calculation of stroke volume is technically more difficult and has been less commonly applied.[48] [49] Several approaches have been assessed for measurement of stroke volume from the mitral inflow velocity waveform.[46] [47] [48] [49] The simplest method employs Doppler sampling in the center of the mitral annulus and measurement of the mitral annulus, assuming a circular geometry for calculation of cross-sectional area (Fig. 26-6) . The mitral annular method for calculation of stroke volume and cardiac output also shows close correlation with thermodilution measurement but with larger interobserver variability than with the outflow method. Because of the noncircular geometry of the mitral annulus, alternative approaches to the calculation of mean mitral valve area during diastole utilize M-mode correction of twodimensional measurements as well as biplane measurement of mitral annulus diameter, assuming an elliptical geometry. These approaches have also shown good correlation with thermodilution cardiac output but are more tedious and do not appear to offer significant advantage. Pulmonary artery flow calculation of stroke volume has been less widely used in adult patients because of limited visualization of the pulmonary

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artery boundaries but has been extensively applied in pediatric patients.[50] The pulmonary artery dilation often observed in patients with dilated cardiomyopathy may improve visualization of the pulmonary boundaries and thus facilitate the use of this method in adults. Because of the difficulties encountered with calculation of cross-sectional area, use of the flow velocity integral alone to obtain a stroke distance has been proposed as a correlate of stroke volume.[51] Measurement of stroke distance 576

Figure 26-5 Calculation of cardiac output using the left ventricular outflow method. The diameter of the left ventricular outflow immediately proximal to the aortic cusp is measured from the parasternal long-axis view (A, upper and lower). Pulsed Doppler sample volume is placed proximal to the aortic valve in the apical view (B, upper) to obtain the left ventricular outflow flow velocity waveform (B, lower). LA, left atrium; LV, left ventricle.

for serial evaluation of patients undergoing therapeutic intervention appears to be a reasonably accurate alternative to stroke volume measurement. Ejection phase indices derived from M-mode and Doppler echocardiographic measurements have also been used to assess left ventricular systolic function. These indices are significantly influenced by loading conditions of the ventricle. On the other hand, indices related to isovolumic contraction, such as the rate of pressure rise Figure 26-6 Calculation of cardiac output using the mitral inflow method. A, Diameter of the mitral annulus is measured from the apical four-chamber view during maximal excursion of the mitral valve. B, Doppler sample volume is placed in the center of the mitral annulus to obtain the mitral flow velocity waveform (lower). LA, left atrium; LV, left ventricle.

during this period (dP/dt), appear to be less influenced by load and are especially useful for evaluating directional changes of myocardial contractility. The mitral regurgitant jet velocity is largely a consequence of temporal changes in the relationship between left ventricular and left atrial pressures. During isovolumic contraction, left atrial pressure does not change appreciably in patients with chronic mitral regurgitation and a

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compliant left atrium. Thus, the rate of change in velocities (and derived pressures) in 577

Figure 26-7 (Figure Not Available) Drawing of a mitral regurgitant flow velocity jet illustrating the basis for determining rate of pressure rise (RPR) in the left ventricle. Two points are selected along the velocity curve (A, 1 m/sec = 4 mm Hg; B, 3 m/sec = 36 mm Hg), and the time interval (t) between them is measured. ECG, electrocardiogram. (From Bargiggia GS, Bertucci C, Recusani F, et al: Circulation 1989; 80:1287–1292, with permission.)

this pre-ejection phase provides information about ventricular systolic performance. [52] [53] [54] [55] Bargiggia et al[52] used Doppler echocardiography to obtain dP/dt from mitral regurgitant jet velocities and found good correlation with peak dP/dt measured at cardiac catheterization (Fig. 26-7) (Figure Not Available) . Doppler-derived dP/dt is obtained by digitization of mitral regurgitant jet velocities at 1 msec intervals to obtain the rate of increase in velocity. This rate of velocity change is converted to rate of pressure increase using the modified Bernoulli equation (pressure gradient = 4[velocity]2 ). In the normal heart, the rate of pressure rise exceeds 1200 mm Hg per second. A pressure rise of less than 400 mm Hg per second is consistent with severe systolic dysfunction.[54] Assessment of Left Ventricular Diastolic Function and Estimation of Left Ventricular Filling Pressure

Left ventricular diastolic function plays an important role in the pathophysiology of a variety of diseases.[17] [18] , [56] [57] [58] [59] In patients with systolic dysfunction, abnormalities of diastolic function may importantly contribute to clinical manifestations of disease. Indeed, diastolic function appears to be significantly related to the severity of cardiac symptoms and prognosis in patients with heart failure.[41] [42] [60] [61] [62] [63] [64] [65] [66] [67] Transmitral flow velocity obtained by pulsed Doppler echocardiography has been extensively used to assess left ventricular diastolic function[68] [69] [70] [71] [72] [73] [74] [75] (see Chapter 6) . The normal mitral waveform is characterized by an early peak flow velocity and a second, late peak with atrial systole (Fig. 26-8) . A number of diastolic indices have been used to assess left ventricular diastolic function, including peak velocity during early filling (E), peak velocity following atrial contraction (A), the time integrals of early and late filling velocities, the ratio of early and late peak

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velocities (E/A), and deceleration time (measured as the time from peak early filling to descent of filling to the baseline). Mitral inflow waveform patterns have been correlated with hemodynamic findings and therefore provide important noninvasive hemodynamic information.[66] [67] [70] A pattern of impaired relaxation is characterized by reduced early peak flow velocity, prolonged deceleration time, and augmented late flow velocity [70] (see Fig. 26-8) . This pattern has been observed in a variety of conditions (e.g., systemic hypertension, coronary artery disease, and early amyloidosis) and is associated with abnormal left ventricular relaxation with relatively normal left ventricular diastolic pressure. In comparison, a "restrictive" pattern of filling has been observed with marked elevation of left atrial and left ventricular diastolic pressure and is most commonly observed in advanced congestive heart failure[41] [42] [66] , [67] [70] [76] (see Fig. 26-8) . Although the transmitral flow velocity waveform provides important information regarding left ventricular diastolic function, the appearance of the transmitral waveform is also influenced by a number of variables, including age, heart rate, and left atrial/left ventricular crossover pressure at the time Figure 26-8 Spectrum of mitral inflow patterns. A, Normal mitral velocity flow pattern. B, Pattern of impaired relaxation with decreased peak early velocity (E) and increased peak late velocity (A). C, Restrictive filling pattern showing increased E velocity, short deceleration time, and reduced A velocity.

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Figure 26-9 Illustration of left ventricular and left atrial pressures with simultaneous mitral flow velocity waveforms in a normal ventricle, a ventricle with impaired relaxation, and a ventricle with increased preload. Note the relation of the atrioventricular gradient on the appearance of the mitral waveform. Hatched areas represent the atrial filling fraction; large arrows denote isovolumic relaxation time; small arrows indicate deceleration time (Dec Time). A, peak late velocity; E, peak early velocity; LA, left atrium; LV, left ventricle. (From Mulvagh S, Quinones MA, Kleiman NS, et al: J Am Coll Cardiol 1992;20:112– 119, with permission from the American College of Cardiology.)

of mitral opening[70] [72] [77] [78] [79] (Fig. 26-9) . The latter accounts for the "pseudonormal" pattern observed in patients with impaired relaxation and

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elevated left atrial pressure. The dependence of transmitral filling on factors other than left ventricular diastolic dysfunction presents an important consideration for the use of mitral indices of left ventricular filling for assessment of diastolic function. Assessment of pulmonary vein flow velocity waveforms provides information complementary to that obtained from the transmitral flow patterns.[80] [81] [82] [83] Pulmonary venous sampling is most readily obtained from a transesophageal study but with practice can be obtained with the transthoracic approach in most patients. The normal pulmonary vein flow pattern is characterized by antegrade systolic and diastolic waves and a retrograde diastolic wave following atrial systole (Fig. 26-10) . During forward systolic pulmonary vein flow, the left atrium functions as a reservoir. Systolic flow from the pulmonary vein into the left atrium is influenced by contractility of the left ventricle and descent of the mitral annulus, as well as left atrial pressure. Thus, impaired left ventricular systolic function and elevated left atrial (or pulmonary capillary wedge) pressure are associated with decreased systolic antegrade flow in the pulmonary veins[81] [83] (Fig. 26-11) (Figure Not Available) . A ratio of pulmonary vein systolic to diastolic velocity integrals of less than 0.40 correlates with left atrial pressures of greater than 15 mm Hg. During forward diastolic flow of the pulmonary vein, the left atrium functions as a conduit. Pulmonary venous diastolic flow is therefore largely influenced by left ventricular diastolic pressure, as well as factors that affect early transmitral filling: age, heart rate, and differences in left atrial/left ventricular crossover pressure at the time of mitral opening. Retrograde diastolic flow (atrial reversal) depends on the integrity of atrial systole and left atrial pressure. Elevated left atrial pressure is usually associated with a pulmonary vein retrograde diastolic flow velocity of greater than 40 cm per second.[81] An integrated approach to assessment of left ventricular diastolic function utilizes both transmitral and pulmonary venous flow velocities. In the presence of impaired relaxation with relatively normal left ventricular diastolic pressure, transmitral filling shows the classic pattern of E to A reversal (E/A ratio 150 msec). The pulmonary venous waveform shows a ratio of forward systolic to diastolic flow of 1.0 or greater and a retrograde diastolic flow velocity of less than 40 cm per second. In the presence of elevated left Figure 26-10 Pulmonary vein flow velocity waveforms obtained by

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transesophageal study in a patient with normal flow pattern (A) and a patient with severe mitral regurgitation (B). There is marked systolic flow reversal in the presence of severe mitral regurgitation.

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Figure 26-11 (Figure Not Available) Scatterplot of correlation of systolic fraction (pulmonary venous velocity time integral as fraction of the sum of systolic and early diastolic velocity time integral) with pulmonary capillary wedge pressure (PCWP). SEE, standard error of estimate. (From Kuecherer HF, Muhiudeen IA, Kusumoto FM, et al: Circulation 1990;82:1127–1139, with permission.)

atrial pressure, early peak mitral flow velocity is increased, followed by shortened deceleration and reduced late peak velocity. Pulmonary venous flow in this situation shows reduced forward systolic flow, a systolic to diastolic ratio of less than 0.4, and increased retrograde diastolic (atrial systolic) flow velocity. The duration of transmitral late flow velocity (A) relative to the duration of pulmonary vein retrograde diastolic flow (Ar) is a useful indicator of left ventricular end-diastolic pressure. In a study by Rossvoll and Hatle, a duration of the pulmonary venous Ar wave exceeding the transmitral A wave duration predicted an end-diastolic pressure of greater than 15 mm Hg, with a sensitivity of 85% and specificity of 79%[84] (Fig. 26-12) . A number of formulas have been derived for estimation of pulmonary capillary wedge and left ventricular end-diastolic pressures (Table 26-3) .[84] [85] [86] [87] [88] [89] [90] The formulas vary considerably in complexity but provide reasonable assessment TABLE 26-3 -- Calculation of Left Ventricular Diastolic Pressure by Echocardiography Study Pozzoli et al[50] Giannuzzi et al[87] Nagueh et al[89] Nagueh et al[84] Garcia et al[86] Mulvagh et al[85]

Equation PCWP = 1.85 × DR - 0.10 × SF + 10.9 PCWP = 32.16 - 0.104E + 0.1345A - 0.17DT + 4.95E/A PCWP = 45 - 0.16DT PCWP = 1.24 (E/Ea) + 1.9 PCWP = 5.27 (E/Vp) + 4.66 PWCP = 46 - 0.22IVRT - 0.10AFF - 0.03DT - 2E/A + 0.05MAR

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Mulvagh et al[85] LVEDP = 46 - 0.22IVRT - 0.03DT - 0.01AFF - (2/E/A) + 0.05MAR Nagueh et al[88] mean PCWP = 17 + 5.3E/A - 0.11IVRT Pozzoli et al[90] PCWP = 0.93DR - 0.155F + 0.03 (dZ - dA) + 0.87E/A + 16.2 A, mitral inflow peak late diastolic velocity; AFF, mitral atrial filling fraction; DT, early mitral velocity deceleration time; DR, early mitral inflow velocity deceleration rate; dZ - dA, difference in duration of reverse pulmonary venous and mitral velocity at atrial contraction; E, mitral inflow peak early velocity; Ea, peak early velocity measured by tissue Doppler at mitral annulus; IVRT, isovolumic relaxation time; MAR, time from mitral closure by Doppler to R wave on ECG; PCWP, pulmonary capillary wedge pressure; SF, peak pulmonary venous flow velocity systolic fraction; Vp, early diastolic color flow propagation velocity. of pressures in patients with reduced left ventricular systolic function. Assessment of Pulmonary Artery Systolic Pressure

Pulmonary artery pressure measured invasively has been commonly employed to assess left ventricular diastolic function. The relation of tricuspid regurgitant jet velocity to right ventricular pressure (and pulmonary artery pressure) as estimated by the modified Bernoulli equation (pressure gradient = 4[velocity]2 ), combined with the frequent finding of Doppler-detected tricuspid regurgitation, even in the absence of structural cardiac disease, affords the opportunity to noninvasively estimate pulmonary artery systolic pressure.[91] Thus, PASP = 4V2 + RAP where PASP is pulmonary artery systolic pressure, V is peak velocity of the tricuspid regurgitant jet, and RAP is estimated right atrial pressure. Figure 26-12 Bar charts showing the effect of different left ventricular (LV) pressures before atrial contraction (pre-a) (A) and of LV pressure (awave) increases at atrial systole (B) on the mean duration of pulmonary venous retrograde velocity (PV-a) and mitral A wave, and the difference in flow duration. The duration of flow on the vertical axis is in milliseconds. + P 60 years of age to those 10 mm Hg caused by raised pericardial pressure).[49] As well, the clinical transformation from stable to unstable can occur abruptly with small changes in any of the factors that influence the hemodynamic effect of a given pericardial effusion. Therefore, echocardiography plays a pivotal role in the management of patients with pericardial effusion, because some echocardiographic findings occur when intrapericardial pressure is elevated, but before clinical compromise. It must be appreciated that the physiologic effects of an increasing pericardial effusion lie on a continuum, and therefore any separation into distinct stages is arbitrary. We find it useful clinically, however, to divide patients with pericardial effusions echocardiographically into three hemodynamic categories. First, we describe those without echocardiographic evidence of hemodynamic compromise (no right ventricular collapse, no right or left atrial collapse, physiologic changes in intracardiac flows with inspiration) as "no evidence of hemodynamic effect" on the echocardiographic report. Second, we describe those with any degree of right ventricular diastolic collapse, prolonged (>35% of the cardiac cycle) right atrial collapse, or marked respiratory flow variation (>25% left ventricular or >80% right ventricular early filling [E] velocity changes with inspiration) as showing echocardiographic indications of "tamponade." Tamponade is in quotation marks to acknowledge our understanding that tamponade is a clinical syndrome. Thirdly, we report patients that fit into neither of the abovementioned categories as having echocardiographic indicators of elevated pericardial pressure without echocardiographic features of tamponade. These rules are applicable to patients with relatively normal pericardial and cardiac physiology; however, it cannot be overemphasized that with localized cardiac compression, or abnormal physiological states, hemodynamic compromise may be present owing to elevated pericardial pressure without any classic M-mode, two-dimensional or Doppler echocardiographic indicators of raised intrapericardial pressure.[46] [47] [48]

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Echocardiographically Guided Pericardiocentesis Before two-dimensional echocardiography, percutaneous pericardiocentesis was viewed with trepidation by even the most experienced clinicians. In cardiac catheterization laboratories, with the procedure performed under continuous fluoroscopic, electrocardiographic, and hemodynamic monitoring, experienced clinicians in large volume centers achieved success rates of only 86% in obtaining fluid, with death rates of 4%, and a further 4% risk of other major complications.[69] In contrast, echocardiographically guided series have indicated success rates of greater than 99%, with no deaths and total complication rates of 3% to 5% (pneumothorax, hemothorax, subsequent purulent pericarditis, transient ventricular tachycardia). [70] [71] [72] Multiple techniques exist for echocardiographically guided pericardiocentesis, [72] [73] [74] and the best technique in an individual case depends on the amount and location of the pericardial fluid, the clinical status of the patient, and the operator's experience. In all but emergency situations, we prefer to perform the procedure in our coronary care unit, under continuous echocardiographic, electrocardiographic, noninvasive or invasive blood pressure, and oximetry monitoring. The steps we employ for nonemergency echocardiographically guided pericardiocentesis are as follows: 1. The patient's echocardiogram is reviewed to determine the amount and location of pericardial fluid, the presence of loculations, the possible percutaneous approaches, and any underlying cardiac pathology. 2. As a minimum the patient's chart is reviewed; if needed a history is taken and a directed physical examination is performed. We determine the clinical effects of the pericardial effusion, the presence of any bleeding diathesis, and underlying general medical or specific cardiac issues that could modify our approach (e.g., avoidance of areas documented to have adhesions, allergies). 3. Laboratory tests are ordered or reviewed. As a minimum we suggest a hemoglobin, platelet count, electrolytes, creatinine, INR, * and APTT. † Any coagulopathy or * INR, international normalized ratio. † APTT, activated partial thromboplastin time. 651

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652

electrolyte disturbance (especially hypokalemia) should be corrected. If the patient is significantly anemic, a cross-match or blood type and antibody screen should be performed. In the presence of severe renal failure, we may choose to administer desmopressin (DDAVP) to improve platelet function. 4. Informed consent is obtained, a large bore peripheral IV is placed, a noninvasive blood pressure cuff (if an arterial line is not present) is applied and readings taken every 2 minutes. Oxygen (O2 ) saturation monitoring is performed and O2 by nasal prongs is provided.

5. If an echocardiographer is performing the study, we prefer to image the patient ourselves to obtain a "feel" for the correct approach. We choose the approach that provides the most direct route to the largest collection of fluid, as far removed from vital structures as possible. Special attention should be made to avoid the internal thoracic arteries (located 0.5 to 2 cm lateral to the sternum). We then mark a proposed entry point (with a permanent marker or indentation of the skin with the top of a syringe cap), and then re-image from this location to determine the depth to the fluid, the depth to the nearest cardiac structure, and the correct angle. We then determine if an acoustic window is available, remote to the proposed puncture site (that will not interfere with the sterility of the procedure), to directly visualize the procedure. If so, we have our sonographers image from this window while the procedure is performed. If not, we cover the imaging probe with a sterile cover and have it available for the physician performing the procedure to use if needed. 6. We then prepare and drape the patient and open a commercial pericardiocentesis kit. If the effusion is at a depth greater than 5 cm from the surface, or if there is less than 2 cm of fluid between the pericardium and any cardiac structure at the proposed puncture site, we prepare a three-way stop-co*ck device for injection of echo contrast. This is performed by connecting two 10-mL Luer lock syringes, one syringe filled with 5 mL of sterile saline agitated with 0.25 to 0.5 mL of air (similar to the set up used for a peripheral venous contrast study). We perform the procedure while wearing sterile gown and gloves. 7. The skin (including an area for an eventual suture) and subcutaneous tissue along the proposed approach are then thoroughly anesthetized

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with 1% or 2% lidocaine using a small (19- to 25-gauge) needle. We use a needle, if possible, that is long enough to reach the pericardial fluid, but not any cardiac structures. Adequate local anesthetic is a must. The needle is advanced along the previously determined pathway until the pericardial fluid is reached, or the predetermined appropriate length of the needle is inserted. 8. We then attach a needle (that we have confirmed will accommodate the guidewire) to a 10-mL Luer lock syringe with 5 mL of 1% lidocaine. Under direct imaging if possible, the needle is advanced until pericardial fluid is obtained, or a depth of needle is inserted that could contact a cardiac structure (i.e., if the pericardial fluid is 4 cm from the skin surface at the entry point and there is 2 cm of fluid in this area, we limit our insertion to 180°

severe, as shown in Fig. 30-12B , irrespective of the duration after transplantation. Validation with Coronary Angiography and Histologic Examination

Early studies compared measurements of the coronary artery lumen derived from intracoronary ultrasound with measurements determined by angiography. [71] In 20 cardiac transplant patients with no angiographic coronary artery disease, measurements from multiple sites in the left anterior descending artery were performed using both methods. Luminal dimensions using the two imaging systems correlated closely, with a correlation coefficient of 0.86. Of note was that the more the imaging catheter deviated from the long axis of the vessel, the greater was the discrepancy between ultrasound and angiographic measurements. Validation of the three-layered appearance of the coronary artery was obtained from histologic studies that included transplanted hearts imaged in vivo early after transplantation and again at autopsy.[73] In this important study, 16 hearts from patients aged 16 to 55 years with no history of coronary artery disease were examined. By comparing 72 cross sections with corresponding histologic sections, the authors concluded that the intracoronary ultrasound image appearance of young, morphologically

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normal coronary artery walls is hom*ogeneous, with no layering. A threelayered appearance suggests the presence of at least 0.2 mm of intimal thickening. Taken together with further autopsy studies that indicate an intimal thickness of greater than 0.3 mm to be pathologic,[74] [75] these data have allowed the application of intravascular ultrasonography to prospectively evaluate the 674

Figure 30-12 Spectrum of images recorded from heart transplant recipients. A, Images recorded from a patient 8 years after cardiac transplantation showing minimal intimal thickening (arrow). B, Images from a patient with severe intimal thickening (arrow) 4 years after transplantation. Horizontal and vertical calibration marks are at 0.5-mm intervals.

prognostic significance of intimal thickening in heart transplant patients. Safety in Heart Transplant Patients

After the initial introduction of intravascular ultrasonography to assess coronary artery morphology in heart transplant patients, concerns were raised regarding the risks for endothelial damage leading to accelerated atherosclerosis. To address this question, coronary artery lumen dimensions of 38 heart transplant patients were measured by quantitative angiography in matched angiograms, at an interval of 1 year after the initial intravascular ultrasound examination.[76] The angiographic measurements in the vessel that had previously held the intravascular ultrasound catheter were compared with vessels that had not been catheterized. There were no differences in the absolute and percentage change in the angiographically measured mean-vessel diameters in intravascular ultrasound-imaged and nonimaged vessels. Acute coronary spasm, however, occurred in 8% of the patients undergoing intravascular ultrasound imaging but resolved promptly in response to nitroglycerin in all cases. Intravascular ultrasonography was not associated with any clinical morbidity. Clinical Application

Intravascular ultrasonography (IVUS) has been used to characterize the in vivo morphologic characteristics of transplant coronary artery disease in terms of incidence and severity, and to define the relationship of intimal thickening to angiographic evidence of coronary artery disease. The relationship of stress-test results to intimal thickening, as detected by

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IVUS, has been evaluated with the hypothesis that coronary angiography may not provide a sufficiently sensitive gold standard against which to test the reliability of stress-induced myocardial ischemia as a marker of transplant coronary artery disease. The technique has also been applied to the evaluation of risk factors that predispose to intimal thickening distinct from coronary artery stenosis and to define the prognostic significance of intimal thickening for predicting mortality and angiographic disease. Focusing on the pathophysiologic basis of transplant coronary artery disease, recent studies have applied IVUS to examine the relationship of intimal thickening with microvascular endothelial cell surface markers and cytokine expression in endomyocardial biopsy. Finally, IVUS is emerging as the gold standard with which to evaluate the efficacy of new therapies in clinical trials for prevention of transplant coronary artery disease. Incidence and Severity of Transplant Coronary Artery Disease.

The severity, distribution, and characteristics of transplant coronary artery disease, as defined by IVUS were reported from 304 intravascular ultrasound studies performed in 174 heart transplant patients.[77] Images were obtained during the initial 2 months following transplantation and up to 15 years after heart transplantation. This study provides a reference point for IVUS measurements of mean intimal thickness, index, and classification, and for morphologic characteristics, including calcification. Compared with studies obtained during the initial months after heart transplantation, patients studied at year 1 had greater intimal thickness, a greater intimal index, and a high intimal class. Thereafter, all three parameters increased over time, reaching peak values between 5 and 15 years. Calcification was detected in 12% of patients at years 0 to 5 but increased to detection in 24% of patients 5 to 15 years after transplantation. This study demonstrated that the greatest rate of progression of transplant coronary artery disease occurred during the initial 2 years after transplantation. This information is crucial because it suggests that measurements obtained from IVUS can provide end points for testing the effect 675

of therapeutic strategies targeted at the prevention of transplant coronary artery disease. Relationship of Coronary Artery Intimal Thickening to Angiographic Findings.

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Several studies have now reported underestimation of transplant coronary artery disease by coronary angiography, confirming earlier pathologic observations. In the initial 80 heart transplant patients undergoing IVUS examination,[78] 60 patients studied at 1 year or greater had some intimal thickening, which was graded as minimal or mild in 35%, moderate in 28%, and severe in 35%. Despite normal angiographic findings in 42 of the 60 patients, however, 50% of the patients had moderate or severe intimal thickening. This observation led to the concept of "angiographically silent" intimal thickening and to the possibility that patients with moderate or severe intimal thickening may be at risk for the subsequent development of angiographically significant disease or for cardiac events. Of 20 patients studied within 1 month of transplantation, an intimal layer was visualized in 13, all of whom had normal coronary angiographic findings. This observation has led to the question of whether disease that is present in the donor heart before transplantation accounts for intimal thickening seen within 3 months after transplantation. It has been suggested that the presence of eccentric lesions, particularly in older donor hearts, probably reflects pre-existing disease. [79] Because most of the baseline studies were not performed until 6 weeks after transplantation, the possibility that intimal thickening occurs as a consequence of the acute alloimmune response requires further evaluation. Prognosis Stratification and Risk-Factor Assessment.

The initial experience with IVUS indicated that 50% of heart transplant patients with moderate or severe intimal thickening had normal coronary angiographic findings, thus confirming that coronary angiography underestimated the severity of the disease. A 3-year follow-up of 120 patients confirmed the prognostic importance of intimal thickening, as detected by IVUS examination.[80] Intimal thickness in excess of 0.3 mm predicted the development of angiographic disease, overall survival, and graft loss resulting from transplant coronary artery disease. Our results on the reproducibility, safety, and prognostic significance of IVUS measures of intimal thickness paved the way for the application of this technology for the quantitative assessment of the early phase of transplant coronary artery disease. To examine the pathophysiology of transplant coronary artery disease, several groups, including our own, have defined the immunologic, metabolic, infectious, donor, and recipient risk factors for intimal thickening.[80] [81] By univariate analysis of metabolic versus immunologic risk for transplant coronary artery disease, 14 of 37 factors were

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significantly associated with intimal thickening. Factors that positively correlated with mean intimal thickness included the pretransplant lowdensity lipoprotein cholesterol level, the duration after transplantation, the average posttransplantation body weight, the number of moderate rejection episodes, the total number of rejection episodes, and the average plasma glucose and insulin levels 2 hours after an oral glucose load. Factors that inversely correlated with intimal thickening included the posttransplant average high-density lipoprotein cholesterol level, the average daily weight-adjusted dose of cyclosporine, and diltiazem treatment. By multivariate regression analysis with the presence of disease shown by IVUS as the dependent variable, average triglyceride levels and the mean post-transplantation body weight remained the only independent predictors for intimal thickening (R = 0.55, P < .0001). Likewise, angiographic evidence of transplant coronary artery disease was significantly correlated with average triglyceride levels and weakly with donor age. In a subgroup analysis of 39 patients studied 1 year after transplantation, a higher average triglyceride level (R = 0.55, P < .003) was the only factor associated with intimal thickening by intravascular ultrasonography. The results of these statistical analyses, as in prior studies, do not indicate acute cellular rejection as an independent predictor of transplant coronary artery disease but rather implicate an important role for lipoprotein abnormalities in the development of both early and late disease. Furthermore, prevention of transplant coronary artery disease by lipid-lowering agents[82] and calcium antagonists[83] suggests that factors other than acute cellular rejection are involved in the pathophysiology of transplant coronary artery disease. Thus, the results of clinicopathologic studies using IVUS to detect early and late disease provide a number of insights into potential pathophysiologic mechanisms of transplant atherosclerosis. Further investigation is needed about the role of vascular injury and the ensuing injury-response model, as postulated for nontransplant atherosclerosis. Relationship of Intimal Thickening to Microvascular Cell Surface Markers and Inflammatory Cell Phenotypes on Endomyocardial Biopsy.

Our group has performed studies aimed at defining the cellular and molecular mechanisms in transplant coronary artery disease. We examined the hypothesis that alterations of microvascular cell surface markers occur in parallel in the microvasculature and epicardial vessels, and that these changes may be important in the pathophysiology of intimal proliferation. [84] Forty-three heart transplant patients beyond 1 year posttransplantation were examined by IVUS, with concurrent analysis of right ventricular endomyocardial biopsies obtained at the time of IVUS. An inverse

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relationship between intimal thickening and microvascular cell surface markers was noticed. The rejection incidence was higher, and the duration after transplantation longer, in intimal classes II, III, and IV, compared with class I. These results are consistent with alterations of microvascular endothelial cell surface markers occurring in association with intimal thickening in epicardial coronary vessels. The changes in the expression of surface antigens by vascular cells could provide the substrate for coronary artery intimal proliferation and narrowing. Relationship of Intimal Thickening to Stress Test Results.

Dobutamine stress results indicate that positive tests coincident with normal angiographic findings are frequently associated with coronary artery intimal thickening, suggesting that ischemia may be occurring as a consequence of intimal hyperplasia in the microvasculature.[85] Similarly, intimal thickening was a frequent finding in exercise echocardiographic false-positive tests. Intravascular ultrasonography provides information regarding 676

early stages of transplant coronary artery disease in patients in vivo, before the development of obstructive lesions. It can be performed safely and is unassociated with a risk of an increasing rate of disease progression or of acute complications. It is superior to coronary angiography because it provides prognostically important information before the development of severe obstructive disease. Thus, it can be used in parallel with molecular analysis methods to characterize the pathophysiologic mechanisms that lead to rapid intimal proliferation in heart transplantation. Finally, because the most rapid phase of intimal proliferation occurs during the initial 2 years after heart transplantation, IVUS provides an invaluable method for monitoring the response to pharmacologic strategies for prevention of transplant coronary artery disease. Application of Intravascular Ultrasound in Clinical Trials.

The studies cited previously set the stage for the use of intravascular coronary artery ultrasound in clinical trials. Kobashigawa et al[82] demonstrated that patients randomized to pravastatin had significantly less intimal thickening 1 year after transplant compared with controls. A similar observation was reported by Wenke et al,[86] who used IVUS and coronary

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angiography to evaluate the effect of another HMG-CoA reductase inhibitor, simvastatin. In a randomized trial of mycophenolate mofetil (MMF) versus azathioprine, patients treated with MMF demonstrated less intimal area compared with controls. This was the first evidence in humans to suggest that the drug inhibits the disease process.[87] Given the limitations of coronary angiography to detect transplant coronary artery disease, as discussed earlier, it is anticipated that in the future clinical trials will use IVUS as the primary end point with which to test efficacy.

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Section 6 - Echocardiography in the Pregnant Patient

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Chapter 31 - The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy Catherine M. Otto MD Thomas R. Easterling MD Thomas J. Benedetti MD

Echocardiography is often requested in pregnant women either to evaluate known pre-existing heart disease or to check the possibility of heart disease in women with cardiac symptoms or abnormal findings on physical examination. Evaluation of heart disease in pregnancy is complicated by the fact that many healthy women experience symptoms of fatigue, decreased exercise tolerance, or dyspnea during pregnancy. Clinical examination alone may be nondiagnostic, prompting a request for echocardiographic evaluation. Similarly, although a "flow murmur" is present in most pregnant women, this normal finding cannot always be distinguished from a pathologic murmur on physical examination. With

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diagnostic testing, it is important to differentiate the normal alterations in cardiovascular 680

physiology and anatomy due to pregnancy from pathologic findings. In pregnant patients with known cardiac disease, expected findings (and appropriate normal reference values) may be different from those in nonpregnant patients. In some cases, echocardiography may be used to monitor cardiovascular function during pregnancy and in the peripartum period. In pregnant patients with concurrent systemic disease or with preeclampsia, echocardiography can provide important insights into the effect of the disease process on cardiovascular physiology and can assist in the management of individual patients. In this chapter, the normal hemodynamic and echocardiographic changes of pregnancy are reviewed and the role of echocardiography in the management of pregnant women with known or suspected cardiac disease is summarized.

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Normal Hemodynamic and Echocardiographic Changes with Pregnancy Normal Hemodynamic Changes During normal pregnancy, plasma volume, erythrocyte volume, and cardiac output increase substantially over baseline values (Fig. 31-1 (Figure Not Available) ; Table 31-1 ). Many of the original studies on the hemodynamic changes of pregnancy were based on right heart catheterization with Fick or thermodilution cardiac output data. Thus, these studies included small numbers of patients with evaluation of only a few time points during pregnancy.[1] [2] The more recent use of Doppler cardiac output measurement techniques has greatly increased our understanding of the magnitude and timing of cardiac output changes during pregnancy.[3] [4] [5] [6] Overall, cardiac output increases progressively during pregnancy by as much as 45% over baseline values.[5] [7] [8] [9] A consistent finding using noninvasive Doppler measurements is that a definite increase in cardiac output occurs as early as 10 weeks of gestation. Some studies suggest that maximum cardiac output is reached at 24 weeks' gestation, with no further increases in later pregnancy Figure 31-1 (Figure Not Available) Plasma and erythrocyte volumes increase during pregnancy. (From Pitkin PM: Clin Obstet Gynecol 1976;19:489–513.)

TABLE 31-1 -- Normal Anatomic and Hemodynamic Changes of Pregnancy Anatomic Aortic root Left ventricle

Slight increase in diameter (2–3 mm) Slight increase in end-diastolic dimension and slight decrease in end-

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Left atrium Hemodynamic Cardiac output

Stroke volume Heart rate Blood pressure Systemic vascular resistance Pulmonary artery pressure Left ventricular end-diastolic pressure

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systolic dimension Slight increase in size Increased beginning in first trimester; maximum increase (at term) of 45% over baseline value Increased Increased by 25%–30% Unchanged Decreased Unchanged Unchanged

(Fig. 31-2) . Other studies ( Fig. 31-3 and Fig. 31-4 ) show a continued increase in cardiac output throughout pregnancy, with increases in stroke volume accounting for much of the first-trimester increase, followed by a continued increase in heart rate (and thus cardiac output) in the last two trimesters. On average, heart rate increases by 25% to 30% over baseline values during pregnancy (Fig. 31-5) . [6] The underlying mechanism of the increase in cardiac output with pregnancy is presumably hormonal, but the exact sequence of events remains unclear. [10] Recent data suggest that an increase in venous tone during pregnancy contributes to preload augmentation.[4] In addition, a decrease in aortic stiffness reduces afterload.[6] The fall in systemic vascular resistance allows blood pressure to increase only slightly despite an increased stroke volume (see Fig. 31-5) . Some studies suggest that pregnancy is associated with an increased wall stress[11] however, this view is challenged by other studies that suggest that wall stress decreases by about 30%. [5] [12] Left ventricular contractility appears to be depressed in pregnancy, based on measurement of the afterload-adjusted velocity of circumferential fiber shortening.[11] [12] Left ventricular systolic performance is maintained, despite this possible decrease in contractility, because of the altered loading conditions of pregnancy. Pulmonary pressures also remain normal during pregnancy,[13] suggesting a similar decrease in pulmonary vascular resistance to balance the increased

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blood flow volume. Diastolic filling pressures in both the right and the left heart also remain normal in pregnancy.[14] Technical Aspects of Doppler Cardiac Output Measurements Doppler measurement of cardiac output in pregnancy is based on the same principles as in nonpregnant patients. Stroke volume (SV) is calculated from the cross-sectional area (CSA) of flow multiplied by the velocity time integral (VTI) of flow at that site: 681

Figure 31-2 Increase in cardiac output from the nonpregnant state throughout pregnancy. P-P, prepregnancy; PN, postnatal. (From Hunter S, Robson SC: Br Heart J 1992;68:540–543.)

SV = CSA × VTI Typically, cross-sectional area is assumed to be circular and is calculated from a two-dimensional echocardiographic diameter measurement recorded with the ultrasound beam perpendicular to the flow diameter. The velocity time integral is measured by either pulsed or continuous wave Doppler ultrasonography, with the Doppler beam aligned parallel to the flow stream. As in nonpregnant patients, it is critical that (1) diameter be measured accurately, (2) the Doppler beam be aligned parallel to the direction of blood flow, and (3) diameter and velocity data be obtained almost simultaneously from the same intracardiac site. In addition, this method assumes that flow is laminar with a relatively flat (or blunt) flow-velocity profile, and that flow fills the anatomic cross-sectional area. Whereas these assumptions appear to be warranted in nonpregnant patients according to numerous studies validating this approach[15] (see Chapter 26) , the potential effect of the altered flow conditions during pregnancy warrants re-evaluation. Specific concerns in pregnant patients include the possibility that the flow profile may not be blunt or may be asymmetric, given the higher flow volumes. Possible changes in cross-sectional flow areas during pregnancy may also affect these measurements. Validation of cardiac output measurements in pregnancy has been performed by several groups of investigators using either of two basic Doppler approaches (Table 31-2) . Some investigators have applied the technique of measuring ascending aortic flow with a continuous wave

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Doppler probe from a suprasternal approach.[16] [17] The cross-sectional area of flow is calculated from a carefully recorded A-mode aortic diameter (Fig. 31-6) measured at the sinotubular junction, the narrowest segment of the aorta, since the highest flow velocity (as obtained with continuous wave Doppler) will correspond to the smallest flow area. Doppler cardiac outputs calculated with this method correlated well with simultaneous thermodilation cardiac outputs in pregnant women undergoing right heart catheterization for clinical indications.[16] Of note, Figure 31-3 Hemodynamic changes during pregnancy and post partum. (From Mabie WC, DiSessa TG, Crocher LG, et al: Am J Obstet Gynecol 1994;170:849–856.)

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Figure 31-4 Serial changes in heart rate (A), stroke volume (B), and cardiac output (C) recorded using Doppler echocardiography in a series of 89 women with no cardiac disease and a normal pregnancy. (Data from Easterling TR, Benedetti TJ, Schmucker BC, Millard SP: Obstet Gynecol 1990;76:1061– 1069.)

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Figure 31-5 Sequential changes in mean arterial pressure (A) and a total peripheral resistance (B) in 89 women with no cardiac disease and a normal pregnancy. (Data from Easterling TR, Benedetti TJ, Schmucker BC, Millard SP: Obstet Gynecol 1990;76:1061–1069.)

serial studies in pregnant women suggest that aortic root diameter increases during pregnancy,[18] [19] so that repeat aortic diameter measurements are needed at each time point. This contrasts with the situation in nonpregnant adults in whom both left ventricular outflow tract (LVOT) and aortic diameters tend to remain relatively constant over time. Other investigators have measured cardiac output in

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TABLE 31-2 -- Validation of Doppler Cardiac Output Measurements in Pregnancy Standard Gestational Doppler of Author n Age Method Reference r Easterling 23 Third CWD TD 0.93 [16] et al trimester A-mode Ao Robson et 15 Nonpregnant PD asc Fick 0.93 [22] al Ao 2D Aoleaflets Ao Doppler 0.96 Robson et 40 Pregnant [22] al Nonpregnant MV vs. MV 0.96 PA PA 0.97

Regression Equation SEE (L/min) (L/min) Dop = 1.07 TD - 0.58

Fick = 1.0 Dop + 0.8 0.4

Ao = 1.02 0.37 MV - 0.96 Ao = 0.97 0.47 PA + 0.40 MV = 0.92 0.34 PA + 0.62 Lee et al 16 Pregnant LVOT TD 0.94 TD = 0.74 0.64 [20] LVOT + 1.91 Ao, aorta; asc, ascending; CWD, continuous wave Doppler; Dop, Doppler; LVOT, left ventricular outflow tract; MV, mitral valve; PA, pulmonary artery; PD, pulsed Doppler; SEE, standard error of estimate; TD, thermodilution; 2D, two-dimensional; Fick, Fick method of cardiac output measurement. pregnant women using standard clinical cardiac ultrasonography systems.[7] [20] [21] [22] LVOT diameter is measured from a two-dimensional parasternal long-axis view; LVOT flow is recorded via an apical approach using pulsed Doppler echocardiography, with the sample volume positioned just proximal to the aortic valve plane.[23] This method correlates well with simultaneous Fick cardiac outputs in nonpregnant patients.[15] In a group of pregnant women, internal 684

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Figure 31-6 Doppler measurement of cardiac output based on a continuous wave Doppler recording of the velocity time integral [v(t)] in the ascending aorta, heart rate (HR), and an A-mode aortic diameter (D) for calculation of cross-sectional area (CSA) at the sinotubular junction. Stroke volume (SV) and cardiac output (CO) are calculated as shown. (From Easterling TR, Watts HD, Schmucker BC, Benedetti TJ: Obstet Gynecol 1987;69:845–850. Reprinted with permission from The American College of Obstetricians and Gynecologists.)

consistency between Doppler cardiac outputs measured from diameter and flow data across the aortic, mitral, and pulmonic valves was demonstrated. [24]

Reproducibility, in addition to accuracy, is critical for the application of these methods in following individual patients during the course of pregnancy. Several studies suggest that both these methods can be performed reproducibly with an acceptable degree of recording and measurement variability in pregnant patients, with a coefficient of variation of 5% to 8%.[16] [24] [25] Numerous studies on the reproducibility of Doppler cardiac output measurements have been reported in nonpregnant patients as well. Although there is still concern that these methods have been validated against invasive standards in only small numbers of pregnant women, the data should still accurately reflect hemodynamic changes over time (if not absolute values) both in individuals and in groups of patients. Compared with the two-dimensional pulsed wave Doppler approach, the advantage of the A-mode continuous wave method is that a smaller, less expensive, dedicated instrument can be used for cardiac output measurements. Although optimal results require careful data acquisition, focused education and training of appropriate individuals allow more widespread application of this technique. Potential disadvantages include (1) the possibility of a nonperpendicular measurement of aortic root diameter (resulting in overestimation of cardiac output); (2) a nonparallel intercept angle between the Doppler beam and the direction of aortic flow (resulting in underestimation of cardiac output); and (3) failure to recognize abnormal aortic flow conditions (e.g., aortic stenosis or regurgitation) that invalidate the Doppler method. When any of these problems are suspected, a standard clinical echocardiographic examination should be performed to resolve the difficulty. M-mode and Two-Dimensional Echocardiographic Changes The increased cardiac output of pregnancy is reflected in changes in left

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ventricular dimensions, volumes, and geometry (Table 31-3) . M-mode studies show that left ventricular end-diastolic dimension increases slightly (by 2 to 3 mm on average) and end-systolic dimension is unchanged, so that there is a slight increase in fractional shortening during pregnancy.[19] [26] [27] [28] These changes in left ventricular diastolic dimension correlate with increased preload due to changes in systemic venous tone.[4] Left ventricular wall thickness also increases slightly, with a corresponding increase in calculated left ventricular mass. Similar changes in right ventricular dimensions have been noted. With two-dimensional echocardiography, a slight increase in end-diastolic volume and in ejection fraction is seen, with little change in end-systolic volume. [8] [19] , [26] [29] [30] [31] These findings are consistent with the altered loading conditions of an increased end-diastolic volume and decreased systemic vascular resistance and do not imply an increase in left ventricular contractility. There are conflicting data on the changes in contractility with pregnancy.[5] [12] [14] , [26] There have been few studies evaluating left ventricular geometry in normal pregnancy; however, no dramatic changes in ventricular shape have been observed. Several investigators have found consistent increases in aortic and LVOT diameters during pregnancy, with the magnitude of this change averaging 1 to 2 mm.[18] [32] Even this small average change is significant for accurate cardiac output calculations, and given the wide range of values, some individuals have more pronounced changes in outflow tract geometry. Left atrial anteroposterior dimension increases by about 4 mm, with the maximum change seen at term compared with a study performed several weeks post partum.[19] Changes in atrial dimension in the peripartum period are associated with changes in serum atrial natriuretic peptide levels.[33] A small increase in mitral annulus diameter has been documented in conjunction with a much larger change in tricuspid annulus diameter.[19] A small pericardial effusion is seen on echocardiography in as many as 25% of healthy pregnant women, with a higher prevalence in women with preeclampsia. [33] Doppler Flows The increases in annular diameters partially compensate for the increased

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transvalvular volume flow of pregnancy, 685

TABLE 31-3 -- Normal Echocardiographic Measurements in Pregnancy (M Changes) Measurement Modality Aortic root M-mode A-mode LVOT (cm2 ) 2D area LA dimension 2D (mm) M-mode M-mode LV EDD M-mode (mm) M-mode M-mode M-mode M-mode 2D LV ESD (mm)

M-mode

Mean ± SD 30 ± 12 25 ± 2 3.5 ± 0.3 38 ± 4 36 37 47 ± 4 46 ± 3 51 ± 3 48 49 52 ± 4 32

M-mode 29 ± 3 2D 33 ± 4

Gestational Comparison Time of Age Value Comparison Third tri 28 ± 3 2 mo pp Term

24 ± 4

10 wk

Term

3.2 ± 0.3

2 mo pp

Term

34 ± 5

2 mo pp

Term Term Term

31 33 48 ± 4

Preconception 24 wk pp 12 wk pp

24–32 wk

43 ± 3

Third tri

50 ± 4

Nonpregnant controls 2 mo pp

Third tri Term Term

45 47 50 ± 3

Preconception 24 wk pp 2 mo pp

Term

24 wk pp

Term

30 ± 2

Term

34 ± 5

Nonpregnant controls 2 mo pp

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PWT (mm)

M-mode 10 ± Term 9±1 12 wk pp 1 M-mode 7 ± 1 Third tri 6±1 2 mo pp 2D 8 ± 1 Term 7±1 2 mo pp LV mass (gm) M-mode 175 ± Term 135 ± 25 12 wk pp 37 M-mode 203 Term 157 24 wk pp M-mode 183 Term 120 Preconception M-mode 186 ± Term 151 ± 34 2 mo pp 39 FS (%) M-mode 40 ± Term 33 ± 7 12 wk pp 7 35 ± 5 2 mo pp M-mode 30 ± Term 5 LV EDV 2D 108 ± Term 102 ± 13 2 mo pp (mL) 14 LV ESV (mL) 2D 44 ± Term 44 ± 7 2 mo pp 10 EF (%) 2D 60 ± Term 57 ± 4 2 mo pp 4 RV (mm) M-mode 20 ± Third tri 18 ± 1 2 mo pp 1 M-mode 19 ± 24–32 wk 15 ± 2 Nonpregnant 3 controls Mitral annulus 2D 24 ± Third tri 21 ± 4 2 mo pp (mm) 5 Tricuspid 2D 27 ± Third tri 18 ± 3 2 mo pp annulus (mm) 3 EDD, end-diastolic dimension; EDV, end-diastolic volume; EF, ejection ESD, end-systolic dimension; ESV, end-systolic volume; FS, fractional shor LA, left atrial; LV, left ventricular; LVOT, left ventricular outflow tract; pp partum; PWT, posterior wall thickness; RV, right ventricular; tri, trimester. but increases in transvalvular flow velocities are also seen[21] (Table 31-4) . Both the maximum aortic and LVOT flow velocity increase by

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approximately 0.3 m per second compared with the nonpregnant state. Less dramatic changes in transmitral velocities are seen with an increase in E velocity of only 0 to 0.1 m per second and an increase in A velocity of only 0.1 to 0.2 m per second. However, the TABLE 31-4 -- Normal Doppler Flow Velocities in Pregnancy Measurement Modality Aorta (m/s) CWD LVOT (m/s)

Mitral E (m/s) MV-tips

Mitral A (m/s) MV-tips

E/A

Heart rate (bpm)

Cardiac output (L/min)

MV-tips

Flow Velocity 1.4 ± 0.2 1.3 ± 0.1 0.7 ± 0.2 0.9 ± 0.1 0.6 ± 0.1 0.6 ± 0.1 1.5 ± 0.2 1.3 ± 0.3 84 ± 10

Gestational Comparison Time of Age Value Comparison Term 1.1 ± 0.2 12 wk pp

89 ± 15 87 77 ± 10 6.5 ± 1.5

Term

1.0 ± 0.1

12 wk pp

Third tri

0.8 ± 0.1

2 mo pp

6–12 wk

0.8 ± 0.1

12 wk pp

Third tri

0.5 ± 0.1

2 mo pp

24–27 wk

0.5 ± 0.1

12 wk pp

Term

1.8 ± 0.2

12 wk pp

Third tri

1.6 ± 0.4

2 mo pp

Third tri

70 ± 16

2 mo pp

32–35 wk Term Term Term

69 ± 12 69 70 ± 7 4.3 ± 0.6

12 wk pp 24 wk pp 2 mo pp 2 mo pp

7.6 Term 5.0 24 wk pp CWD, continuous wave Doppler; MV, mitral valve; PD, pulsed Doppler; partum; tri, trimester.

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relative increase in E and A velocities being unequal, the E/A ratio changes from the normal pattern in young women (higher E than A with an E/A ratio of >1.5) to a pattern of equalized or reversed E/A velocities (E/A ratio of 0.45) even in the absence of increased LV mass (14 years) lead to sustained hypercholesterolemia (level >200 mg/dL). Patients with inactive SLE have high levels of VLDL and triglycerides and low levels of high-density lipoprotein. These abnormalities are worse in patients with active SLE.[55] [56] Antiphospholipid antibodies have also been associated with coronary artery disease. They produce peroxidation of low-density lipoprotein and endothelial dysfunction leading to vasoconstriction and thrombosis by release of platelet-derived growth factor and thromboxane A2 and decreased production of prostacyclin and prostaglandin I.[56] In SLE patients, angina, myocardial infarction, and left ventricular dysfunction may also result from coronary arteritis or embolization to a coronary artery.[57] Coronary arteritis should be suspected in a young patient with an acute coronary syndrome, especially if accompanied by active SLE and evidence of vasculitis affecting other organs. Coronary embolism or in situ thrombosis are rare but warrant consideration when myocardial infarction occurs with no anginal prodrome or in association with a cardioembolic substrate or an underlying procoagulant state such as elevated antiphospholipid antibodies. [35] [36] [55] [56] [57]

The echocardiographic detection of myocardial infarction is summarized in Table 34-3 . Dobutamine echocardiography is useful for detection and for risk stratification of patients with suspected or known coronary artery disease and arthritis precluding exercise testing. Newly suspected coronary artery disease may warrant coronary angiography because of the relative youth of these patients and the need for accurate risk stratification, and to guide choices of SLE treatment, such as steroids, immunosuppressives, or both if coronary arteritis is suspected.

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Pulmonary Hypertension

Pulmonary hypertension occurs in 5% to 14% of SLE patients. The most common causes include interstitial lung disease, vasculitis, and thromboembolism. Myocardial and valve disease should also be considered. Doppler echocardiography is valuable in the diagnosis, assessment of severity, and follow-up of SLE-associated pulmonary hypertension.[58] [59]

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Rheumatoid Arthritis Background Rheumatoid arthritis is a chronic autoimmune disease characterized by symmetric arthritis, potentially involving any synovial joint but usually affecting the metacarpophalangeal and proximal interphalangeal joints and wrists. In this disease, the patient's serum contains rheumatoid factor, a group of IgM or IgG antibodies directed against autologous IgG. Nonarthritic manifestations of rheumatoid arthritis include rheumatoid nodules, systemic vasculitis, glomerulonephritis, pulmonary fibrosis, and several cardiovascular diseases: pericarditis, valve disease, myocarditis, coronary arteritis, aortitis, and cor pulmonale. Clinically apparent heart disease occurs in as many as 25% of patients with rheumatoid arthritis and is more likely in patients with long-standing disease; active extra-articular, erosive polyarticular, and nodular disease; systemic vasculitis; and high serum titers of rheumatoid factor. Heart 769

disease is the third leading cause of death in patients with rheumatoid arthritis. [60] [61] Associated Cardiovascular Involvement Pericarditis

Echocardiographic studies have shown pericardial effusions in as many as 50% of rheumatoid arthritis patients, but symptomatic pericarditis is unusual.[61] [62] [63] Episodes of pericarditis tend to occur in patients with active arthritis, high serum levels of rheumatoid factor, rheumatoid nodules, an erythrocyte sedimentation rate greater than 55 mm per hour, and positive antinuclear antibodies. Immunoflurescent staining of the biopsied pericardium reveals deposits of IgG, IgM, C3, and C1q, indicating

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autoimmune injury.[64] The pericardial effusion is exudative and bloody with a low glucose level, and it may contain rheumatoid factor.[65] [66] As with SLE pericarditis, tamponade and constriction are rarely reported.[67] [68] The role of echocardiography in the diagnosis and management of rheumatoid effusions parallels its role in SLE pericarditis[69] [70] (see Table 34-3) . Valve Disease

Estimates of the prevalence of valve disease in rheumatoid arthritis are highly variable. A few early echocardiographic studies reported prevalence rates of nonspecific valve abnormalities as high as 30%.[63] [71] [72] Valve disease is probably more common in patients with erosive polyarticular and nodular disease, systemic vasculitis, and high serum titers of rheumatoid factor. Valve disease in rheumatoid arthritis occurs as leaflet fibrosis and valve granulomas. The leaflet fibrosis is indistinguishable from that seen in SLE. In contrast, valve granulomas appear to be unique to rheumatoid arthritis. [73] [74] These granulomas or nodules can also be seen on valve rings, papillary muscle tips, and atrial or ventricular endocardium. Histologically, the granulomas resemble subcutaneous rheumatoid nodules, containing a central portion of fibrinoid necrosis surrounded by a mononuclear infiltrate and sometimes by Langhans cells and giant cells. It is thought that these nodules result from a process of focal vasculitis. On an echocardiogram, rheumatoid valve nodules usually appear as small (86 msec), reduced E peak velocity (65 m per second), reduced E/A ratio (50%) Asymmetric septal hypertrophy (variable frequency)

Diastolic Dysfunction (>50%) ↓ Peak early filling velocity ↓ E/A ratio ↑ Early filling deceleration time ↑ Isovolumetric relaxation time Abnormal SVC flow

LV enlargement Increased LV mass (38–81%) RV hypertrophy E/A, early to atrial velocity; LV, left ventricular; RV, right ventricular; SVC, superior vena cava. relaxation time and abnormal left ventricular diastolic filling, characterized by reduction of early filling and augmentation of atrial contribution to filling, occur in most acromegalic patients, even in the absence of hypertension, diabetes mellitus, or coronary artery disease.[70] [71] [72] , [74] Disease duration and increased left ventricular mass are important factors in the severity of impaired left ventricular filling.[72] Abnormalities of right ventricular filling similar to those of the left ventricle also occur.[67] [71] Systolic Function and Acromegaly

In the absence of long-standing, severe acromegaly complicated by

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hypertension, coronary artery disease, or diabetes mellitus, left ventricular systolic dysfunction in acromegalic patients appears uncommon.[58] [59] [60] [61] [62] [70] [71] , In patients with short-term acromegaly uncomplicated by hypertension, coronary artery disease, or diabetes mellitus, left ventricular systolic function, as assessed by shortening fraction, stroke volume, and cardiac output, typically is enhanced.[75] However, prolonged untreated acromegaly may lead to dilated cardiomyopathy and heart failure.[76] Acromegaly is characterized by excessive apoptosis of myocytes and nonmyocytes, which correlates with the extent of impairment in ejection fraction and disease duration, possibly explaining acromegalic cardiomyopathy. [76] Echocardiographic Findings in Acromegaly

Echocardiography is well suited to delineate the protean cardiac manifestations of acromegaly (see Table 35-3) . M-mode and twodimensional echocardiographic findings include concentric left ventricular hypertrophy,[58] [59] [61] , [67] [74] 785

septal hypertrophy that may simulate hypertrophic cardiomyopathy,[60] [62] right ventricular hypertrophy,[71] and left ventricular dilation.[58] [59] [61] [63] Pulsed Doppler echocardiography of transmitral valve velocities in these patients shows a reduction of peak early filling velocity and E/A ratio and an increase in peak atrial filling velocity and deceleration time of early filling.[67] [71] [72] , [74] Abnormalities of transtricuspid valve Doppler velocities similar to those of the mitral valve are a feature of acromegaly.[67] , [71] Isovolumetric relaxation time, assessed by Doppler echocardiography, is prolonged in acromegalic patients.[67] [71] [74] Pulsed Doppler echocardiography has shown abnormal superior vena caval flow, characterized by a decrease in peak forward diastolic velocity and an increase in peak flow velocity reversal during atrial contraction.[71] These findings are consistent with biventricular diastolic dysfunction, possibly reflecting impaired ventricular relaxation. Clinical Utility

Acromegaly frequently leads to heart disease, which may be asymptomatic. Clinical studies have demonstrated that suppression of growth hormone release by octreotide acetate, a long-acting somatostatin synthetic peptide analog, in acromegalic patients significantly reduces left ventricular

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hypertrophy and reduces abnormalities of isovolumetric relaxation time and left and right ventricular filling.[77] [78] The echocardiographic evaluation of cardiac size and function in patients with acromegaly is of value to assess ventricular hypertrophy and cardiac dysfunction. Prolongation of isovolumetric relaxation time is the most sensitive echocardiographic finding of cardiac involvement in acromegaly and may be useful in the evaluation in the subclinical stage of the disease.[74] Ventricular hypertrophy and dysfunction are important indicators for aggressive treatment to control growth hormone levels as a means of improving heart disease in patients with excessive growth hormone.[68] [75] [77] , [78] Hyperparathyroidism and Heart Disease Cardiac Calcification

The major cause of death in primary hyperparathyroidism patients is cardiovascular disease.[79] [80] [81] Hypercalcemia due to primary hyperparathyroidism may induce calcification of coronary arteries,[82] valves,[83] [84] [85] and myocardium.[83] [84] [85] [86] Aortic valve calcification occurs in 46% to 63% of primary hyperparathyroidism patients, and mitral valve or submitral annulus calcification has been reported in 33% to 49% of these patients.[83] [84] [85] Aortic and mitral stenosis may result from primary hyperparathyroidism.[83] [84] Myocardial calcific deposits have been reported in 62% to 74% of patients with primary hyperparathyroidism.[83] [84] [85] Myocardial calcification mainly involves the interventricular septum and may result in third-degree heart block.[83] [84] Structure and Function in Hyperparathyroidism

Left ventricular hypertrophy is a common feature of primary hyperparathyroidism and may be caused by an excessive serum concentration of parathyroid hormone or elevated extracellular calcium concentration.[84] [85] [86] [87] [88] Partial regression of left ventricular hypertrophy may occur 6 months to 1 year after parathyroidectomy in these patients.[84] [85] , [87] [88] Primary hyperparathyroidism is associated with hypercontractile function and may be a cause of hypertrophic cardiomyopathy.[86] A reduced transmitral valve E/A ratio by pulsed Doppler echocardiography has been reported in patients with primary hyperparathyroidism and suggests that left ventricular diastolic dysfunction may be a feature of this disease.[89] [90] Echocardiographic Findings in Hyperparathyroidism

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Two-dimensional echocardiography is useful for determining the extent of myocardial and valvular calcification in patients with primary hyperparathyroidism (Table 35-4) . The presence and severity of aortic or mitral stenosis can be assessed by Doppler echocardiography. M-mode and two-dimensional echocardiographic methods are useful for evaluation of possible hypertrophic cardiomyopathy.[86] Clinical Utility

Echocardiography helps identify left ventricular hypertrophy and valvular stenosis in patients with primary hyperparathyroidism. Parathyroidectomy may promote regression of myocardial hypertrophy.[84] Adrenal Diseases and Heart Disease Cushing's Syndrome and Echocardiographic Features

Cushing's syndrome is caused by excessive secretion of adrenocortical hormones. Left ventricular hypertrophy frequently occurs in patients with this syndrome and is partially attributable to associated hypertension. An echocardiographic TABLE 35-4 -- Echocardiographic Findings in Primary Hyperparathyroidism Structural Valvular Disease Abnormalities Aortic valve calcification Myocardial calcification (46–63%) (62–74%) Mitral valve/annulus LV hypertrophy calcification (33–49%) Asymmetric septal hypertrophy Aortic stenosis Mitral stenosis LV, left ventricular.

Enhanced Systolic Function ↑ LV ejection fraction

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study showed left ventricular hypertrophy and asymmetric septal

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hypertrophy in 75% of patients with Cushing's syndrome.[91] Asymmetric septal hypertrophy in this syndrome is common and severe, with interventricular septal thickness ranging from 1.6 to 3.2 cm and the ratio of septal to posterior wall thickness ranging from 1.33 to 2.67.[91] Primary Hyperaldosteronism and Echocardiographic Features

Left ventricular wall thickening without asymmetric septal hypertrophy is a feature of primary hyperaldosteronism.[91] , [92] Several investigators have reported concentric left ventricular hypertrophy in primary hyperaldosteronism,[93] [94] [95] evidence of diastolic dysfunction as reflected by reduced mitral valve peak early filling velocity and E/A ratio, and increased atrial contribution to filling.[94] [95] Clinical Utility

Regression of left ventricular hypertrophy in Cushing's syndrome after surgical treatment frequently occurs and may be dramatic.[91] Echocardiographic findings of severe left ventricular hypertrophy or hypertrophic cardiomyopathy without obvious cause should raise the clinical suspicion of glucocorticoid excess, possibly from Cushing's syndrome. Regression of left ventricular hypertrophy may occur after surgical excision of an aldosterone-producing tumor in patients with primary hyperaldosteronism.[95]

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End-Stage Renal Disease and Heart Disease Uremic Cardiomyopathy Congestive heart failure commonly occurs in patients with end-stage renal failure.[96] The pathogenesis of heart failure in uremic patients is complex and multifactorial and may include anemia, electrolyte and acid-base abnormalities, volume overload, hypertension, coronary artery disease, and uremic toxins. Although some studies have reported normal left ventricular function in patients with uremia,[97] [98] many support the presence of a specific uremic cardiomyopathy.[99] [100] [101] [102] [103] The features of uremic cardiomyopathy include cardiac enlargement, impaired left ventricular systolic function, and ventricular hypertrophy. In addition, after renal transplantation systolic function improves, left ventricular volume decreases, and left ventricular hypertrophy regresses, independent of blood pressure control.[104] Secondary hyperparathyroidism is a suspected cause of left ventricular systolic dysfunction due to uremia.[102] Structural and Valvular Heart Disease in Renal Disease Calcification of the myocardium, valves, or cardiac skeleton is found in most patients with end-stage renal disease and is caused by derangements in calcium and phosphorus metabolism.[105] [106] [107] [108] [109] Calcification of the aortic valve has been reported in 28% to 31% of patients with end-stage renal disease.[108] [109] Mitral annular calcification has been described in 10% to 36% of patients on dialysis. [107] [108] A recent study using transesophageal echocardiography with enhanced two-dimensional resolution has shown that calcification may also occur in "atypical" areas such as the base of both mitral leaflets and intervalvular fibrosa.[110] Aortic valve regurgitation is a feature of renal failure and is explained by valvular calcification[109] [111] it occurs in 13% of renal failure patients.[109] Mitral regurgitation may occur in 38% of renal failure patients and may be caused by mitral annular calcification or left ventricular dilation.[109]

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Tricuspid and pulmonic insufficiency occur with the same frequency as do mitral and aortic regurgitation, respectively, in patients with chronic renal failure.[109] [112] However, the mechanism of right-sided valvular regurgitation consists of increased pulmonary artery pressures from mitral regurgitation as opposed to valvular calcification.[109] , [113] Calcific aortic and mitral stenoses are important valvular abnormalities of renal failure. Occasionally, aortic and mitral stenoses may rapidly progress in patients with chronic renal failure, possibly because of associated secondary hyperparathyroidism.[114] Pericardial disease from renal failure may manifest as pericardial effusion, pericardial thickening, or cardiac tamponade.[106] Concentric left ventricular hypertrophy or asymmetric septal hypertrophy may be seen in renal failure patients with or without associated systemic hypertension.[115] [116] [117] [118] In renal failure patients with secondary hyperparathyroidism, eccentric left ventricular hypertrophy may occur, characterized by left ventricular dilation and normal wall thickness. [119]

Diastolic Function and Renal Disease Left ventricular diastolic dysfunction as assessed by Doppler echocardiography is associated with renal failure and may persist after renal transplantation. [120] [121] Echocardiographic Findings in Renal Disease Structural or valvular abnormalities of the heart detectable by echocardiography occur in most patients with end-stage renal disease and may include atrial or ventricular dilation; concentric hypertrophy; asymmetric septal hypertrophy; mitral annulus calcification; aortic and mitral valve calcification; myocardial calcification; aortic, mitral, tricuspid, and pulmonic valvular regurgitation; aortic and mitral valve stenosis; and pericardial effusion ( Fig. 35-6 and Fig. 35-7 , Table 35-5 ).[99] [100] [101] [102] [103] [105] [106] [107] [108] [109] [111] [112] [113] [114] [115] [116] [119] Despite the many echocardiographic features of end-stage renal disease, none are diagnostic of a specific structural or valvular abnormality or of cardiomyopathy due to renal failure. Hemodialysis is a commonly used treatment in patients with end-stage renal disease. An acute reduction in intravascular volume is associated with hemodialysis. It is not unanticipated that this treatment would significantly alter loading conditions. Left ventricular end-diastolic diameter derived by

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M-mode echocardiography may decrease on average by 4 mm after hemodialysis.[122] The decrease in left ventricular end-diastolic diameter after hemodialysis 787

Figure 35-6 Transthoracic two-dimensional parasternal long-axis view in a patient with chronic renal failure demonstrating associated mitral annular calcification (MAC), pericardial effusion (PE), a calcified aortic valve (arrow), and hypertrophy of the septal (SW) and posterior (PW) left ventricular walls.

results from a decrease in early filling without a compensatory increase in atrial contribution to filling, as assessed by transmitral valve Doppler echocardiography. [122] The influence of hemodialysis on systolic function, as assessed by M-mode or two-dimensional echocardiography, or both methods, is complex and may be influenced by dialysate composition,[123] dialysis-induced changes in serum Figure 35-7 Two-dimensional short-axis (A) and continuous wave (B) Doppler echocardiography of the mitral valve in a patient with chronic renal failure demonstrating mitral stenosis from encroachment upon the mitral orifice by mitral annular calcification (MAC). The planimetered mitral orifice area (A) was 2.77 cm2 , and the peak gradient by modified Bernoulli equation was 10 mm Hg. IW, inferoposterior wall; PE, pericardial effusion; SW, septal wall.

TABLE 35-5 -- Echocardiographic Findings in Renal Disease Structural Valvular Disease Abnormalities Aortic valve calcification Concentric LV (28–31%) hypertrophy Mitral annular calcification Eccentric LV hypertrophy (10–36%) Aortic regurgitation (13%) LV enlargement Mitral regurgitation (38%) Asymmetric septal hypertrophy

Systolic Dysfunction ↑ LV ejection fraction

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Aortic stenosis Mitral stenosis Tricuspid regurgitation Pulmonic insufficiency

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Atrial enlargement Pericardial effusion Pericardial thickening Myocardial calcification

LV, left ventricular. electrolytes,[124] left ventricular mass,[125] and previous treatment with a beta antagonist.[125] Systolic function after hemodialysis, as assessed by echocardiographically derived shortening fraction, left ventricular ejection fraction, velocity of circumferential fiber shortening, or ratio of fractional shortening to end-systolic stress, may be enhanced,[123] [124] [125] [126] depressed, [125] [126] or unchanged.[122] [123] [127] Doppler echocardiographic findings of diastolic dysfunction in patients with renal failure include reduced transmitral peak early filling velocity and E/A ratio and prolonged isovolumetric relaxation time.[120] [121] Ultrasonic backscatter of myocardium in renal failure is increased, reflecting cardiac calcification (Fig. 35-8) (Figure Not Available) .[128] Clinical Utility Echocardiography is a useful noninvasive method of evaluating patients with end-stage renal disease who present 788

Figure 35-8 (Figure Not Available) Illustration of ultrasonographic videodensitometric analysis of myocardium in end-stage renal disease. Left panels show digitized two-dimensional echocardiographic images of the left ventricle (parasternal long-axis view) of a control subject, a hypertensive patient, and a dialysis patient. The graph on right demonstrates variation in echocardiographic intensity in the region of interest placed at the posterior wall level during one cardiac cycle divided into 12 frames for the control (closed circle), hypertensive (open rectangle) and dialysis (closed triangle) groups. Time 0 is end-diastolic frame and time 4 is endsystolic frame. (From Di Bello V, Panichi V, Pedrinelli R, et al: Nephrol Dial Transplant 1999;14:2184–2191.)

with cardiovascular symptoms. An accurate diagnosis of the cause of congestive heart failure in renal failure patients on the basis of clinical assessment is challenging. Congestive heart failure in renal disease patients is frequently multifactorial and could be diagnosed on the basis of

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congestive cardiomyopathy, inadequate ventricular hypertrophy, valvular regurgitation, or stenosis. Pericardial effusion with secondary cardiac tamponade could simulate congestive heart failure. M-mode, twodimensional, and Doppler echocardiography are useful in the diagnosis of the many structural and valvular abnormalities that may cause heart failure in the renal failure patient. Echocardiography is useful for predicting survival in chronic dialysis patients.[129] Echocardiographic assessment of left ventricular size and function is a significantly better predictor of prognosis than clinical evaluation or electrocardiographic findings.[129] Patients on dialysis with abnormal left ventricular systolic function and dilated left ventricular cavities have a poor prognosis, with one study reporting a mean survival of 7.8 months in such patients.[129] A prospective study using serial echocardiography has shown that improvement in renal failure-related cardiac abnormalities (e.g., left ventricular hypertrophy and systolic dysfunction) 1 year after the patient starts dialysis is associated with an improved cardiac outcome over a mean follow-up period of 41 months.[130] Thus, serial echocardiography adds prognostic information beyond the initial study, a potentially important application of echocardiography in the evaluation of patients with end-stage renal disease. Systemic hypotension induced by hemodialysis is occasionally serious or life threatening. In patients with dialysis-induced hypotension refractory to conventional therapy, echocardiography helps assess potential causes of hypotension after dialysis, such as intravascular volume depletion, impaired systolic function, or a hyperdynamic state with secondary intraventricular obstruction. Patients with impaired early left ventricular filling and a short duration of early filling are at higher risk for hemodynamic instability during hemodialysis and may be identified prospectively by Doppler echocardiography.[131] In the preoperative evaluation for renal transplantation, echocardiography is useful for predicting patient and renal graft survival.[132] M-mode echocardiographically derived increased left ventricular end-systolic diameter (≥4.0 cm) and a decreased shortening fraction (4.0 cm, shortening fraction 70 years) was compared with the youngest group (21–30 years). The mean septal thickness and LV free-wall thickness increased from 9.8 and 10.1 mm, respectively, in the youngest group to 11.8 mm (for both) in the oldest group, an increment of 20% and 18%, respectively. An estimated 15% increase in LV mass was observed; however, between these extremes in age, wall thickness showed only minimal changes, such that the mean values for septal and free-wall thickness increased by only 0.3 mm for each decade between the third and seventh decades. A study by Pearson et al[3] of 53 healthy normotensive subjects (21 men and 32 women, 25–75 years of age) demonstrated that posterior wall thickness

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(10 mm vs. 8 mm, P < .05) was significantly greater in elderly than in younger subjects. These results supported previous investigations. In each of these echocardiographic studies, LV end-diastolic and endsystolic cavity dimensions showed little or no changes with increasing age. The increases in LV mass associated with aging resulted largely from increases in wall thickness rather than cavity enlargement. The Cardiovascular Health Study,[6] involving a cohort of 5201 men and women over 65 years of age, investigated the effects of age, gender, hypertension, and coronary heart disease (CHD) on LV mass and systolic function in the elderly. LV mass adjusted for body weight increased modestly with age (P < .001), increasing less than 1 g/y for men and women. After adjusting for body weight, LV mass was significantly greater in men than in women, and greater in participants with clinical CHD compared with participants with neither CHD nor hypertension (P < .001).

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TABLE 36-1 -- Distribution of Mean Left Ventricular Mass, WeightAdjusted Left Ventricular Mass, and Blood Pressure Among Obese and Nonobese Participants by Disease Status

Parameter Nonobese Patients LV mass (g)

Neither Clinical Heart Disease nor Clinical CHD Hypertension Hypertension MEN WOMEN MEN WOMEN MEN WOMEN 188.2 135.6 P

Weight-adjusted LV mass 195.4 148.3 (g) Systolic BP (mm Hg) 132.7 138.7

165.7 131.0 P

156.7 116.4 P

172.7 139.6

161.1 120.2

146.0 145.2

121.0 119.2 P

Diastolic BP (mm Hg)

69.2 68.1

75.0 71.2

67.2 P 64.8 P

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Obese Patients LV mass (g) 197.6 160.0 198.8 152.9 172.6 132.2 Weight-adjusted LV mass 179.3 140.8 186.5 139.0 157.7 121.1 (g) Systolic BP (mm Hg) 134.7 138.8 144.4 143.4 124.2 120.7 Diastolic BP (mm Hg) 70.9 68.6 75.7 71.5 69.4 67.4 BP, blood pressure; CHD, coronary heart disease; LV, left ventricular. Adapted from Gardin JM, Siscovick D, Anton-Culver H: Circulation 1995;91:1739–1748. Reproduced with permission. Copyright 1995 American Heart Association. P < 0.001. P < 0.01. P < 0.05 for nonobese versus obese participants. All comparisons were performed separately for each age-disease group combination.

The weight-adjusted LV mass and blood pressure values for obese and nonobese participants are listed by disease status in Table 36-1 (see also Chapter 32) . Weight-adjusted LV mass was significantly higher for men (P < .001) and for subjects with CHD than for other groups. Participants with hypertension had significantly higher LV mass than those without hypertension or clinical CAD. LV mass increased with age (P < .001), but as seen in Figure 36-1 , after adjusting for weight, the age effect was small. The minimal effect of age in this study may reflect the highly truncated age range; no subjects were younger than 65 years. Gardin et al[6] developed reference equations for calculating the expected LV mass of men or women, in grams: LV mass (men) = 16.6 [weight (kg)]0.51 LV mass (women) = 13.9 [weight (kg)]0.51 If the ratio of observed-to-expected LV mass is between 0.69 and 1.47, the patient's LV mass should not be considered larger than expected for his or her body weight. Chamber Dimensions

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The influence of aging on LV cavity dimensions are shown in Table 36-2 and Figure 36-2 . There is a minor decrease or no change seen in LV internal dimensions with age. [1] A significant increase in the aortic root and left atrial dimensions occurs with age, specifically when the oldest group (>70 years) is compared with the youngest group (21–30 years).[1] [2] [3] [4] [8] Changes in aortic and left atrial dimensions are outlined in Figure 36-3 and Figure 36-4 and Table 363 . It is important to consider these age-related changes when taking echocardiographic measurements of the size of the left atrium to make quantitative statements about the effect of various diseases such as hypertension and coronary artery disease. Cardiac Valves Aging is associated with morphologic changes of the cardiac valves, most prominently on the aortic and mitral valves and is presumably related to increased ventricular systolic pressure.[7] [8] [9] [10] A review of necropsy data of 765 patients revealed that all indexed mean valve circumferences increased progressively throughout adult life, although this trend was greater for semilunar than for atrioventricular valves. The mean circumference of the aortic valve surpassed that of the pulmonic valve in the fourth decade and approached that of the mitral valve.[7] Krovetz[10] Figure 36-1 Bar graph shows weight-adjusted mean left ventricular (LV) mass displayed by sex (women on left, men on right for each age group) and disease status group across 5-year age intervals. Data are computed using the lower age end point and the mean weight for each age category (65–69, 70–74, 75–79, 80–84, 85+ years). Weight-adjusted LV mass was significantly associated with sex, disease status, and age. Of interest, within each age group the magnitude of the sex effect exceeded that of the effect of the disease (e.g., clinical coronary heart disease [CHD], hypertension [HTN]). (From Gardin JM, Siscovick D, Anton-Culver H: Circulation 1995;91:1739–1748.)

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TABLE 36-2 -- Mean Values of Echocardiographic Parameters for Three Age Groups Group I (25–

Group II

Group III

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Parameter Mitral valve E-F slope (mm/sec) Aortic root, diastole (mm) LV wall thickness (mm) Systolic Diastolic Systolic/m2 Diastolic/m2

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44 yr) 102.3 ± 3.7 (52) 30.9 ± 0.6 (45)

(45–64 yr) 79.0 ± 3.8 (35) * 32.0 ± 0.6 (34)

(65–84 yr) 67.1 ± 5.2 (18) † 32.9 ± 0.8 (17) ‡

15.4 ± 0.5 17.6 ± 0.7 18.8 ± 0.6 (33) (15) (12) * 8.7 ± 0.3 (33) 9.8 ± 0.5 (16) 10.7 ± 0.5 (13) * 7.6 ± 0.3 (33) 9.2 ± 0.3 (15) 10.0 ± 0.4 † (12) † 4.3 ± 0.1 (33) 5.0 ± 0.2 (16) 5.7 ± 0.2 (13) *

†§

LV dimension (mm) Systolic

34.4 ± 1.1 32.1 ± 0.89 32.1 ± 1.4 (37) (17) (11) Diastolic 51.8 ± 1.03 50.8 ± 1.3 51.2 ± 1.4 (37) (17) (11) 17.3 ± 0.5 16.7 ± 0.5 16.8 ± 0.6 Systolic/m2 (37) (17) (11) 26.0 ± 0.5 26.4 ± 0.6 27.0 ± 0.7 Diastolic/m2 (37) (17) (11) Fractional shortening of the 0.34 ± 0.01 0.36 ± 0.01 0.37 ± 0.02 minor semiaxis (37) (17) (11) VCF (circ/sec) 1.17 ± 0.04 1.23 ± 0.04 1.30 ± 0.08 (37) (17) (11) LV, left ventricular; VCF, velocity of circumferential fiber shortening. Adapted from Gerstenblith G, Frederiksen J, Yin FCP: Circulation 1977;56:273–277. * P < 0.01 as compared with group I. The number of subjects is given in parentheses next to the mean and standard error of the mean. † P < 0.001 as compared with group I. ‡ P < 0.05 as compared with group I. § P < 0.05 as compared with group II.

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reviewed published reports of aortic annulus size measured at autopsy. When corrected for body surface area, the aortic annulus size was found to increase with age in both men and women after 20 years of age.[10] Aging is also associated with thickening and calcification of the aortic and mitral valves. Calcific deposits are common in the bases of the aortic cusps, at the margins of closure on the atrial aspect of the mitral leaflets, and in the mitral valve annulus.[7] [8] [9] [10] [11] [12] [13] [14] [15] [16] Many elderly patients have calcific deposits in the aortic valve cusps, the mitral valve annulus, and the epicardial coronary arteries; this triad of calcific deposits is known as the "senile calcification syndrome."[8] Sahasakul et al[9] demonstrated that the mean thickness found at various sites of the aortic and mitral valves, as measured in 200 autopsy specimens, increased significantly (P < .001) with age. In subjects over 60 years of age, the valves were more than twice the thickness of those under 20 years.[9] Figure 36-2 Left ventricular (LV) end-diastolic and end-systolic dimensions in millimeters versus age in years. For each age group the mean and 95% prediction intervals for normal values are depicted. (From Gardin JM, Henry WL, Savage DD, et al: J Clin Ultrasound 1979;7:439–447.)

Mitral annular calcification (MAC) is a degenerative process that increases with age and occurs more frequently in women than in men (Fig. 36-5) .[7] [8] In a prospective study of 976 unselected elderly persons in a long-term health care facility (mean age, 82 ± 8 years; range, 62–103 years), conducted with technically adequate M-mode and two-dimensional (2D) echocardiograms of the mitral valve, MAC was detected in 402 (57%) of 714 women and 124 (47%) of 262 men.[14] The prevalence of MAC with increasing age in elderly men and women is shown in Table 36-4 .[14] The amount of calcium may vary from a few spicules to a large mass located behind the posterior leaflet, often forming a ridge or ring that encircles the mitral valve. Calcification Figure 36-3 Aortic root dimension in late diastole is plotted in millimeters versus age in years. The mean value for each age group is depicted by a circle plotted at the mean age in the age group. The

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bracket and shaded area on either side of the circle represents the interval for normal values for a subject with a body surface area (BSA) of 1.8 m2 . The 95% prediction intervals are also shown for subjects with BSA values of 1.4 m2 (dotted lines) and 2.2 m2 (solid lines). (From Gardin JM, Henry WL, Savage DD, et al: J Clin Ultrasound 1979;7:439–447.)

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Figure 36-4 Left atrial dimension in late diastole in millimeters versus age in years. For each age group the mean and 95% prediction intervals for normal values are depicted. (From Gardin JM, Henry WL, Savage DD, et al: J Clin Ultrasound 1979;7:439–447.)

may interfere with normal cyclic changes in annular size and, in conjunction with mechanical stretching of the leaflets, can cause mitral regurgitation, which is usually mild.[16] [17] MAC may restrict leaflet motion, but actual calcification of leaflets and mitral stenosis is rare.[15] , [17] Although the annular calcium is covered with a layer of endothelium, ulceration of the lining can expose underlying calcific deposits, which may serve as a nidus for platelet aggregation and subsequent thromboembolism. [14] In patients with endocarditis associated with MAC, the avascular nature of the annulus predisposes to periannular and myocardial abscesses. Calcific deposits in the aortic valve are common in elderly persons and may lead to valvular aortic stenosis. In an autopsy series, calcific deposits on the aortic valves were found in 22 (55%) of 40 patients between 90 and 103 years of age.[18] In a prospective 2D echocardiographic study of subjects 62 years and older, a calcified aortic valve was detected in 22 (18%) of 119 men and 67 (19%) of 354 women.[19] Calcific aortic stenosis was observed in 12% of the elderly; it was mild in 10% (Doppler-derived peak gradient < 25 mm Hg), moderate in 6% (peak gradient 20 to 49 mm Hg), and severe in 2% (peak Doppler gradient > 30 mm TABLE 36-3 -- Data Describing the Left Ventricular Outflow Tract and Aortic Valve in Different Age Groups Age Group (yr)

55–71

75–76

80–81

85–86

P Value

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Parameter (n=76) (n=197) (n=155) (n=124) Left ventricular 19.9±2.3 † 18.5±2.6 17.9±2.7 17.8±3.0 outflow tract diameter (mm) Peak velocity in left 101±17 90±19 90±20 93±25 ventricular outflow tract (cm/sec) Peak velocity across 126±27 127±53 131±53 143±55 aortic valve (cm/sec) 0.82±0.11 0.76±0.19 0.75±0.20 0.71±0.21 Velocity ratio ‡ 2.56±0.63 2.07±0.72 1.91±0.74 1.77±0.75 Aortic valve area (cm2 ) Adapted from Lindroos M, Kupari M, Heikkila J, et al: J Am Coll Cardiol 1993;21:1220–1224.

0.000

0.002 0.001 0.000

* Significance (P) values refer to comparison between age groups with the KruskalWallis test. † Data are presented as mean value±standard deviation. ‡ Velocity ratio is equal to the peak velocity in the left ventricular outflow tract divided by the peak velocity across the aortic valve.

Hg). The frequency of aortic stenosis increases with age. Lindroos et al[20] reported the prevalence of aortic valve abnormalities detected by echocardiography in 552 older subjects. Mild calcification was found in 40% and severe calcification in 13% of subjects. Critical aortic stenosis (aortic valve area < 0.8 cm2 ) existed in 2.2%, and aortic regurgitation, mostly mild, was found in 29% of subjects. LV outflow and aortic flow velocities also change with age (see Table 363) . There is a statistically significant decrease in LV outflow tract diameter and velocity while aortic valve area also decreases with age. In contrast, aortic velocity increases with age.

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Normal Changes in Left Ventricular Function Systolic Function Previous studies evaluating age-associated changes in cardiovascular function have demonstrated that resting LV systolic function is maintained with advancing age.[21] [22] [23] [24] [25] Noninvasive investigations using Mmode echocardiography in healthy elderly subjects screened for cardiovascular disease have consistently revealed that LV ejection fraction, percentage of fractional shortening, and cardiac output are preserved with aging. [21] [23] Animal model studies indicate that contractile function is maintained with aging. Lakatta et al[22] demonstrated in isolated rat papillary muscle that resting tension, peak active isometric tension, and maximal rate of tension development were similar in young and senescent cardiac muscle. Similarly, Yin et al[23] showed that contractile function in the intact dog heart is not altered with age. LV systolic function has also been evaluated by Doppler aortic-flow velocity parameters. Gardin et al[24] studied the relationship between age and Doppler aortic-flow velocity measurements in 97 healthy adults (45 men and 52 women, 21 to 78 years of age) who were carefully screened for cardiac disease by history, cardiac examination, electrocardiography, chest radiography, and M-mode and 2D echocardiography. Multiple linear regression analysis showed that the aortic peak flow velocity, aortic average acceleration, and aortic flow velocity integral were all significantly lower in subjects 61 to 70 years of age than in those 21 to 30 years of age (all P < .001). This 801

TABLE 36-4 -- Prevalence of Mitral Annular Calcification

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Age (yr) Men Women 7/35 (20) * 62–70 4/22 (18) * 71–80 13/42 (31) 40/116 (34) 81–90 44/75 (59) 146/226 (65) 91–100 19/22 (86) 56/63 (89) 101–103 3/3 (100) Adapted from Aronow WS, Koenigsberg M, Kronzon J, et al: Am J Cardiol 1987;59:181–182. * Number affected per total number, with the percentage affected given within parentheses.

study concluded that the age-related decrease in aortic peak velocity and aortic flow velocity integral resulted partly from the increases in aortic root diameter that occurred with aging. Pearson et al[3] demonstrated similar results in a study involving 53 healthy subjects. These observations are relevant to differentiating the normal aging heart from certain pathologic states. For example, patients with dilated cardiomyopathy have markedly reduced aortic peak flow velocities, flow velocity integrals, and average acceleration parameters compared with normal subjects.[25] These age-dependent changes must be kept in mind when using Doppler aortic flow parameters in evaluating LV performance. Diastolic Function Unlike the preserved systolic function, age-related alterations in LV diastolic function have been demonstrated in the healthy elderly population. [26] [27] [28] [29] [30] [31] [32] [33] [34] [35] [36] [37] [38] [39] Earlier investigators using Mmode echocardiography revealed a decrease in the E–F slope (closing velocity of the mitral valve) and E/A ratio (ratio of early-to-late diastolic flow velocity).[34] Later studies using Doppler echocardiography showed that aging is associated with changes in mitral Doppler flow velocity.[35] [36] [37] [38] There is a progressive increase in end-diastolic transmitral flow velocity (A) and a decrease in the E/A ratio. Gardin et al[34] studied the relationship between age and pulsed Doppler transmitral flow velocity measurements in 66 adults between 21 and 78

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years of age who were without evidence of cardiovascular disease. These researchers demonstrated that aging is associated with progressive decreases in early diastolic transmitral peak flow velocity (E) and early diastolic deceleration. They detected progressive increases in A and mitral A/E (Fig. 36-6) . These findings concur with a study by Miyatake et al,[35] which reported that the ratio of peak velocity in the atrial contraction phase to the peak velocity in the rapid filling phase showed a significant increase with aging (r = 0.82, P < .001). Pearson et al[3] reported a doubling of the percentage of atrial contribution (37% vs. 19%, P < .0001) and a halving of ratio of peak early to peak atrial (E/A) velocity (0.85 vs. 1.77, P < .01), which was similar to the atrial contribution found by Arora et al[33] with the use of radionuclide angiography (36% for a mean age of 75 years; 16% for a mean age of 26 years). The preponderance of data demonstrates that normal aging is associated with alterations in LV diastolic performance: an age-related decline in early diastolic LV filling, with a compensatory, increased contribution of atrial systole to maintain adequate resting ventricular filling volume. Because congestive heart failure increases in prevalence with age and an estimated 40% of adult patients with cardiac failure have symptoms resulting from diastolic LV dysfunction, it is essential to define and detect LV diastolic dysfunction in order to provide appropriate therapy (see Chapter 6) . The availability of reference Doppler diastolic indices may provide an alternative modality for the identification of LV dysfunction in the elderly. Using the original Framingham Figure 36-5 Mitral annular calcification in left parenteral long-axis (top) and short-axis (bottom) views. Ao, aortic root; LA, left atrium; LV, left ventricle; MAC, mitral annular calcification.

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Figure 36-6 Doppler mitral flow velocity recordings from a young 32-yearold normal subject (top) and an older 82-year-old normal subject (bottom). The peak velocity in early diastole (E) is lower and the late diastolic velocity (A) is higher in the older subject than in the younger subject.

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Heart Study population, Sagie et al[39] established reference values for various Doppler parameters (Table 36-5) based on a large cohort of rigorously defined healthy subjects (26 men and 88 women between 70 and 87 years of age). This study demonstrated that TABLE 36-5 -- Mean and Percentile Values of Doppler Diastolic Filling Indices for 114 Study Subjects Over 70 Years of Age Lower Median Upper Percentiles Percentiles Percentiles Diastolic Indices Mean 5% 10% 50% 75% 90% 95% E-velocity (m/sec) 0.44 0.25 0.26 0.41 0.51 0.69 0.76 A-velocity (m/sec) 0.59 0.38 0.43 0.56 0.68 0.80 0.84 E/A (ratio) 0.76 0.48 0.52 0.70 0.86 1.05 1.21 E/A TV1 (ratio) 1.36 0.79 0.90 1.33 1.57 1.76 1.94 AFF (ratio) 0.40 0.29 0.32 0.40 0.44 0.49 0.52 AT (sec) 0.06 0.02 0.03 0.05 0.07 0.08 0.09 DT (sec) 0.14 0.09 0.10 0.14 0.16 0.19 0.23 AFF, atrial filling fraction; AT, acceleration time; DT, deceleration time; A-velocity, peak velocity A; E-velocity, peak velocity E; E/A, ratio of early-to-late peak velocities; E/A TV1, ratio of early-to-late timevelocity integrals. Modified from Sagie A, Benjamin EJ, Golderisi M, et al: J Am Soc Echocardiogr 1993;6:570–576. 87% of the elderly population had peak velocity E/A ratios of less than 1.0, 75% had values less than 0.86, and 25% had values less than 0.62. Because healthy, younger subjects frequently have peak velocity E/A ratios greater than 1.0, it may be inappropriate to apply reference values based on younger subjects to elderly populations for assessment of diastolic LV dysfunction. The exact mechanisms responsible for these age-related diastolic alterations are not fully known, but multiple factors have been postulated. Normal physiologic and morphologic changes of aging that could contribute to the decreased early diastolic filling include prolonged isovolumic relaxation secondary to delayed calcium uptake by the sarcoplasmic reticulum; increased ventricular stiffness from quantitative and qualitative changes in the myocardial collagen and fibrous tissue content; sclerosis of the mitral

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leaflets with subsequently prolonged diastolic closure time; and an increase in LV wall thickness, and an increase in afterload. As the elderly population increases, recognition of the normal ageassociated changes in cardiovascular structure and function becomes imperative for assessing cardiac disease in the elderly. Aging changes seen in the normal older population are summarized in Table 36-6 . Response to Stress and Exercise Exercise capacity declines with age because of a blunted heart rate response to the stress.[21] The stroke volume and cardiac output, however, are maintained because of a larger increase in LV end-diastolic volume and a decrease in end-systolic volume during exercise.[21] [40]

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Clinical Value of Echocardiography in the Older Population Left Ventricular Hypertrophy Data from the Framingham study indicate that LV hypertrophy determined from M-mode echocardiographic mass is an independent predictor of mortality and morbidity from coronary heart disease and stroke.[41] [42] [43] Since echocardiographic LV mass is the gold standard for diagnosing LV hypertrophy, it is important to define 803

TABLE 36-6 -- Summary of Aging Changes Seen on Echocardiography Parameter Left ventricular mass Left ventricular dimensions Left atrial size Aortic root size Left ventricular systolic function Left ventricular diastolic function (E/A) Mitral annular calcification Aortic valve calcification or stenosis ↑, increase; ↓, decrease.

Change ↑ Normal ↑ ↑ Normal ↓ ↑ ↑

normal limits for age, body weight, and gender, according to criteria established by Gardin et al.[6] Inter- and intraobserver variability in the measurement of LV mass should be defined for each echocardiographic laboratory.

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Congestive Heart Failure Heart failure is a common problem in the elderly. Many elderly persons with heart failure have normal or only slightly reduced LV systolic function. [44] Proper definition and accurate detection of LV diastolic dysfunction are needed to provide appropriate treatment for patients with congestive heart failure. Because Doppler echocardiography is commonly used to assess LV diastolic dysfunction, it is important to know the reference values for Doppler indices of diastolic function in the elderly. The reference values established by Sagie et al[39] should be used. In the Cardiovascular Health Study, Gardin et al[45] examined patterns of LV diastolic filling in several subgroups of elderly subjects. As demonstrated in other studies, peak early velocity on transmitral Doppler examination decreased, peak late velocity increased, and the early-to-late velocity ratio decreased with advancing age and hypertension. In multivariate analyses, congestive heart failure caused by LV systolic dysfunction was associated with an increase in early and late diastolic velocities as well as an increase in the early-to-late velocity ratio compared with age-matched normal subjects. This difference is likely related to an increase in early left atrial-to-LV pressure difference.[45] Diagnosis of Coronary Artery Disease LV segmental wall motion abnormalities indicating coronary artery disease are as accurate in the elderly as they are in younger patients. Wall motion abnormalities affect a high percentage of the older population, including almost 2% of those without overt coronary disease, 43% of patients with hypertension alone, and 18% of patients with coronary disease who are living in the community.[6] Because this prevalence of coronary artery disease is high among older women, the prevalence of wall motion abnormalities is also high. Stress echocardiography is safe and accurate for diagnosis of ischemic disease in the elderly ( see also Chapter 13 and Chapter 14 ). In a preliminary study of 93 patients over 65 years of age (mean, 72 years), including 34 patients with acute myocardial infarction, dobutamine-stress echocardiography (DSE) was performed without any complication; it had a sensitivity of 85% and a specificity of 94%. The peak dose of dobutamine was not significantly different from that administered in patients younger than 61 years (authors' unpublished data, 2001). Hiro et al,[46] in a study that examined results and safety of DSE in the elderly, found no significant

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difference in the prevalence of positivity between age groups but found more frequent asymptomatic hypotension and ventricular arrhythmias in subjects older than age 75 years. Valvular Heart Disease There is a high prevalence of aortic valve disease among the elderly. [47] [48] In 35 patients with ejection systolic murmur, nonsignificant aortic stenosis (peak gradient < 20 mm Hg) was found in seven, significant aortic stenosis (peak gradient > 30 mm Hg) in seven, and mitral regurgitation in seven.[44] Aronow and Kronzon[48] reported the prevalence of aortic stenosis to be 12% for 721 patients with a mean age of 82 ± 8 years. Severe aortic stenosis affected 2%, moderate aortic stenosis affected 6%, and mild stenosis affected 2% of these patients.[48] Otto and Pearlman[49] demonstrated that Doppler echocardiography was cost-effective for the diagnosis of aortic stenosis in the elderly. The incidence of mitral valve prolapse and MAC also is higher in this group of patients. Mitral valve prolapse is a common cause of isolated mitral regurgitation in the elderly.[4] Previous analyses have shown that aortic valvular stenosis is associated with adverse cardiovascular outcomes. The echocardiographic diagnosis of aortic sclerosis, in the absence of hemodynamically significant valvular obstruction, has also been found to be associated with significant cardiovascular morbidity and mortality. Otto et al[50] found an increase of approximately 50% in the risk of death from cardiovascular causes and the risk of myocardial infarction. The clinical factors associated with degenerative calcific aortic valve disease are also similar to the risk factors for atherosclerosis; factors include advanced age, male gender, present smoking, and hypertension.[51] Thromboembolism Cardiogenic embolism is the presumed cause of ischemic strokes in 20% of patients. Potential cardiac sources of emboli more specific to the elderly are arteriolosclerotic intra-aortic debris and MAC. Both of these represent arteriolosclerosis, which is more prevalent in the elderly. In the previously cited analysis by Otto that examined the association of aortic valve sclerosis with cardiovascular mortality and morbidity, the risk of stroke, when adjusted for age and gender, was increased by 30%.[50] The rates of other cardiogenic embolic phenomena such as those associated with LV

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thrombus, left atrial thrombus, vegetation, atrial myxoma, and paradoxical emboli, are the same as for younger subjects. Amyloidosis

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Senile amyloidosis is a frequent postmortem finding in patients over 80 years of age. It is an infrequent cause of heart failure and syncope. Echocardiographic criteria for the diagnosis of amyloidosis include increased myocardial echogenicity and wall thickness, myocardial speckle, increased atrial septal thickness, and thickened valves (see Chapter 28) . These criteria however, have not been validated in the elderly, who may have thickened valves due to aging, and the characteristics of amyloid protein are different from those of the primary amyloidoses.

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Cost-Effectiveness of Echocardiography Echocardiography is cost-effective compared with other noninvasive and invasive imaging techniques. Otto and Pearlman[49] developed a noninvasive diagnostic approach and tested it prospectively in 77 patients with symptomatic aortic stenosis. They reported a sensitivity of 98%, a specificity of 89%, and a total error rate of 3.9%. They concluded that this approach could have resulted in cost savings between 24% and 34% compared with an invasive diagnostic approach. Although their study did not specifically target the older population, presumably a similar diagnostic approach could be applied to the elderly. Although LV function, pericardial disease, and coronary disease can be evaluated with other noninvasive imaging techniques such as nuclear imaging and magnetic resonance imaging, echocardiography is the least expensive. No data are available to determine the cost-benefit ratio and outcome analysis of echocardiography in the elderly population. Echocardiography, however, appears to be cost effective in the elderly because a correct diagnosis allows optimizing therapy and enhancing clinical decision making. Echocardiography differentiates normal aging changes from pathologic changes. Additional studies are needed to define changes in the right ventricle and to assess the impact of echocardiography on the management of elderly patients.

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806

Chapter 37 - Echocardiographic Evaluation of the Patient with a Systemic Embolic Event Edmond W. Chen MD Rita F. Redberg MD

Cerebrovascular Ischemia Stroke, a sudden development of a focal neurologic deficit, remains the third leading cause of death in the United States. There were 600,000 strokes that resulted in 280,000 deaths and over 1 million hospitalizations, in 1997 alone. [1] With 4.4 million survivors today, the medical and social costs are estimated to range between $15 and $30 billion annually.[2] Five percent to 13% of strokes occur in patients younger than 45 years of age[3] up to 40% of strokes occur in patients without occlusive cerebrovascular disease; and it is estimated that the source is of cardiac origin in 15% to 20%.[4] Another 30% to 40% (100,000 to 200,000 per year) are in the category of stroke of undetermined cause, also known as cryptogenic stroke. [5] [6] An increasing number of echocardiographic findings have been found in this group of cryptogenic stroke patients and in patients with embolic stroke (Table 37-1) . Cardiac tumors can be a source of emboli, but the most commonly implicated sources are thrombi from the left atrial appendage or left ventricle, left atrial spontaneous contrast, atrial septal aneurysm associated with a patent foramen ovale (PFO), thrombi traversing a PFO (i.e.,

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paradoxical emboli), valve vegetations (infected or sterile), fibrinous mitral valve strands, protruding aortic atheroma of the aortic arch and ascending aorta, and emboli associated with mitral and aortic prostheses. Echocardiography is most helpful in defining the cause of cerebrovascular ischemia in patients without occlusive cerebrovascular disease. This chapter discusses indications for, clinical value of, and the limitations of transthoracic, transesophageal, and contrast echocardiography in this setting; particular emphasis is placed on the utility and insights provided by transesophageal echocardiography (TEE) in cases of stroke and the impact of echocardiography on patient management.

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Transthoracic Echocardiography Indications As with other diseases, the work-up for an embolic event includes taking the patient's history, performing a TABLE 37-1 -- Stroke Occurrence by Type Type of Stroke Atherosclerotic thrombosis Lacunae Embolism Hemorrhage Vascular Indeterminate

Occurrence (%) 20 5–10 20 10–20 5 35–40

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physical examination, and obtaining an electrocardiogram (ECG), often followed by a carotid duplex ultrasound. If significant carotid stenosis is identified, some centers proceed with magnetic resonance angiography, with or without cerebral angiography and endarterectomy. In the search for a cardiac source of emboli, the history and physical examination can be helpful in deciding which patients should undergo an echocardiogram. In the group without occlusive cerebrovascular disease, findings in the history, such as myocardial infarction, congestive heart failure, rheumatic heart disease, prosthetic valve replacement, or atrial fibrillation or flutter, become more conclusive when combined with findings from an echocardiographic examination for the source of embolus.

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[7]

Similarly, the yield of data is augmented if there are findings in the physical examination that suggest left ventricular dyskinesia, cardiac enlargement, left-sided valvular regurgitation, mitral stenosis, or a midsystolic or late systolic click. An ECG examination showing features of atrial fibrillation, transmural myocardial infarction, or left atrial enlargement increases the probability for a cardiac source of emboli. If there is no evidence of cardiac disease indicated by the history, physical examination, or ECG, the yield of findings from a transthoracic echocardiogram (TTE) for the identification of a source of lesions usually is less than 1%.[7] [8] [9] [10] [11] A pooled analysis of 13 studies found that TTE yielded a source incidence of 0.7% in patients with no cardiac history; in patients with clinical cardiac abnormalities, the yield increased to 13%.[12] In a review of 280 patients between 19 and 96 years of age who underwent TTE for assessing suspected systemic emboli, Come et al[7] found a 35% incidence of abnormalities that might have predisposed patients to systemic embolism and a 4% incidence of lesions that were possibly or probably responsible for emboli. If patients were classified according to clinically evident cardiovascular disease, the incidence of findings in the group with cardiovascular disease was 47% TABLE 37-2 -- Echocardiographic Evaluation of Cardiac Source of Embolus

Left ventricular thrombus Vegetation, mitral or aortic (>10 mm) Myxoma

H&P Factors that Increase the Likelihood of this Finding Mitral valve disease, atrial fibrillation CAD, history of myocardial infarction Fever, weight loss, changing murmurs Systemic symptoms

Possible Source of Embolus Patent foramen ovale

No specific

Probable Source of Embolus Left atrial thrombus

Atrial septal aneurysm No specific

Best Age Diagnostic Group Test Any TEE age >50 yr TTE Any age Any age

TEE (preferred)/TTE TTE/TEE

60 yr Any age Any age >55 yr

TTE TEE TEE TTE TTE

No specific or decreased exercise tolerance No specific

65 years), a growing body of data implicates atheromas in the aorta as a source of embolic events, which may increase the yield of TEE findings in this group as well. Findings and Techniques Left Atrial Size

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Transthoracic echocardiography is an excellent method to evaluate left atrial size. The left atrial diameter can be measured in the parasternal longaxis and short-axis views by M-mode or directly from the 2D image (online or offline), using commercially available measurement packages. Normally, the left atrial diameter is less than 4.0 cm. Measurements of left atrial diameter should be made at end-systole, from leading edge to leading edge. M-mode echocardiography has been shown to predict angiographic left atrial area,[15] but it has limitations that compromise accurate volume estimates. Two-dimensional apical imaging correlates well with cinecomputed tomographic measurements of atrial volume.[16] [17] [18] The left atrium is best imaged in the two- and four-chamber apical views, with the patient in steep left recumbency, and with suspended respiration. Atrial volume can then be calculated by a single-plane area-length method from each view or by using the biplane method of discs. Normal left atrial

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volume is approximately 36 mL, or 20 mL/m2 . This volume is increased in athletes.[17] The atrial appendage, especially in enlarged atria, can sometimes be visualized in the apical views. Occasionally, a particularly large thrombus can be seen in the enlarged left atrium by TTE (Fig. 37-1) . The sensitivity of TTE for the detection of left atrial thrombus is 25% to 57% overall and 63% to 83% for left atrial cavity thrombus. Specificity is 94% to 99%, as confirmed at surgery. Most thrombi occur, however, in the left atrial appendage, which is a posterior structure, and the sensitivity of TTE for detecting left atrial appendage thrombi drops to 0% to 16%. An enlarged left atrium, particularly in a patient Figure 37-1 Left atrial thrombus seen in four-chamber apical view on TTE. This 78-year-old woman had severe congestive cardiomyopathy with a giant left atrium and was in atrial fibrillation. There was no intrinsic mitral valve disease. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

with atrial fibrillation, may have an intra-atrial thrombus, suggesting the need for TEE to better visualize left atrial appendage thrombus or the need for presumptive anticoagulation. Mitral Annular Calcification

Despite a number of studies that have suggested an association between mitral annular calcification and stroke,[8] [11] [19] [20] [21] [22] [23] [24] the role of mitral annular calcification in stroke remains unclear. In an analysis of Mmode echocardiograms in 1159 members of the Framingham study, Benjamin et al[25] contended that mitral annular calcification was an independent risk factor for stroke, especially embolic stroke. This association was maintained in subjects without atrial fibrillation, congestive heart failure, or clinically apparent coronary artery disease. These authors postulated that the mechanism may be calcific emboli or that the mitral annular calcification may serve as a nidus for thrombus.[25] In another prospective study of 2148 subjects, patients with mitral annular calcification were more likely to suffer a cerebrovascular event, with a risk ratio of 2.6 (P = .001). This risk was further increased in the presence of mitral stenosis and atrial fibrillation[24] however, the Stroke Prevention in Atrial Fibrillation (SPAF)-II trial of 568 patients failed to find such an association. [26] A more recent prospective cohort study of 657 patients with

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mitral annular calcification identified by 2D echocardiography showed no increased incidence of stroke.[27] Mitral annular calcification is easily detected by TTE. Using 2D criteria, it is best identified in the same views in which the mitral valve is seen: the parasternal long-axis and short-axis views, as well as the two- and fourchamber apical views. Mitral annular calcification is visually defined as increased echodensity in the mitral annulus, which is a C-shaped structure and distinct from the mitral valve. Annular calcification occurs posteriorly, may extend toward the base of the heart, and can appear to infiltrate the myocardium. Extensive mitral annular calcification can obscure visualization of the thin mitral valve leaflets and can cause decreased mitral valve excursion, although usually not severe mitral stenosis. Mitral annular calcification can be graded as mild, moderate, or severe. Autopsy studies reveal this condition in approximately 10% of patients. [28] [29] It is associated with obesity, elevated systolic blood pressure, aging, aortic stenosis, and hypertrophic obstructive cardiomyopathy. It is found predominantly in elderly women, with an incidence of 12% in women over 70.[28] Mitral annular calcification occurs earlier in renal dialysis patients, and it may be associated with the presence of aortic atheroma as well.[30] [31] Left Ventricular Wall Thickness

Left ventricular mass index has been identified as an independent risk factor for carotid atherosclerosis in normal and hypertensive subjects.[32] Roman et al[32] studied a group of 486 adults without cardiovascular disease, using 809

echocardiography to determine left ventricular mass and carotid ultrasound for measurement of common carotid artery dimensions and detection of carotid atherosclerosis. Patients with left ventricular hypertrophy were twice as likely to have carotid atheroma (35% vs. 18%; P < .01). As with left atrial size, left ventricular mass can be measured by M-mode echocardiography or 2D planimetry. Left Ventricular Wall Motion

Transthoracic echocardiography is an excellent method for evaluating left ventricular wall motion abnormalities in most patients. Exceptions are

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patients with technically difficult echocardiographic windows, those with chronic obstructive pulmonary disease, or very obese patients. The anterior septum and inferior wall are well seen in the parasternal long-axis view; the anterior, anteroseptal, posterior, lateral, and septal walls are seen in the parasternal short-axis view; the inferoseptal, septal, lateral, apical, and anterolateral walls are seen in the four-chamber apical view; and the inferior and anterior walls are visualized in the two-chamber apical view. Regional wall motion abnormalities are an indicator of ischemic heart disease. The identification of wall motion abnormalities, particularly of an aneurysm, greatly increases the likelihood of finding an associated left ventricular thrombus. Left Ventricular Thrombus

Transthoracic echocardiography also is the best imaging modality for detecting intracardiac thrombus in the left ventricle. These masses generally are seen in the setting of wall motion abnormalities, particularly anterior and apical, or cardiomyopathy. Identification of an aneurysm in the apical view necessitates a careful search by the echocardiographer for the presence of apical thrombi. Thrombi are visually defined as a distinct mass of echoes in the left ventricular cavity that are seen clearly throughout the cardiac cycle in at least two different echocardiographic views. They appear as irregular sessile or mobile structures that are contiguous with the endocardium in an area of abnormal wall motion, such as ischemic or infarcted myocardium (Fig. 37-2) . Thrombi are best seen in the four-chamber apical view by TTE, because the transducer is closest to the cardiac apex in this view. Identification of thrombi can be made more certain by using off-axis views that are directed toward or across the apex. In some cases, the transducer may be directed inferiorly or caudally across the apical impulse location. We call this maneuver the "backhanded" apical view. In this process, it is best to use a high-frequency transducer (3.5 or 5 MHz). This view combined with the use of a higher-frequency transducer increase the examiner's ability to detect apical thrombus. Ventricular thrombus should be associated with a wall-motion abnormality in the same location. Rarely, thrombi may form in the left ventricle, in the setting of transient ischemia or coronary spasm, with normal wall motion seen by echocardiography. Thrombi also are seen in patients with dilated cardiomyopathies secondary to ischemic Figure 37-2 Left ventricular apical thrombus seen in the two- (left) and

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four-chamber (right) views in TTE from a 56-year-old man with ischemic cardiomyopathy. The thrombus appears as a cap adherent to the apex. (Courtesy of Ray Stainback, MD.)

or nonischemic causes. These patients have diffuse hypokinesis, generally with an ejection fraction of less than 30%, and the thrombus is most often found in the apical third of the left ventricle. Flow patterns in the left ventricle can predict thrombus formation after myocardial infarction. An abnormal Doppler-flow pattern is highly associated with the formation of thrombus. In a study of 62 patients, no patient with a normal Doppler-flow pattern seen within 24 hours of myocardial infarction went on to develop a thrombus.[33] In this study, oral anticoagulation did not prevent the formation of thrombus, although it did decrease significantly the incidence of peripheral embolization in patients with left ventricular thrombus. The incidence of embolization from ventricular thrombus in dilated cardiomyopathy is approximately 1% to 4% per year.[4] [34] [35] [36] [37] The independent risk factors for stroke are low ejection fraction, older age, and the absence of aspirin or anticoagulation therapy. Thrombi that are protruding and mobile are most likely to embolize.[38] In the latest consensus recommendation for the management of chronic heart failure, the panel did not endorse routine anticoagulation, emphasizing that "in the absence of definitive trials, it is not clear how anticoagulants should be prescribed in patients with heart failure."[35] The European Society of Cardiology, while acknowledging the lack of data in this area, suggested that anticoagulation "may be advisable in selected patients with large hearts and a low ejection fraction."[39] Echocardiography is useful in this setting to identify thrombi and to target patients who may benefit from anticoagulation.[4] [19] [34] [37] , [38] , [40] Patients known to be at high risk for embolization, such as those in atrial fibrillation or those with a history of previous embolization, should also undergo anticoagulation therapy. Definitive recommendations addressing the need for anticoagulation therapy for patients with dilated cardiomyopathy and normal sinus rhythm await results of clinical trials such as WATCH and WARCEF (see "Studies in Progress"). In cases of anterior myocardial infarction, embolic risk is greatest in the first 3 months after the infarction.[41] [42] [43] [44] [45] [46] After that period, the clot has organized and is less of an

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810

embolic risk, and 40% of clots resolve spontaneously.[47] More recent data suggest an increased incidence of stroke long after the initial infarction. In the Survival and Ventricular Enlargement (SAVE) trial, 2231 patients with left ventricular dysfunction following an episode of myocardial infarction were prospectively followed for a mean of 42 months.[48] During the study, 4.6% of these patients experienced strokes, with an estimated 5-year rate of stroke of 8.1%.[48] Presently, anticoagulation therapy is recommended following myocardial infarction in patients unable to take aspirin, patients with persistent atrial fibrillation, and patients with left ventricular thrombus. The American College of Cardiology and American Heart Association Task Force on acute myocardial infarction considers anticoagulation therapy a class II indication in patients with extensive wallmotion abnormalities, paroxysmal atrial fibrillation, or severe left ventricular dysfunction, with or without congestive heart failure.[49] Chronic anticoagulation therapy in patients with left ventricular dysfunction or dilated cardiomyopathy remains controversial.

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Transesophageal Echocardiography Indications Transesophageal echocardiography offers higher resolution imaging than TTE because the adjacent, airless imaging pathway allows the use of 5- to 7.5-MHz probes. This TABLE 37-3 -- Transthoracic versus Transesophageal Echocardiography in Evaluation of Cardiac SOE in Patients with Cerebral Ischemia

Studies Cujec[51]

No. Patients 63

Mean Yield Age ± of SD Yield TEE (Range of TTE n in yr) n (%) (%) 63 ± 15 -0 -0 (18– 87)

de Belder

131

—

[52]

— Pearson[56]

59 (17– 84)

+9 (14) +26 (41)

72 (55)

92 (70)

Patients with Clinical Findings Heart Seen by Disease n TEE Only (%) ASA/PFO— 24 (38) 2 LAA thrombus—1 Myxoma MV—2 PFO—18 53 (40)

SEC—27 Vegetation— 2 12 (15) 45 ASA/PFO— (57) 9 -7 (19) -15 LASEC—13 (39)

41 (52)

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Comess[59]

Lee[55]

Pop[57] †

Hofmann

153

[54]

+5 (12) +30 LA clot—6 (73) 62 -6 (30) -18 — (60) +9 (19) +35 (76) 63 ± 13 0 26/50 LA/LAA (Except (52) clot—5 MAC) (20– LA/LV 82) SEC—9 MV strands—11 60 -0 (0) -5 (9) LAA thrombus—2 +6 (32) +6 LAA mass— (32) 1 Ao dissection— 1 MVP—1 42 -20 -49 Intracardiac (19) (46) masses (16– +35 +39 60) (76) (88)

46 (70)

29 (58)

19 (26)

46 (30)

84 (cerebral ischemia) 50 (peripheral embolus) 19 (retinal ischemia) Ao, aorta; ASA, atrial septal aneurysm; LA, left atrium; LAA, left atrial appendage; MV, mitral valve; MVP, mitral valve prolapse; SEC, spontaneous echo contrast; LV, left ventricle; MAC, mitral annular calcification; PFO, patent foramen ovale.

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* All patients had transient ischemic attack or cerebrovascular accident unless otherwise noted. -, patients without cardiovascular disease; +, patients with cardiovascular disease. † TEE showed thoracic aortic plaque in 32 patients (44%).

advantage becomes particularly evident when studying structures close to the probe, such as the left atrium (and left atrial appendage) and thoracic aorta. All series that compare TTE with TEE show that the latter is superior for identifying potential sources of arterial emboli (Table 37-3) . [10] [14] , [50] [51] [52] [53] [54] [55] [56] [57] For example, Pearson et al,[10] in a study of 79 patients, found that the yield of potential sources of embolism rose from 15% to 57% when comparing TTE with TEE in patients known to have preexisting cardiac disease, and from 19% to 39% in those patients without pre-existing cardiac disease. The data for the effect of age on the usefulness of TEE in evaluating emboli are evolving. As stated previously, patients with no cardiac disease have an extremely low likelihood of positive findings on TTE, generally less than 1%. Even though TEE is superior to TTE in identifying potential sources of emboli in patients without known cardiac disease, overall yield is increased to only 1.6% in a pooled analysis.[32] Thus, patients with a history of ischemic stroke and who are under 45 to 55 years of age tend to have a low overall yield as well. Although some authorities recommend TEE evaluation of embolic events as the initial diagnostic test for patients younger than 45 to 55 years of age with no other heart disease,[3] [14] others do not recommend such an approach.[12] In any case, this age group is less likely to have occlusive cerebrovascular disease. Findings best visualized by TEE, such as PFO, atrial septal aneurysm, atrial septal defect, and spontaneous contrast, have been associated with embolic events in this group of patients. All comparative studies show a higher 811

TABLE 37-4 -- Grading of Aortic Plaques Class Characteristics

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I II III IV

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Normal intima Minimal intimal thickening Raised irregular plaque 3 mm) of the bellies of the anterior and posterior mitral leaflets above the annulus, with the coaptation point at or above the annular plane in the four-chamber apical view; (3) increased mitral leaflet thickness (>5 mm); and (4) pathologic mitral regurgitation. Ischemic neurologic events were previously thought to be highly correlated with mitral valve prolapse, especially in patients under 45 years of age. [192] [193] Some of these studies, however, were done using M-mode criteria for mitral valve prolapse. By these criteria, 7% to 21% of a healthy population were defined as having mitral valve prolapse. Since then, there has been more accurate definition of mitral valve prolapse using 2D criteria. Using the currently accepted criteria for mitral valve prolapse, the association between mitral valve prolapse and ischemic neurologic events is no longer seen. Earlier studies found mitral valve prolapse in up to 40% of younger patients with stroke or transient ischemic attack, but Gilon et al found mitral valve prolapse in only 1.9% to 2.7% of younger patients, using accepted 2D criteria. Furthermore, this case-control study of 213 patients 45 years of age or younger suggested that mitral valve prolapse was not associated with an increased incidence of stroke.[194] In a population-based

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cohort study of 1079 residents of Olmsted County, Minnesota, patients with echocardiographic diagnosis of mitral valve prolapse between 1975 and 1989, without prior stroke or transient ischemic attack, were followed until the development of their first stroke. Patients with mitral valve prolapse had a twofold increase of incidence of stroke (standardized morbidity ratio, 2.1; 95% confidence interval, 1.3 to 3.2). After adjustment of risk factors such as age, diabetes, congestive heart failure, atrial fibrillation, and mitral valve replacement, however, no association between mitral valve prolapse and stroke was seen. Of note, the mean age at initial stroke was 78 years of age.[195] In subsequent follow-up of 49 patients with mitral valve prolapse and a history of ischemic stroke, no increased incidence of recurrent stroke was identified.[196] More recently, in the offsprings of the Framingham Heart Study, mitral valve prolapse was seen in 2.4% of 3491 subjects. The natural history, as in other studies, was benign, with no increase in ischemic stroke risks.[197]

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Studies in Progress Warfarin Antiplatelet Recurrent Stroke Study The Warfarin Antiplatelet Recurrent Stroke Study (WARSS)[198] is a randomized, double-blind, multicenter study funded by the National Institute of Neurological Disease and Stroke. It enrolled 2206 patients from 1993 to 1998. The average age of patients enrolled was 63 ± 11 years; 41% were female and the population was ethnically diverse. Patients all underwent TTE and were randomized to warfarin or aspirin and followed for recurrent embolic events for a minimum of 2 years. Results showed no difference in recurrent stroke or death for either of the two treatment arms. For major secondary outcomes, there was no difference in recurrent stroke or death or major hemorrhage. Subgroup analysis showed no difference when analyzed by race, ethnicity, gender, or baseline stroke subtype. Overall, the result favored aspirin, with an 11% benefit over warfarin; however, this difference was not statistically significant (www.conferencecapture.com/cc/aan; accessed July 26, 2001). Patent Foramen Ovale in Cryptogenic Stroke Study The Patent Foramen Ovale in Cryptogenic Stroke Study (PICSS)[198] is a substudy of WARSS. The study focuses on 500 patients with cryptogenic stroke. This subset of patients undergoes TEE for identification of PFO. This group is followed separately and may be randomized in future trials for surgical or percutaneous closure of the PFO. Results will be available in 2002. Warfarin-Aspirin Reduced Cardiac Ejection Fraction Study Warfarin-Aspirin Reduced Cardiac Ejection Fraction Study (WARCEF) [199] is a randomized, double-blind,

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823

multicenter study with a target enrollment of 2860 and mean follow-up of 3 years. Patients with low ejection fractions are randomized to warfarin or aspirin. The primary outcome is death, recurrent stroke, or intracerebral hemorrhage. Warfarin and Antiplatelet Therapy in Chronic Heart Failure Warfarin and Antiplatelet Therapy in Chronic Heart Failure (WATCH) [199] is a randomized, multicenter study of patients with a history of congestive heart failure and low ejection fraction. The patients are randomized to warfarin, aspirin, and clopidogrel. Primary outcome includes death, stroke, and myocardial infarction.

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Attribution of Embolic Events to a Cardiac Source Approximately 20% of strokes are thought to result from a cardiac source of embolism, and 40% are of undetermined origin, but an increasing number in the latter category have been associated with the various echocardiographic findings discussed in this chapter. Despite the strong association between echocardiographic findings of a source of embolus and stroke, it remains difficult to show a true cause-and-effect association. The scientific difficulty was demonstrated in a paper by Sansoy et al.[200] This group at the University of Virginia compared two groups of patients, one group undergoing echocardiography who had embolic events versus an age-matched group undergoing echocardiography but with no history of embolic events. It was observed that the incidence of echocardiographic findings believed to be cardiac sources of emboli, such as left ventricular thrombus and left atrial appendage thrombus and PFO, were similar in these two groups. This observation led the authors to question whether the finding of a cardiac thrombus in a patient with stroke is unrelated to the cause of the stroke. Because we must make medical decisions with the best data we have available, the findings of a probable source of embolus by echocardiography in a patient with embolic events is strong enough evidence to mandate anticoagulation therapy, preferably with warfarin. The finding of a possible source of embolus by echocardiography in a patient with embolic events, based on currently available data, also suggests a benefit from anticoagulation with aspirin or warfarin, preferably aspirin. More definitive recommendations for this group can be made when the results of large, randomized trials such as WARSS are available.

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Influence of Echocardiographic Evaluation on Patient Management Several studies have examined how echocardiographic evaluation of patients with embolic events influences patient management. In the Value of Transesophageal Echocardiography (VOTE) study, 847 of the 3001 patients underwent TEE because of a history of cerebrovascular accident or transient ischemic attack; TEE led to a change in clinical management of 27% of patients and a change in drug regimen for 15.7% in this group. This was a higher percentage of change in drug regimen (14.1%) but a lower percentage of change in clinical management (38.5%) than for the group as a whole. The data suggested that TEE is useful for determining the management of patients with cerebrovascular ischemia, particularly in establishing pharmacologic therapy.[201] In the Significance of Transesophageal Echocardiography in the Prevention of Recurrent Stroke (STEPS) study, 242 patients with unexplained cerebral ischemia underwent TEE and were followed for 1 year. Recurrent stroke occurred in 17 of 132 (13%) of the patients in the aspirin group versus 5 of 110 (5%) of the patients receiving warfarin (P 1 year) atrial fibrillation, rheumatic mitral valve disease, and prominent left atrial enlargement (>6.0 cm), however, are far less likely to be maintained in sinus rhythm after conversion.[54]

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Detection of Atrial Thrombi in Atrial Fibrillation Atrial fibrillation is believed to be responsible for almost half of cardiogenic thromboembolism. Several large, multicenter, randomized studies have now confirmed the beneficial effect of chronic anticoagulation (International TABLE 38-1 -- Characteristics of Patients at Risk for Atrial Thrombi *

Total number Age (yr)

Left No Left Entire Atrial Atrial P Group Thrombus Thrombus Value 70 463 533 † 71.6 ± 70.7 ± 71.7 ± 13.2 .55 13.0 14.0 45.9 54.3 44.4 .16 60.0 64.3 59.1 .49 4.4 ± 9.3 5.8 ± 15.4 3.9 ± 8.0 .18 8.3 28.9 7.3 .003

Gender (% female) First episode of AF (%) Duration of AF (wk) History of thromboembolism (%) Left atrial SEC (%) 48.0 85.5 36.9 .0001 Left atrial dimension (cm) 4.6 ± 0.7 4.7 ± 0.7 4.6 ± 0.7 .29 Mitral regurgitation (0–3 +) 1.3 ± 0.9 1.2 ± 0.6 1.3 ± 0.9 .35 Left ventricular dysfunction 40.9 60.7 38.1 .002 (%) AF, atrial fibrillation; SEC, spontaneous echocardiographic contrast. * Data presented are mean value ± SD. † TEE could not be completed in six patients. Data for these six are excluded.

Normalized Ratio [INR] 2.0 to 3.0) in patients with atrial fibrillation[55] [56] [57] [58] [59] for clinical stroke prevention. Since transthoracic echocardiography is so limited for the assessment of atrial thrombi,[14] [15] [16] data on the prevalence of left atrial thrombi was not available until the introduction of TEE. Among patients presenting with atrial fibrillation of greater than 2 days' or of unknown duration, we found atrial thrombi in 13%,[60] [61] of which more than 92% were left atrial thrombi and nearly all

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of these involved the left atrial appendage. These data are similar to those reported by others,[62] [63] [64] but higher than the approximately 6% incidence of clinical thromboembolism following cardioversion without anticoagulation.[65] [66] [67] [68] This apparent discrepancy can be explained by the fact that some thrombi may not migrate and some embolic events may be clinically silent.[69] Patients at particularly high risk for atrial thrombi (Table 38-1) included those with rheumatic mitral valve disease, depressed left ventricular systolic function, recent thromboembolism,[70] and TEE evidence of severe left atrial spontaneous echocardiographic contrast and complex aortic debris.[71] Duration of atrial fibrillation and left atrial dimension are not predictive of left atrial thrombi.[60] [61] In contrast to data suggesting that moderate or worse mitral regurgitation is protective against clinical thromboembolism,[72] [73] we have found that mitral regurgitation is not protective against left atrial thrombi (see Table 38-1) among those with new onset atrial fibrillation.[60] Immediate cardioversion is generally advocated for patients with atrial fibrillation of less than 24 hours' duration,[74] under the assumption that the prevalence of atrial thrombi in this group was very low. This common teaching was challenged when Stoddard et al[75] reported a 14% prevalence of atrial thrombi among patients with atrial fibrillation of less than 3 days' duration and a prevalence of 27% in those with a duration 3 days or more in a predominantly male population. In contrast, we found an incidence of clinical thromboembolism following cardioversion (without antecedent TEE or prolonged warfarin anticoagulation) of less than 1% among patients with atrial fibrillation of less than 2 days' duration.[76] Thus, prolonged warfarin or screening TEE are likely not needed in this group (unless they have a history of thromboembolism, severe left ventricular dysfunction, or mitral 835

stenosis). Although we perform cardioversion of atrial fibrillation of less than 48 hours' duration without prolonged warfarin or screening TEE, we do initiate therapeutic anticoagulation at presentation (rather than delaying anticoagulation until the patient has been in atrial fibrillation for 48 hours). As might be expected, atrial thrombi are more common among patients with atrial fibrillation who present with acute thromboembolism. In our experience, residual left atrial thrombi are found in more than 40% of these

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patients.[77] Right atrial thrombi appear to be far less common among patients with atrial fibrillation and represent less than 5% of all atrial thrombi.[60] [61] [78] Right atrial spontaneous echocardiographic contrast is distinctly unusual. It is seen in only 10% of patients with atrial fibrillation[60] but is highly predictive for right atrial thrombi. Chronic Atrial Fibrillation and Predictors of Thromboembolism

Compared with patients who present with new-onset atrial fibrillation and undergo TEE prior to cardioversion, risk factors of thromboembolism differ in patients with chronic atrial fibrillation. Left ventricular systolic dysfunction is among the strongest independent predictors of thromboembolism in patients with chronic atrial fibrillation.[70] The TEE substudies of the Stroke Prevention in Atrial Fibrillation Investigators Committee (SPAF) III study[71] have extended echocardiographic indexes known to be associated with thromboembolism to include dense spontaneous echocardiographic contrast, depressed (2 days') duration had demanded that these patients receive several weeks of anticoagulation before cardioversion, followed by several weeks of anticoagulation after cardioversion while atrial mechanical function recovers.[80] [81] Although no randomized and only two prospective studies[62] [67] have been reported, 3 to 4 weeks of warfarin therapy appears to decrease the risk of an embolic event following cardioversion to less than 1.6%.[62] [67] [68] Use of warfarin, however, carries a risk of major (2%) and minor (10-20%) hemorrhagic

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complications.[62] [80] In addition, many patients develop a subtherapeutic INR during the month leading to cardioversion. For these individuals, the warfarin dose is increased and the "1-month clock" restarted. Finally, conventional therapy leads to a delay in cardioversion for the majority of patients who do not have an atrial thrombus, and a second hospitalization is needed later for cardioversion. Rationale and Advantages

The risks and benefits of a TEE-guided approach to cardioversion are summarized in Table 38-2 . A TEE-guided approach to early and safe cardioversion has several advantages over traditional strategies for hospitalized patients with atrial fibrillation. Currently, up to 8 weeks of oral anticoagulation are recommended with cardioversion,[74] [80] [81] including 3 to 4 weeks before and after cardioversion. This period of anticoagulation exposes patients to a significant risk of a hemorrhagic complication[62] [80] by doubling the exposure of systemic anticoagulation. For unclear reasons, the atrial fibrillation population appears to be at increased risk of hemorrhagic complications during the second month of anticoagulation.[62] Early cardioversion offers physiologic advantages over traditional therapy. A shorter duration of atrial fibrillation prior to cardioversion is among the strongest predictors for long-term maintenance of sinus rhythm.[46] Almost 60% of patients hospitalized for atrial fibrillation at our hospital[60] [61] have been in atrial fibrillation for less than 1 month. For these individuals, traditional treatment of 3 to 4 weeks of anticoagulation prior to cardioversion serves to more than double the total period of atrial fibrillation prior to cardioversion. Early cardioversion may also lead to a more rapid return to normal atrial function. The time required for return of atrial mechanical function is directly related to the duration of atrial fibrillation prior to cardioversion.[81] [82] Patients with atrial fibrillation less than 2 weeks prior to cardioversion appear to have complete return of atrial TABLE 38-2 -- Benefits and Risks of Transesophageal Echocardiography (TEE)-Guided Cardioversion Benefits Shorter initial duration of atrial fibrillation Enhanced recovery of atrial mechanical function More rapid resolution of symptoms of congestive heart failure

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Increased likelihood that sinus rhythm will be maintained(?) Greater success of pharmacologic cardioversion(?) No need to return for elective cardioversion after 1 month of warfarin anticoagulation Shorter total duration of atrial fibrillation Fewer hemorrhagic complications Lower cost for warfarin medication and monitoring Fewer thromboembolic events than conventional therapy(?) More cost-effective than conventional therapy Identify high-risk population that requires lifelong warfarin regardless of clinical risk factors(?) Risks TEE "misses" clinically relevant thrombi that subsequently migrate and cause stroke/thromboembolism Morbidity associated with TEE Cost of TEE

836

mechanical function within 24 hours of cardioversion, whereas those with atrial fibrillation of 2 to 6 weeks require a week and those with atrial fibrillation for more than 6 weeks require up to 3 weeks. With elimination of a transthoracic echocardiogram, a TEE approach to guide early cardioversion also appears to have cost savings.[83] Finally, a TEE approach may also reduce the incidence of thromboembolism after cardioversion. The "costs" of the TEE approach include the morbidity of TEE, cost of TEE, and risk that TEE will not be adequate to identify atrial thrombi, which subsequently migrate and cause clinical events. Current Data

We reported on our experience with a TEE-guided approach (Fig. 38-6) to early cardioversion among 533 patients with atrial fibrillation of unknown or prolonged duration who underwent precardioversion TEE in the absence of prolonged chronic anticoagulation.[60] [61] [78] Seventy-six

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Figure 38-6 Schematic of the transesophageal echocardiographic protocol. AF, atrial fibrillation; CV, cardioversion; PTT, partial thromboplastin time. (From Manning WJ, Silverman DI, Keighley CS, et al: J Am Coll Cardiol 1995;25:1356.)

atrial thrombi were identified in 70 patients (13%). Of the 463 without TEE evidence of thrombi, 413 (89%) were successfully cardioverted to sinus rhythm, all without prolonged anticoagulation, and 1 (0.2%; 95% CI, 0 to 0.8%) experienced a clinical thromboembolic event. The one adverse event occurred in an elderly woman with mild mitral stenosis who presented 1 week after cardioversion with a brachial artery embolus. She had been therapeutically anticoagulated between TEE and presentation with the adverse event.[61] None of the 70 patients with atrial thrombi were cardioverted, but five (7%) died during the index hospitalization. Repeat TEE to document resolution of atrial thrombi was recommended for all with atrial thrombi, with cardioversion only after documentation of thrombus resolution. Other prospective studies using a similar anticoagulation regimen have shown similar results. Stoddard et al[64] reported on 82 patients scheduled for elective cardioversion of atrial fibrillation. Atrial thrombi were identified in 837

13% of patients. Sixty-six of 71 patients without atrial thrombi underwent successful cardioversion and no patient experienced a clinical embolic event. The pilot study data from the Assessment of Cardioversion Using Transesophageal Echocardiography (ACUTE) trial reported no thromboembolic complications among 47 patients treated with an anticoagulation strategy similar to ours.[62] Finally, data from the 1222patient, multicenter, randomized ACUTE trial were recently reported,[64] [84] which demonstrated "equivalence" for the TEE and the conventional approaches. The ACUTE trial directly compared conventional therapy of 4 weeks of warfarin with a strategy of anticoagulation followed by TEE and early cardioversion if no atrial thrombi are seen. While these reports are encouraging, several adverse events have occurred among patients with a "negative" TEE for atrial thrombi who have undergone early cardioversion using monoplane TEE or in the absence of

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systemic anticoagulation. [85] Many underwent electrical cardioversion several days or weeks following TEE with no anticoagulation during this interval. For these patients, it is impossible to exclude the possibility that atrial thrombi may have formed either between the TEE and cardioversion, or even after cardioversion. Impaired atrial mechanical function,[86] impaired atrial appendage function,[87] [88] or new spontaneous contrast[64] [88] have all been documented following cardioversion. As in our original report[78] we strongly recommend that all patients being considered for multiplane TEE-guided early cardioversion be anticoagulated with intravenous heparin or a therapeutic dose of warfarin at the time of TEE, continuing through cardioversion, and that warfarin anticoagulation be continued for at least 1 month after cardioversion. Multiplane TEE should be performed (without transthoracic echocardiography) immediately prior to cardioversion to adequately visualize the atria and appendages and to exclude the presence of atrial thrombi. Heightened vigilance for thrombi is necessary if there is prominent spontaneous echo contrast or poor (2 up to 6 weeks) and prolonged (>6 weeks) duration as compared with the patients with atrial fibrillation of only brief (≥2 weeks) duration.[81] This depression in peak A velocity persisted until at least 1 week following cardioversion. In addition, 1 week after cardioversion, both peak A velocity and percentage A wave filling were depressed in the group with atrial fibrillation of prolonged duration as compared with the group with atrial fibrillation of moderate duration. As compared with 3-month postcardioversion data, full recovery of atrial mechanical function was achieved within 24 hours for patients with brief (6 weeks) duration of atrial fibrillation. Twenty-seven 840

Figure 38-9 Comparison of transmitral pulsed Doppler peak A-wave velocity among patients with brief (6 weeks) atrial fibrillation immediately after, at 24 hours, and at 1 week after cardioversion. *P < .05 vs. brief duration. †P < .05 vs. moderate duration. (From Manning WJ, Silverman DI, Katz SE, et al: J Am Coll Cardiol 1994;23:1537.)

patients (45%) reverted to atrial fibrillation during follow-up. Those reverting to atrial fibrillation had a longer duration prior to cardioversion (10.2 vs. 5.3 weeks; P = .04). There were no differences in left atrial dimension, patient age, mode of cardioversion, peak A wave velocity, or percentage of A wave filling among patients who reverted to atrial fibrillation compared with those with sustained sinus rhythm. Evidence of Electrical Injury to the Atria Left ventricular myocardial injury as a result of electrical cardioversion has been previously described.[95] [96] TEE data acquired with electrical cardioversion have shown new or more pronounced spontaneous left atrial contrast following electrical cardioversion[64] [88] as well as depressed left atrial appendage ejection velocity.[88] We reported on transmitral Doppler data from 33 patients with atrial fibrillation of less than 5 weeks' duration following elective electrical or pharmacologic (primarily quinidine or procainamide) cardioversion using transmitral Doppler examination.[97]

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Immediately following cardioversion, patients who underwent electrical cardioversion demonstrated lower peak A wave velocity as compared with those who were cardioverted pharmacologically (Fig. 38-10) . This depression in atrial systolic function was also present at the 24-hour study but had resolved at 1 week. Similarly, Mattioli et al[103] randomized 64 patients with atrial fibrillation (duration 1 day to 6 months) to either directcurrent shock or pharmacologic cardioversion. They found that the recovery of atrial mechanical function occurred sooner with pharmacologic cardioversion. Finally, Pollak and Falk[104] performed electrical cardioversion in 37 patients receiving sotalol or placebo. They found relatively depressed atrial function among the group receiving sotalol as compared with those receiving placebo. Spontaneous Echo Contrast Spontaneous echo contrast, or "smoke," refers to the presence of dynamic smokelike echoes in a cardiac cavity and is occasionally seen by transthoracic echocardiography in the left atrium in patients with mitral stenosis and atrial fibrillation. More commonly, spontaneous echo contrast is identified on transthoracic imaging of the left ventricular apex with a high-frequency transducer in patients with an apical aneurysm. Spontaneous echo contrast likely represents stasis of blood within the cavity, but it may also reflect alterations in blood components such as platelets, red cells, and fibrinogen. Black et al[105] found an association between spontaneous echo contrast and erythrocyte aggregation in low shear rate conditions. Aspirin and warfarin therapy do not appear to affect the presence of left atrial spontaneous echo contrast.[105] At least mild spontaneous echo contrast may be seen in over half of patients with atrial fibrillation,[60] [71] [78] and in over 80% of patients with atrial fibrillation and left atrial appendage thrombi.[60] Among patients with nonvalvular atrial fibrillation, Chimowitz et al[106] found that left atrial spontaneous echo contrast was associated with an increased risk of stroke. Black et al[105] found that spontaneous echo contrast by TEE was an independent predictor of left atrial thrombus among patients with suspected cardioembolism. Although unproved, it seems likely that recovery of atrial mechanical function would decrease or abolish spontaneous echo contrast. SPAF-III TEE data[71] suggest that warfarin anticoagulation decreases the risk of thromboembolism in patients with spontaneous echo contrast.

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Echocardiography and Atrial Flutter Sustained atrial flutter is far less common then atrial fibrillation. As a result, there are fewer data regarding atrial function at baseline and following cardioversion. It has generally been accepted that the relatively preserved atrial mechanical function (Fig. 38-11) with atrial flutter results in a lower risk of thromboembolism (as compared with atrial fibrillation). In a retrospective review, Arnold Figure 38-10 Comparison of transmitral peak A wave velocity among patients who underwent pharmacologic and electrical cardioversion. (From Manning WJ, Silverman DI, Katz SE, et al: Am J Cardiol 1995;75:626, with permission from Excerpta Medica Inc.)

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Figure 38-11 M-Mode echocardiographic image depicting motion of the anterior mitral leaflet (arrows) corresponding to flutter waves on the electrocardiogram in a patient with atrial flutter.

et al[68] reported on 122 patients with atrial flutter at the time of cardioversion, including 74% who were not receiving anticoagulation. No patient experienced a clinical thromboembolic event. These data would support the concept that patients with atrial flutter do not require anticoagulation prior to cardioversion. However, there have been reports of atrial thrombus identified during TEE study among patients with atrial flutter[107] [108] and postcardioversion thromboembolism. A limitation of interpreting the literature on atrial flutter is the definition of the arrhythmia. For many studies,[68] a patient is defined as having atrial flutter if it is the

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rhythm during the intervention or period of observation (e.g., at the time of TEE or cardioversion). Many patients may have alternating periods of atrial fibrillation and flutter, making clinical distinction of pure atrial flutter difficult. Irani et al[109] performed TEE in 47 consecutive patients with atrial flutter (and without atrial fibrillation by history or Holter monitoring). They found that 11% of patients had left atrial thrombus, and 31% had spontaneous echo contrast, values similar to those found in patients with atrial fibrillation. Similar to our findings for atrial fibrillation, [60] [61] , [78] moderate or severe mitral regurgitation was not protective against thrombus formation for this group. Jordaens et al[110] studied 22 patients with atrial flutter with serial transmitral Doppler echocardiography after cardioversion. Analogous to data on atrial fibrillation, they found that 20% of patients had Doppler evidence of atrial standstill immediately after cardioversion. There was a progressive increase in peak A wave velocity and percentage of A wave filling over a 6-week period. Based on these data, our recommendation is to treat patients with atrial flutter who have periods of atrial fibrillation ("atrial flutter-fibrillation") in the same manner as those with isolated atrial fibrillation. When it is certain that a patient has sustained atrial flutter, particularly for a short period of time, it may be reasonable to cardiovert without anticoagulation, although individualized risk-benefit considerations are most appropriate. We would generally treat conservatively patients who had atrial flutter in the setting of rheumatic mitral valve disease, a history of thromboembolism, or left ventricular systolic dysfunction, with shortterm anticoagulation and screening TEE or several weeks of anticoagulation prior to attempted cardioversion.

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Current and Future Areas of Investigation As the ability of echocardiography to provide detailed structural and functional information about the heart continues to grow, so likely will its role in the evaluation and optimal management of patients with atrial fibrillation. Among the areas of current and future investigation are 1. Improved methods of assessment of atrial mechanical function, such as measurement of atrial ejection force. 2. Randomized prospective studies to further define the safety of TEE to guide early cardioversion among patients with atrial fibrillation, as in the ACUTE Trial. 3. Randomized trials to examine the need for repeat TEE prior to cardioversion among patients with a thrombus on initial TEE. 4. Clinical studies examining TEE risk stratification for aspirin or warfarin in patients with chronic atrial fibrillation. 5. Assistance in localization of structural abnormalities and foci of abnormal electrical activity, including assistance in radiofrequency ablation of arrhythmic foci. 6. Identification of clinical or echocardiographic indexes that predict recurrence of atrial fibrillation or identify a group at low risk for thromboembolism so as to minimize postcardioversion anticoagulation. 7. Anatomic and Doppler descriptions of right atrial appendage in health and disease.

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Section 8 - Echocardiography in Adult Congenital Heart Disease

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Chapter 39 - General Echocardiographic Approach to the Adult with Suspected Congenital Heart Disease A. Rebecca Snider MD

Two-dimensional (2D) echocardiography has had a major impact on our ability to diagnose complex congenital heart defects. With this technique, one can image detailed structural anatomy even more precisely than with cardiac catheterization in most patients. The echocardiographic approach to the diagnosis of complex congenital heart disease is very logical and systematic, requiring a basic knowledge of how cardiac chambers are identified on the 2D echocardiogram. In this chapter, we review (1) the echocardiographic approach to segmental analysis of the heart, (2) the echocardiographic features used to determine the morphology of the cardiac chambers and great vessels, and (3) the echocardiographic appearance of the more frequently encountered forms of complex congenital heart disease.

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Echocardiographic Approach to Segmental Analysis of the Heart General Considerations The echocardiographic approach to the diagnosis of complex congenital heart disease involves a segmental analysis of the heart.[1] [2] [3] [4] [5] [6] In this type of analysis, one can think of the heart as being much like a house. To describe a house completely, one must say where the rooms or chambers are located on each floor. For the "cardiac house," this description includes where each atrium is on the ground floor, where the ventricles are on the second story, and where each great artery is positioned at the top 846

TABLE 39-1 -- Summary of Segmental Approach to Cardiac Diagnosis Atrial situs: describes location of atria Solitus: morphologic RA on right Inversus: morphologic RA on left Ambiguus: undifferentiated atria Asplenia: bilateral right-sidedness Polysplenia: bilateral left-sidedness Bulboventricular loop: describes location of ventricles d-Loop: morphologic RV on right l-Loop: morphologic RV on left Ventriculoarterial connections: describes connections of great arteries Concordant: Ao arising from LV, PA from RV

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Discordant (transposition): Ao arising from RV, PA from LV Double-outlet right ventricle Double-outlet left ventricle Single outlet from heart Aortic atresia Pulmonary atresia Truncus arteriosus Ao, aorta; LA, left atrium; LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle. of the house. In addition, a complete description of the house should include the location of the staircases that connect the floors. For the cardiac house, this description includes atrioventricular and ventriculoarterial connections. In this approach, if the atria are not correctly identified, the entire house comes tumbling down.[7] Thus, the approach to echocardiographic diagnosis of the patient with complex congenital heart disease begins with a determination of the atrial situs (Table 39-1) . The word situs refers to the topology or spatial position of the structure. In atrial situs solitus, the morphologic right atrium is on the right and the morphologic left atrium is on the left. In situs inversus, the morphologic right atrium is on the left and the morphologic left atrium is on the right. In situs ambiguus, the atria do not differentiate into right and left atria; instead, both atria can have features of (1) a morphologic right atrium, a condition called asplenia, or (2) a morphologic left atrium, a condition called polysplenia. [2] [6] , [8] The next step in the diagnosis of complex congenital heart disease is determination of the bulboventricular loop (see Table 39-1) . This loop describes the locations of the ventricles. In a d-loop (dextro loop), the morphologic right ventricle is on the right and the morphologic left ventricle is on the left. In an l-loop (levo loop), the morphologic right ventricle is on the left and the morphologic left ventricle is on the right. These definitions of d- and l-loop apply regardless of the atrial situs. Thus, concordant or normal connections between the atria and ventricles (morphologic right atrium to morphologic right ventricle, morphologic left atrium to morphologic left ventricle) occur when there is situs solitus with a d-loop or situs inversus with an l-loop. Discordant or abnormal connections (morphologic right atrium to morphologic left ventricle, morphologic left

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atrium to morphologic right ventricle) occur when there is situs solitus with an l-loop or situs inversus with a d-loop. [1] [2] , [5] In general, the convexity of the aorta points to the position of the right ventricle and thus helps indicate the bulboventricular loop.[2] The definitive indicator of the bulboventricular loop, however, is the relative positioning of the ventricular inlets or atrioventricular valves. Thus, in a d-loop the tricuspid valve is to the right of the mitral valve, and in an l-loop the tricuspid valve is to the left of the mitral valve.[9] [10] In most cardiac defects the inflow and trabecular portions of the right ventricle are on the same side relative to the components of the left ventricle, so that determination of the bulboventricular loop is straightforward (i.e., tricuspid valve to the right indicates d-loop, tricuspid valve to the left indicates l-loop). In some rare complex malformations discussed in detail later in this chapter, the inflow and trabecular portions of the right ventricle can be located on different sides of the left ventricular inflow (e.g., in certain forms of crisscross hearts). The spatial locations of the trabecular and outflow portions of the ventricles alone do not indicate the bulboventricular loop; their final spatial position is determined by the degree of apical rotation in the ninth week of gestation. Normally, the cardiac apex pivots to the hemithorax opposite the bulboventricular loop.[4] [11] In the early embryogenesis of the normal heart, the apex is oriented to the right (following initial rightward loop formation), but it subsequently rotates to the left as the primitive ventricular cavity develops into the left ventricle. Thus, in a normal d-loop the apex pivots to the left hemithorax; in a "normal" l-loop (i.e., one in the setting of situs inversus) the apex pivots to the right hemithorax. When the atrial situs and the loop are alignment concordant, apical pivoting is usually complete. Failure of complete apical pivoting is commonly associated with discordant atrioventricular connections. Partial pivoting in either concordant or discordant atrioventricular connections leads to a sagittally oriented ventricular septum and mesocardia. Rotational anomalies of the cardiac apex cause the ventricular septum and greater ventricular mass to be grossly displaced in space, whereas the inlet relationships of the ventricles are preserved. Abnormal rotation can occur either in the frontal plane, along the longitudinal axis, or in both patterns. The resultant possible spatial relationships of the chambers and septal orientation are listed in Table 39-2 .[11] Rotational anomalies of the cardiac apex also can cause the semilunar valves to be altered in their spatial relationships. An understanding of these apical

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TABLE 39-2 -- Rotational Anomalies of the Cardiac Apex Normal Heart Apex displaced 30 to 60 degrees from a vertical direction in the frontal plane Ventricular septum tilted so that its anterior edge is leftward and superior to its posterior edge Superoinferior Ventricles Abnormal tilting of the apex in the frontal plane Resultant horizontal ventricular septum and superior right ventricle Crisscross Ventricles Abnormal apical rotation along the longitudinal axis Dextroversion Lack of apical pivoting in situs solitus, d-loop Resultant abnormal positioning of the apex to the right Preservation of the relationship between the great arteries

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rotational abnormalities and the resultant changes in the plane of the ventricular septum, the positioning of the greater ventricular mass, and the positioning of the great arteries is an essential component of the echocardiographic approach to segmental analysis of complex cardiac defects. If the echocardiographer does not understand the effects that rotational anomalies of the apex have on the standard imaging planes, imaging artifacts can be created easily and incorrect assessments made of the adequacy of chamber size. In most congenital cardiac defects, there is harmony between the situs (topology) and alignment (connections) information[12] which means that situs concordance nearly always predicts alignment concordance, and situs discordance nearly always predicts alignment discordance. For example, situs solitus with an l-loop (discordant situs information) almost always predicts discordant atrioventricular connections or alignments (right atrium on the right connected to left ventricle on the right). The rare and notable exception to this rule is the heart with crisscross atrioventricular relations (discussed later). In this case, knowledge of the atrial situs and the

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bulboventricular loop might be wrongly predictive of the alignment or connections of these segments. In other words, there is disharmony between the situs and alignment information. The final step in the diagnosis of complex congenital heart disease is a description of the great artery connections (see Table 39-1) . In normal or concordant connections, the pulmonary artery arises from the morphologic right ventricle and the aorta arises from the morphologic left ventricle. Normally, the aortic valve is situated posterior and to the right of the pulmonic valve. Transposition is a discordant ventriculoarterial connection in which the aorta arises from the morphologic right ventricle and the pulmonary artery arises from the morphologic left ventricle.[2] [5] [6] Classically, the old definition of transposition was based on spatial relations of the great arteries, that is, that transposition is present when the aortic valve and ascending aorta are anterior to the pulmonary valve and main pulmonary artery.[8] The more current definition of transposition proposed by Van Praagh et al[2] [5] and used in this chapter is based on the ventriculoarterial connections and not the spatial interrelationships. The literal Latin root meaning of the word transposition is from trans (across) and positio (placement). Thus, the great arteries are literally "placed across" the ventricular septum, with the aorta arising from the morphologic right ventricle and the pulmonary artery arising from the morphologic left ventricle.[13] The old definition of transposition based on the anteroposterior relations of the great arteries has been largely abandoned because of the existence of transposition with a posterior aortic valve and an anterior pulmonic valve in 11% of autopsy-proved cases of transposition with dextrocardia.[14] Likewise, when the ventricles are severely rotated, normally connected great arteries can have an anterior aortic valve and a posterior pulmonic valve.[13] Other types of great artery connections include double-outlet right ventricle, double-outlet left ventricle, and single outlet from the heart. Three common forms of single outlet from the heart include truncus arteriosus, aortic atresia, and pulmonary atresia. In Van Praagh's system of nomenclature, any great artery relationship that is neither normally crossed nor transposed is referred to as being malposed.[5] [15] [16] Thus, for the heart with both great arteries arising from the right ventricle, with the aortic valve anterior and to the right of the pulmonic valve, the preferred nomenclature is double-outlet right ventricle connection with d-malposed great artery relationships (not double-outlet right ventricle and transposition, which would be two mutually exclusive types of

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connections). Although this is the terminology used throughout this chapter, there is no single agreed upon system of nomenclature for congenital heart disease. Clarity in the description of cardiac anatomy is undoubtedly the most important focus for the echocardiographer, and several approaches to cardiac nomenclature are available to allow one to accomplish this goal. Definition of Cardiac Chambers from the Two-Dimensional Echocardiogram Before we review how cardiac chambers are identified on the echocardiogram, one of the largest controversies in cardiac nomenclature needs to be addressed: the definition of a ventricle. Anderson et al[6] [17] proposed a rule of 50% for determining whether a cardiac chamber is a ventricle. This rule states that a chamber is a ventricle if it receives 50% or more of an inlet. The inlet consists of the fibrous ring of the atrioventricular valve and need not always include a patent atrioventricular valve with wellformed valve leaflets. For example, in hypoplastic left heart with aortic and mitral atresia, the fibrous ring of the mitral valve contains an imperforate membrane and is situated over the small left ventricle. Thus, this small leftsided chamber is a ventricle because it receives 100% of an inlet (even though there is no antegrade flow across the inlet). A chamber need not have an outlet to be a ventricle. Thus, the left ventricle in double-outlet right ventricle is a ventricle because it receives the mitral valve even though it does not have an outlet. The rule of 50% has also been used to define the ventriculoarterial connections. Thus, if 50% or more of a great artery arises above a chamber, the great artery is defined as being connected to that chamber.[6] [17] Application of the rule of 50% requires definitions for chambers that are not ventricles. According to the original descriptions,[6] [17] rudimentary chambers are chambers that receive less than 50% of an inlet and therefore do not qualify to be ventricles. There are two types of rudimentary chambers. An outlet chamber is one that has less than 50% of an inlet but 50% or more of an outlet or great artery. A trabecular pouch is a chamber that has less than 50% of an inlet and less than 50% of an outlet.[17] More recently, chick embryo studies by de la Cruz et al[18] have shown that the trabeculated portions of the ventricles are the original developmental components. The inlet and outlet components form from the trabeculated component during and after looping; thus, the apical components are the oldest parts of the ventricles and form the basis for subsequent

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development. These and other observations form the basis for the belief by some investigators that chambers in the ventricular mass that possess 848

a trabeculated portion of a ventricle should be considered ventricles regardless of whether they have an inlet or outlet component.[19] Anderson has suggested that when such small chambers lack an inlet, they be called rudimentary ventricles.[20] Anatomic Landmarks on the Septal Surfaces

To diagnose complex congenital heart disease, one must know how cardiac chambers are identified on the 2D echocardiogram (Table 39-3) . The cardiac chambers are largely defined by the anatomic landmarks on their septal surfaces.[21] The morphologic right atrium has a septal surface that receives the tendinous insertion of the eustachian valve and has the limbus of the fossa ovalis. The eustachian valve crosses the floor of the right atrium from the orifice of the inferior vena cava and inserts into the septum primum (the lower portion of the atrial septum adjacent to the atrioventricular valves). This tendinous insertion is along the lower border of the fossa ovalis and is called the inferior limbic band (Fig. 39-1) (Figure Not Available) .[3] [4] [21] The left atrial septal surface has the flap valve of the fossa ovalis. This is the septum primum tissue that covers the foramen ovale and seals it closed after birth (Fig. 39-2) . [21] The flap valve can be seen on the 2D echocardiogram protruding into the left atrium in the fetus when the foramen ovale is open; after birth, however, the flap valve is usually difficult to identify on the transthoracic 2D echocardiogram. With the use of high-frequency transesophageal imaging transducers, the flap valve can be imaged in a large proportion of patients. In cases in which the flap valve is tightly adherent to the left atrial septal surface and therefore cannot be visualized as a separate structure on the 2D echocardiogram, other methods for identification of the left atrium must be used. The morphologic right ventricle is the chamber whose septal surface has prominent muscle bundles crossing from the septum to the parietal free wall (Fig. 39-3) . The largest of the septoparietal muscle bundles is the moderator band. In addition, the septal surface of the right ventricle receives chordal insertions from the tricuspid valve septal leaflet.[3] [4] [21]

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TABLE 39-3 -- Definition of Cardiac Chambers from Two-Dimensional Echocardiography Right Atrium Tendinous insertion of eustachian valve Short, stout appendage Usually receives drainage of inferior vena cava, superior vena cava, and coronary sinus Left Atrium Flap valve of fossa ovalis Long, finger-like appendage Usually receives drainage of pulmonary veins Right Ventricle Septoparietal muscle bundles Atrioventricular valve chordal insertions into septum Tricuspid valve Left Ventricle Smooth septal surface Mitral valve Figure 39-1 (Figure Not Available) Subcostal four-chamber view from a normal patient showing the anatomic features of the morphologic right atrium (RA). The morphologic RA has a septal surface that receives the tendinous insertion of the eustachian valve. In this view the eustachian valve can be seen crossing the floor of the RA from the orifice of the inferior vena cava to its insertion into the septum primum. LA, left atrium; LV, left ventricle. (From Snider AR, Bengur AR: Twodimensional and Doppler echocardiography in the evaluation of congenital heart disease. In Marcus ML, Schelbert HR, Skorton DJ, Wolf GL [eds]: Cardiac Imaging: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1991, p 501.)

The morphologic left ventricle is the chamber whose septal surface is smooth. There are no septoparietal free wall muscle bundles and the mitral valve normally has no chordal insertions into the septum (see Fig. 39-3) .[3] [4] [21]

Additional Features of the Cardiac Chambers

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Another useful anatomic feature for identifying the ventricles is that the atrioventricular valve always belongs to Figure 39-2 Subcostal sagittal view from a normal patient. The flap valve (arrow) of the foramen ovale is seen on the atrial surface of the left atrium (LA). The flap valve of the foramen ovale is an anatomic marker of the morphologic LA. AO, aorta; RA, right atrium; RPA, right pulmonary artery.

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Figure 39-3 Apical four-chamber view from a normal subject. The morphologic right ventricle (RV) has prominent muscle bundles traversing from the septal surface to the parietal free wall and an atrioventricular valve closer to the cardiac apex. The morphologic left ventricle (LV) has a smooth septal surface and an atrioventricular valve farther from the cardiac apex. Note the pulmonary veins draining to the morphologic left atrium (LA). RA, right atrium.

the appropriate ventricle. Thus, the tricuspid valve is always found in the morphologic right ventricle and the mitral valve is always found in the morphologic left ventricle. The tricuspid valve is closer to the cardiac apex (see Fig. 39-3) , has three leaflets, and has chordal insertions into the ventricular septum. The mitral valve is farther from the cardiac apex, is a fish-mouth bicuspid valve, and has chordal insertions only into two papillary muscles in the left ventricle (see Fig. 39-3) .[21] Systemic and pulmonary venous return can help identify the atria. The pulmonary veins usually drain to the morphologic left atrium; however, this is not a constant feature of the left atrium, because the pulmonary veins can drain anomalously. If three or more pulmonary veins drain by separate orifices to a chamber and there is no evidence of a pulmonary venous confluence, that chamber is most likely a morphologic left atrium. The inferior vena cava usually drains to the morphologic right atrium. This relationship is constant in most cases except in patients with situs ambiguus (discussed later). The superior vena cava usually drains to the morphologic right atrium; however, this relationship is not constant, as it can drain to either or both atria.[3] [4] [17] The morphology of the atrial appendages can help identify the atria.[3] The

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right atrial appendage is short and stout, resembling "Snoopy's" nose, and the left atrial appendage is long and finger-like, resembling "Snoopy's" ear (Fig. 39-4) . Also, the abdominal situs may provide helpful information for determining the atrial situs.[3] [4] [21] For example, in most patients with atrial situs solitus, there is also abdominal situs solitus. Thus, subcostal views of the abdomen show that the inferior vena cava is to the right of the spine, the descending aorta is to the left of the spine, the stomach bubble is on the left, and the liver is on the right (Fig. 39-5) . Likewise, in most patients with atrial situs inversus, there is also abdominal situs inversus. Subcostal views of the abdomen show that the inferior vena cava is usually to the left of the spine and the descending aorta is usually to the right. The stomach bubble is on the right and the liver is on the left. In atrial situs ambiguus the liver may be to the right, to the left, or transverse. The stomach bubble can be on either side or in the midline. Several types of anomalies of systemic venous drainage often are present and suggest the diagnosis of situs ambiguus. These anomalies are discussed in detail later in this chapter. When the atrial and abdominal Figure 39-4 Transesophageal echocardiogram from a normal patient showing several basal short-axis transverse views. Top, The aortic valve (AO) is seen in cross section. Middle, The transducer has been rotated rightward to image the right atrial appendage (RAA) and the main pulmonary artery (MPA), which is anterior and to the left of the AO. Note that the RAA is short and stout and resembles "Snoopy's" nose. Bottom, The transducer has been rotated leftward to image the left main coronary artery (LMCA), the left anterior descending coronary artery (LAD), and the left atrial appendage (LAA). Note the long, finger-like appearance of the LAA, which resembles "Snoopy's" ear. The arrow indicates a prominent pulmonary vein shelf, which is a normal structure and should not be mistaken for a thrombus. L, left coronary cusp; LA, left atrium; N, noncoronary cusp; R, right coronary cusp; RA, right atrium; RV, right ventricle.

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Figure 39-5 Subcostal short-axis view from a patient with atrial and abdominal situs solitus. Note that the liver is on the patient's right. The inferior vena cava (IVC) is to the right of the spine and the descending aorta (DAO) is to the left of the spine.

situs are discordant (atrial situs solitus with abdominal situs inversus or vice versa), the incidence of severe, complex congenital heart disease is

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high. Defects with atrioventricular and ventriculoarterial discordance are frequent in this setting. [4] Evaluation of the Patient with Dextrocardia The term dextrocardia simply indicates that the heart is located primarily in the right chest and implies that Figure 39-6 Diagrammatic representation of the types of dextrocardia. In dextroposition (in situs solitus), the entire heart is shifted to the right chest, either because of a space-occupying mass in the left chest or because of absence of the normal lung volume filling the right chest. Usually, the alignment of the major axis of the heart is normal (pointed toward the left) or rotated slightly vertically; however, the entire heart is shifted to the right of midline or to the retrosternal area. The parasternal long- and short-axis views are obtained with the usual orientation of the plane of sound but with the transducer positioned just to the right of the sternum. The apical views are also obtained with the usual orientation of the plane of sound but with the transducer positioned just to the right of the lower sternal border. In dextroversion (in situs solitus), there is failure of apical pivoting. The cardiac apex is to the right of midline and the atria are usually in their normal positions or shifted slightly to the right. The major axis of the heart is aligned from the left shoulder toward the right hip. The parasternal long-axis view is obtained with the plane of sound oriented in the mirror-image direction of normal. Because the atria are usually normally positioned and the great arteries arise normally from the ventricles, the parasternal short-axis view is obtained with a normal orientation of the plane of sound. In mirror-image dextrocardia or situs inversus totalis, the heart is located in the mirror-image position of normal. Both atria are usually entirely to the right of the sternum, and the cardiac apex is usually in the right fifth or sixth intercostal space at the anterior axillary line; hence, the major axis of the heart is aligned between the left shoulder and right hip. The parasternal long-axis view is obtained from the right second or third intercostal space with the plane of sound oriented in a mirror-image direction of normal (from left shoulder to right hip). The parasternal short-axis view is obtained from the same transducer location with the plane of sound also oriented in the mirror-image direction of normal (from right shoulder to left hip). The apical views are obtained with the transducer positioned in the right fifth or sixth intercostal space in the anterior axillary line and with the plane of sound oriented in a mirrorimage direction of normal. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

one of three conditions is present (Fig. 39-6) .[14] , [22] First, dextrocardia can occur because the heart is displaced into the right chest, either because of a space-occupying mass in the left chest or because of absence of the normal lung volume filling the right chest. This form of dextrocardia is commonly called dextroposition. Second, dextrocardia can occur because of failure of

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pivoting of the cardiac apex to the left. This condition is known as dextroversion and is frequently associated with atrioventricular discordance.[4] Third, dextrocardia can occur with abnormal atrial situs (i.e., situs inversus or situs ambiguus). The most common condition in this category is situs inversus totalis, in which the heart is located in the mirrorimage position of normal. When a patient is referred with a diagnosis of dextrocardia,[23] the echocardiographic examination is begun from the subcostal position rather than from the parasternal window, the routine starting position. From the subcostal four-chamber view, patients with dextroposition have the morphologic right atrium and right ventricle to the right of the morphologic left atrium and left ventricle. Usually, the alignment of the major axis of the heart is normal (pointed toward the left) or rotated slightly vertically; however, the entire heart is shifted to the right of midline or to the retrosternal area. In patients with dextroversion the morphologic right atrium is to the right of the morphologic left atrium; however, the major axis of the heart is aligned from the left shoulder toward the right hip.[22] In this condition the cardiac apex is to the right of midline and the atria are usually in their normal positions or shifted slightly to the right (Fig. 39-7) . In dextrocardia with atrial situs inversus, the morphologic left atrium is 851

Figure 39-7 Subcostal four-chamber views from a patient with dextroversion of the cardiac apex. Top, The left-sided ventricle has a smooth septal surface and is therefore the morphologic left ventricle (LV). The LV gives rise to a vessel that arches and is therefore the aorta (AO). Bottom, The plane of sound has been tilted far anteriorly. The right-sided ventricle has a prominent moderator band in its apical portion and is therefore a morphologic right ventricle (RV). The RV gives rise to a vessel that dives posteriorly and is therefore a pulmonary artery (PA). Other echocardiographic views showed that this patient had atrial situs solitus; therefore, the atrioventricular and ventriculoarterial connections are normal. The only abnormality in this heart is failure of pivoting of the cardiac apex to the left. LA, left atrium.

to the right of the morphologic right atrium, and both atria are usually entirely to the right of the sternum ( Fig. 39-8 and Fig. 39-9 ). The cardiac apex is usually in the right fifth or sixth intercostal space at the anterior axillary line; therefore, the major axis of the heart is aligned between the left shoulder and right hip.[22]

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In dextrocardia with atrial situs inversus, the parasternal long-axis view is obtained from the right second or third intercostal space with the plane of sound oriented in a mirror image of normal (from left shoulder to right hip). The parasternal long-axis view has only anteroposterior and superoinferior directions and does not display the right-to-left orientation of cardiac structures. Thus, on the video monitor, cardiac structures appear to be oriented in a normal fashion, and only the examiner knows that the images were obtained in a mirror-image plane. The parasternal short-axis views are obtained from the same transducer location with the plane of sound also oriented in the mirror-image direction of normal (from right shoulder to left hip). Unlike the parasternal long-axis view, the parasternal short-axis view displays the right-to-left orientation of cardiac structures. Thus, on the video monitor, in patients with dextrocardia and atrial situs inversus, the parasternal short-axis view appears to be a backward version of normal. It is important that the examiner not "correct" the image by using the leftright invert button. Inverting the images to make the views appear "normal" is contrary to the accepted guidelines for 2D image orientation and leads to confusion in understanding the spatial anatomy. In dextrocardia with situs inversus, the apical views are obtained with the transducer positioned in the right fifth or sixth intercostal space and with the plane of sound oriented in a mirror-image direction of normal. Like the parasternal short-axis view, the apical four-chamber view in dextrocardia with situs inversus appears to be backward.

MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26082022/1031/333.html/top

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Echocardiographic Features of Frequently Encountered Complex Congenital Cardiac Defects All possible concordant and discordant connections are listed in Table 394 . The following discussion covers Figure 39-8 Subcostal coronal views from a patient with atrial situs inversus, l-loop, and normal great vessels. This patient had total anomalous pulmonary venous return to the upper portion of the inferior vena cava (IVC) and a hypoplastic right lung. Top, The right and left pulmonary veins (RPV and LPV) can be seen connecting to a common pulmonary vein that drains below the diaphragm and connects to the upper IVC. Note that the RPVs are considerably smaller than the LPVs because of diminished drainage from the hypoplastic right lung. Bottom, The plane of sound has been tilted anteriorly to image the subcostal four-chamber view. Note that the heart is in the right chest with the apex to the right. The left-sided atrium receives the superior vena cava (SVC) and the IVC (top) and is therefore the morphologic right atrium (RA). The RA connects to a ventricle on the left that has an atrioventricular valve closer to the apex. These findings indicate that the left-sided ventricle is the morphologic right ventricle (RV) and that there is l-looping. LA, left atrium; LV, left ventricle.

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Figure 39-9 Subcostal views from the same patients as in Figure 39-8 . Top, The plane of sound has been tilted farther than that in Figure 39-8 in order to image the posterior great artery. Note that the morphologic left ventricle (LV) on the patient's right gives rise to a vessel that arches and is therefore the aorta (AO). Bottom, The plane of sound has been tilted even farther anteriorly to image the anterior great artery. Note that the morphologic right ventricle (RV) on the patient's left gives rise to a vessel that crosses from left to right anterior to the AO. This vessel is a normally connected pulmonary artery (PA). LA, left atrium; RA, right atrium.

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the anatomy of these and other frequently encountered complex congenital defects. Associated lesions that should alert one to the diagnosis are also discussed. Atrioventricular Concordance and Ventriculoarterial Discordance or Simple Transposition of the Great Arteries In the most common form of transposition the morphologic right atrium on the patient's right is connected TABLE 39-4 -- Possible Segmental Connections AV Connection Concordant Concordant Discordant Discordant

VA Connection Concordant Discordant Discordant Concordant

Defect Normal heart d-Transposition l-Transposition Isolated ventricular inversion Anatomically corrected malposition AV, atrioventricular; VA, ventriculoarterial.

to the morphologic right ventricle on the patient's right, which in turn is connected to the aorta. On the patient's left the morphologic left atrium is connected to the morphologic left ventricle, which is connected to the pulmonary artery. This defect is called situs solitus, d-loop, d-transposition, or simply d-transposition. The "d" in the third term is used to describe the spatial relations of the aortic and pulmonic valves. The mirror image of this defect is situs inversus, l-loop, l-transposition. In more than 80% of cases the aortic valve spatially is located to the right of the pulmonary valve; hence, the use of the "d." Other spatial relationships are possible. In a small percentage of cases the aortic infundibulum and valve may be to the left of the pulmonary valve. This spatial relationship is frequently found in patients with d-transposition and a large ventricular septal defect, and it is often referred to as situs solitus, dloop, l-transposition. In this nomenclature the "l" in the third term refers to the spatial position of the aorta (to the left). In another small percentage of patients the aortic valve may be directly anterior to the pulmonary valve. The echocardiographic diagnosis of transposition of the great arteries is based on demonstrating an abnormal connection of the right ventricle to the aorta. Although the spatial relationships of the great arteries may provide supportive evidence of the diagnosis, they should never be used as the sole

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diagnostic criteria. The connections between the ventricles and great arteries can be seen in multiple echocardiographic views; however, the subcostal views are particularly useful for complete segmental analysis of the heart (Fig. 39-10) (Figure Not Available) . The anatomic and echocardiographic features of dtransposition are well known and are not reviewed in detail in this chapter. These features include (1) complete subaortic muscular infundibulum, (2) pulmonary valve-mitral valve fibrous continuity, (3) parallel spatial alignment of the outflow tracts and great arteries, (4) straight muscular septum, and (5) posterior angulation of the posterior great artery.[23] [24] [25] Associated Defects Ventricular Septal Defect.

Ventricular septal defects occur in about 33% of patients with dtransposition. Most of these defects are in the outlet septum and are associated with an overriding pulmonary artery. In this situation, anterior displacement of the infundibular septum results in a narrowed right ventricular infundibulum, discontinuity of the infundibular septum and the trabecular septum, and a malaligned-outlet ventricular septal defect.[26] Although the pulmonary artery overrides the ventricular septum, more than 50% of the pulmonary artery is committed to the left ventricle and there is pulmonary-mitral continuity. In patients with a malaligned-outlet ventricular septal defect, tricuspid valve abnormalities are frequent, occurring in 65% of patients in one series.[27] The types of tricuspid valve anomalies that occur are chordal attachments to the infundibular septum or ventricular septal crest, overriding of the tricuspid annulus, straddling tricuspid valve with chordal attachments into the left ventricle, tricuspid valve tissue protruding through the ventricular 853

Figure 39-10 (Figure Not Available) Subcostal views in coronal body planes from a patient with d-transposition of the great arteries. Top, View obtained by tilting the transducer posteriorly to image the inlets of the ventricles. The eustachian valve can be imaged in the morphologic right atrium (RA) and the pulmonary veins can be seen draining to the morphologic left atrium (LA). Middle, The plane of sound has been tilted slightly anteriorly to image the midportion of the heart. The smooth-walled morphologic left ventricle (LV) on the patient's left (d-loop) gives rise to a posterior vessel that bifurcates and is therefore the pulmonary artery (PA). Bottom, The plane of sound has been tilted far anteriorly. The morphologic right ventricle (RV) on the

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patient's right gives rise to the aorta (AO). (From Snider AR, Bengur AR: Twodimensional and Doppler echocardiography in the evaluation of congenital heart disease. In Marcus ML, Schelbert HR, Skorton DJ, Wolf GL [eds]: Cardiac Imaging: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1991, p 497.)

septal defect and causing subpulmonary obstruction, and cleft anterior leaflet of the tricuspid valve. The anterior displacement of the infundibular septum causes subaortic narrowing and produces a long, oblique course from left ventricle to aorta. These anatomic features make intraventricular repair extremely difficult and favor repair with an arterial switch procedure, closure of the ventricular septal defect, and resection of subaortic muscle, if necessary.[26] After closure of the ventricular septal defect, the right ventricle always becomes smaller, and right ventricular outflow gradients that were of minor significance preoperatively may become significant. The subaortic narrowing seen in patients with d-transposition and a malaligned-outlet ventricular septal defect may lead to the development of coarctation and interruption of the aorta. In one review of 129 pathologic specimens with d-transposition, 17% had right ventricular outflow obstruction and 7% had associated aortic arch obstruction as well. Anatomic narrowing of the subaortic region was found only in association with a malaligned-outlet ventricular septal defect. Aortic arch obstruction was present in 44% of specimens with a malaligned-outlet ventricular septal defect and in only 3% of specimens with an intact ventricular septum.[28] Other types of outlet ventricular septal defects occur less commonly in patients with d-transposition. Outlet ventricular septal defects can occur with posterior displacement of the infundibular septum, left ventricular outflow tract narrowing, and posterior malalignment between infundibular septum and trabecular septum.[26] In these cases, muscular subpulmonary obstruction is nearly always present. Because of the posterior deviation of the infundibular septum, a direct route from left ventricle to aorta is present, and patients with this defect are good candidates for repair by way of intraventricular rerouting from left ventricle to aorta.[26] Coarctation of the aorta is not associated with this type of ventricular septal defect. Another type of outlet ventricular septal defect that occurs very infrequently in patients with d-transposition is a subarterial (subaortic)

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ventricular septal defect in which the infundibular septum is hypoplastic or absent, but not displaced.[26] In patients with this defect, the aorta is frequently to the left and anterior. [26] Perimembranousinlet ventricular septal defects are commonly found in patients with d-transposition. This type of defect is also associated with tricuspid valve abnormalities of the type described earlier for a malaligned-outlet defect. In one series, 100% of patients with inlet ventricular septal defect had tricuspid valve abnormalities.[27] Other types of defects found with d-transposition are isolated muscular defects and perimembranous trabecular defects. Left Ventricular Outflow Tract Obstruction.

Obstruction to the pulmonary outflow occurs in patients with dtransposition with or without a ventricular septal defect. With an intact ventricular septum, dynamic subpulmonary obstruction is common, either before or after an intra-atrial baffle procedure. This dynamic obstruction is caused by a prominent systolic bulging of the ventricular septum into the left ventricular outflow tract.[29] On the short-axis views the left ventricle is thin walled and crescent shaped. Only minimal pressure gradients are detected by pulsed or continuous wave Doppler techniques. With significant fixed anatomic obstruction and an intact ventricular septum, the left ventricular pressure increases and the left ventricle becomes spherical and thick walled. The most common forms of fixed pulmonary 854

stenosis in this setting are fibrous subpulmonary diaphragm, fibromuscular ridge, and valvular stenosis (usually a bicuspid pulmonary valve).[30] Subpulmonary stenosis occurs more commonly in association with a ventricular septal defect, and certain types of subpulmonary stenosis are specific for certain types of ventricular septal defect. For example, posterior deviation of the infundibular septum occurs with malaligned-outlet ventricular septal defect,[26] whereas accessory tricuspid leaflet tissue bowing into the left ventricular outflow tract tends to occur with perimembranous-inlet defects.[27] Atrioventricular Discordance and Ventriculoarterial Discordance or lTransposition of the Great Arteries l-Transposition of the great arteries is a condition in which there is both

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atrioventricular and ventriculoarterial discordance; therefore, in situs solitus the morphologic right atrium on the patient's right is connected to the morphologic left ventricle on the patient's right, which in turn is connected to the pulmonary artery. On the left the morphologic left atrium is connected to the morphologic right ventricle, which is connected to the aorta.[31] This defect is called situs solitus, l-loop, l-transposition, or simply l-transposition. The "l" in the third term is used to describe the spatial relations of the aortic and pulmonic valves. In most cases the aortic valve is to the left; hence the use of the "l." Because of the presence of discordant connections at two levels, the circulation is hemodynamically correct (systemic venous blood flows to the pulmonary artery and pulmonary venous blood flows to the aorta); some investigators have called this defect corrected transposition of the great arteries. This terminology is not used in this chapter because of the confusion it creates in distinguishing this defect from surgically corrected d-transposition. The mirror-image situation is situs inversus, d-loop, d-transposition. As with d-transposition, the echocardiographic diagnosis of l-transposition is based on demonstrating abnormal connections between the right ventricle and aorta and also between the atria and the ventricles (Fig. 39-11 (Figure Not Available) and Fig. 39-12 ). The spatial relationships of the great arteries may provide supportive evidence of the diagnosis, but these are never used as the sole diagnostic criteria. In l-transposition the aortic valve is usually supported by a complete muscular infundibulum and is therefore located more superiorly than the pulmonary valve (see Fig. 39-11) (Figure Not Available) . In most cases the muscular infundibulum of the left ventricle is absorbed so that the pulmonary valve is wedged deeply in the heart between the two atrioventricular valves. Direct valvular continuity exists between the posterior cusp of the pulmonary valve and the anterior leaflet of the mitral valve; however, indirect continuity also exists with the tricuspid valve on the left via the central fibrous body and membranous septum.[31] With a slight tilting of the plane of sound in the parasternal longaxis view, "continuity" of the pulmonary valve to both atrioventricular valves can be shown. As in d-transposition, the ventricular outflow tracts and great arteries in ltransposition exit the heart in a parallel Figure 39-11 (Figure Not Available) Subcostal coronal views from a patient with situs solitus, l-loop, l-transposition of the great arteries, a large ventricular septal defect, and severe subvalvular and valvular pulmonary stenosis. Top, View obtained with the transducer tilted posteriorly to image the inlets of the heart. The pulmonary

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veins can be seen draining to the left-sided atrium, indicating that it is the morphologic left atrium (LA) and there is atrial situs solitus. Middle, The plane of sound has been tilted anteriorly. The right-sided ventricle has a smooth septal surface and a shape suggesting that it is the morphologic left ventricle (LV). The LV gives rise to a vessel that bifurcates into two branches and is the pulmonary artery (PA). These findings indicate an l-loop with l-transposition. Note the severe subvalvular and valvular pulmonary stenosis and the poststenotic dilation of the PA. There is an outlet ventricular septal defect. Bottom, The plane of sound has been tilted far anteriorly. The ventricle on the left side is triangular in shape and has prominent septal-parietal free wall muscle bundles, indicating that it is the morphologic right ventricle (RV). The RV gives rise to a vessel that arches and is the aorta (AO). RA, right atrium. (From Snider AR, Bengur AR: Two-dimensional and Doppler echocardiography in the evaluation of congenital heart disease. In Marcus ML, Schelbert HR, Skorton DJ, Wolf GL [eds]: Cardiac Imaging: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1991, p 507.)

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Figure 39-12 (color plate.) A, Apical four-chamber view from a patient with atrial situs solitus, l-loop, and l-transposition of the great arteries. Note that the ventricle on the left has a prominent moderator band and an atrioventricular valve closer to the cardiac apex. These findings indicate that the leftsided ventricle is the morphologic right ventricle (RV) and there is an l-loop. The leftsided tricuspid valve in this patient is much more apically displaced than is normal because of associated Ebstein deformity of the valve. B, Color Doppler examination from the same view shows a tricuspid regurgitation jet (red flow area) with a wide proximal diameter indicating a large regurgitant orifice. Note the massive left atrial (LA) dilation caused by the physiologic mitral regurgitation. LV, left ventricle; RA, right atrium. (From Snider AR, Serwer GA, Ritter SB: Echocardiography in Pediatric Heart Disease, 2nd ed. St. Louis, Mosby–Year Book, 1997, p. 322.)

fashion rather than wrapped around each another. Unlike the normal heart or the heart with d-transposition, however, the right ventricle is usually not anterior to the left ventricle in l-transposition. Typically, the ventricles are positioned side by side and the ventricular septum is oriented in a straight line perpendicular to the frontal plane through the thorax (Fig. 39-13) . In some cases the ventricles are arranged in a superoinferior fashion, the morphologic right ventricle being superior (Fig. 39-14) . The unusual spatial relationships of the ventricles, ventricular septum, and great arteries can lead to unusual and often confusing echocardiographic images (especially in the parasternal views). Associated Defects

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Tricuspid Valve Abnormalities.

Abnormalities of the left-sided tricuspid valve occur in about 90% of patients with l-transposition of the great arteries.[31] The common Figure 39-13 A, Parasternal short-axis view from a patient with situs solitus, l-loop, and l-transposition of the great arteries with partial apical pivoting. The ventricle on the left has a prominent moderator band and is the morphologic right ventricle (RV). Note that the ventricles are positioned side by side, with the septum oriented perpendicular to the frontal body plane. This arrangement of the ventricular mass and septum is due to lack of complete apical pivoting, which commonly occurs in hearts with atrioventricular discordance. B, Parasternal short-axis view from a patient with situs solitus, l-loop, and l-transposition of the great arteries with complete apical pivoting. The apex has pivoted completely to the side opposite the loop and thus points to the right hemithorax. As a result, the ventricular septum is oriented in a plane the mirror image of normal. C, Subcostal coronal view from a patient with situs solitus, l-loop, and l-transposition of the great arteries with complete apical pivoting. The apex has completely rotated to the side opposite the loop. Note the left atrioventricular valve positioned closer to the cardiac apex, indicating that it is a tricuspid valve. The plane of the ventricular septum is the mirror image of normal. LA, left atrium; LV, left ventricle; RA, right atrium.

malformation is an Ebstein-type deformity in which the origin of the valve leaflet is displaced downward so that the basal attachments of the leaflets are from the systemic ventricular wall below the annulus fibrosus. Typically, the anterior leaflet is the least malformed and the septal and posterior leaflets are the most malformed. Occasionally, the valve leaflets are fused together and poorly demarcated. The chordae tendineae may be shortened, irregular, and thickened so that they hinder valve motion. All these anatomic features result in some loss in the size of the functioning right ventricle (the "atrialized" portion of right ventricle is between the annulus and the displaced valve) and a tricuspid valve incapable of closing properly (tricuspid regurgitation).[32] [33] [34] In patients with l-transposition, deformities of the tricuspid valve other than Ebstein malformation occur and lead to the development of tricuspid regurgitation (physiologic mitral regurgitation). Deformities such as deficient valve leaflet tissue, thickened valve leaflets, dilation of the annulus fibrosus, abnormal papillary muscles, and 856

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Figure 39-14 Top, Subcostal coronal view from a patient with situs solitus, l-loop, and l-transposition and superior-inferior arrangement of the ventricles. The left atrium (LA) communicates by way of a straddling and overriding tricuspid valve to a superiorly positioned right ventricle (RV). Note the horizontal position of the ventricular septum and the inferiorly positioned, smooth-walled left ventricle (LV). Bottom, Parasternal view through the inflow tracts of both ventricles. The two atrioventricular valves are seen in the same view aligned parallel, indicating that this patient does not have crisscross atrioventricular relations. RA, right atrium.

shortened chordae tendineae that insert directly into the ventricular wall may all occur and contribute to valvular dysfunction.[33] In patients with ltransposition and a ventricular septal defect (usually perimembranous inlet), chordae can insert through the ventricular septal defect into the morphologic left ventricle (straddling tricuspid valve). Uncommonly, obstruction to right ventricular inflow can occur in patients with l-transposition. This obstruction usually takes the form of a stenosing membrane or ring just above the tricuspid valve. On the 2D echocardiogram a supratricuspid stenosing ring appears as a thin, linear echo just above the left-sided tricuspid valve. Medially, the ring inserts into the left atrial surface just above the crux of the heart, and laterally it inserts into the free wall of the left atrium below the appendage.[35] Ventricular Septal Defect.

Ventricular septal defect occurs in about 70% of patients with ltransposition[31] and is usually perimembranous in location. In ltransposition, ventricular septal defects are frequently accompanied by other malformations (i.e., perimembranous inlet defects are associated with tricuspid valve straddle; anterior outlet defects are associated with mitral valve straddle). Left Ventricular Outflow Tract Obstruction.

Left ventricular outflow tract obstruction occurs in approximately 40% of patients with l-transposition. Usually, the stenosis is subvalvular—either a subvalvular diaphragmatic ring or an aneurysm of fibrous tissue protruding into the left ventricular outflow tract.[36] This fibrous tissue can originate from the membranous septum, mitral valve, tricuspid valve, or pulmonary valve. Right Ventricular Outflow Tract Obstruction.

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Right ventricular outflow obstruction is rare in patients with l-transposition, occurring in only about 10% of patients. [35] Subaortic stenosis can occur in patients with an outlet ventricular septal defect and anterior and leftward displacement of the infundibular septum. Most patients with l-transposition and subaortic stenosis also have aortic coarctation; however, aortic coarctation can occur without subaortic stenosis.[35] Atrioventricular Discordance with Ventriculoarterial Concordance Isolated Ventricular Inversion

Isolated ventricular inversion is a term first used in 1966 to describe the rare congenital cardiac malformation of ventricular inversion without transposition of the great arteries (i.e., atrioventricular discordance and ventriculoarterial concordance).[37] Because isolated ventricular inversion causes a physiologic state identical to that of complete transposition of the great arteries, most patients with this defect are symptomatic in infancy with cyanosis and congestive heart failure. On the 2D echocardiogram, patients with isolated ventricular inversion have atrioventricular discordance.[38] In the usual situation, there is atrial situs solitus and lbulboventricular loop (Fig. 39-15) (Figure Not Available) . The ventriculoarterial connections are normal. Thus, a posterior aorta usually arises from a right-sided morphologic left ventricle and is in fibrous continuity with the right-sided mitral valve (Fig. 39-16) (Figure Not Available) . An anterior pulmonary artery arises from the left-sided morphologic right ventricle and is separated from the left atrioventricular valve by a persistent subpulmonary conus. The normal relationships of the great arteries to one another (aortic valve rightward, posterior, and inferior to the pulmonary valve; great arteries coiled around each other) create a "circle-sausage" appearance in the short-axis views. Anatomically Corrected Malposition

Another rare defect with atrioventricular discordance and ventriculoarterial concordance is anatomically corrected malposition.[5] The echocardiographic techniques described previously are used to diagnose atrioventricular discordance (morphologic right atrium connected to morphologic left ventricle) and ventriculoarterial concordance (aorta arising from morphologic left ventricle).[39] In anatomically corrected malpositions, however, there is an 857

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Figure 39-15 (Figure Not Available) Apical four-chamber view showing normal atrial situs and discordant atrioventricular connections in a patient with isolated ventricular inversion. The pulmonary veins can be seen draining to the left-sided atrium, suggesting that this chamber is the morphologic left atrium (LA); therefore, there is atrial situs solitus. The left-sided ventricle has a prominent septoparietal muscle bundle and an atrioventricular valve closer to the cardiac apex. These features show that this chamber is the morphologic right ventricle (ARV); therefore, there is ventricular inversion. The right-sided morphologic left ventricle (ALV) has no septoparietal muscle bundles and has an atrioventricular valve farther from the cardiac apex. A, apex; R, right; RA, right atrium. (From Snider AR, Enderlein MA, Teitel DR, et al: Isolated ventricular inversion: Two-dimensional echocardiographic findings and a review of the literature. Pediatr Cardiol 1984;5:28.)

abnormal relationship between the aorta and the atrioventricular canal, such that mitral-aortic fibrous continuity does not occur (there is usually bilateral conus). In addition, although the great vessels arise above the correct chamber, the aortic valve is anterior to the pulmonary valve and the great vessels exit the heart in a parallel fashion. Univentricular Atrioventricular Connection Nomenclature and Definitions

Considerable controversy exists surrounding the definition, classification, and nomenclature for various forms of complex congenital heart defects; however, there is no greater controversy than that surrounding the nomenclature of hearts with a large dominant ventricle and a small rudimentary ventricular chamber that lacks an inflow. Terms used to describe these hearts include single ventricle, double-inlet ventricle, univentricular heart, and univentricular atrioventricular connection, among others. The debate started with the use in classic descriptions of the term "single ventricle."[19] As pointed out by Van Praagh et al,[19] the hearts in this category nearly always possess two ventricular chambers; therefore, the term "single ventricle" is inaccurate. In the late 1970s and early 1980s, Anderson et al[40] [41] [42] [43] attempted to clarify the confusion surrounding the terminology and classification of these hearts. They used the term univentricular heart of the left ventricular type to describe hearts in which the dominant chamber was morphologically a left ventricle and the rudimentary chamber had morphologic features of the trabecular portion of the right ventricle, and the term univentricular heart of the right ventricular type to describe hearts in which the dominant chamber was morphologically a right ventricle and the

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rudimentary chamber had morphologic features of the trabecular portion of the left ventricle. These authors introduced a new definition for what constitutes a ventricle and introduced terms to define rudimentary chambers in the heart that were not by definition ventricles.[40] [41] [42] Their proposed nomenclature was based on the following observations: The ventricles of the normal heart possess inlet, trabecular, and outlet Figure 39-16 (Figure Not Available) Subcostal coronal views from the same patient as in Figure 39-15 (Figure Not Available) . These views show discordant atrioventricular connections and normal relationships between the great arteries and the ventricles. Top, The aorta (Ao) and aortic arch can be seen arising from the rightsided ventricle, which the four-chamber view in Figure 39-15 (Figure Not Available) has shown to be the morphologic left ventricle (ALV). Bottom, With even more anterior tilting of the transducer, the anteriorly positioned pulmonary artery (PA) and its bifurcation can be seen arising from the left-sided morphologic right ventricle (ARV). In addition, the great vessels are normally coiled around each other ("circle sausage" appearance). A subaortic ventricular septal defect also can be seen. I, inferior; R, right; RA, right atrium. (From Snider AR, Enderlein MA, Teitel DR, et al: Isolated ventricular inversion: Two-dimensional echocardiographic findings and a review of the literature. Pediatr Cardiol 1984;5:28.)

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portions.[42] The inlet portion extends from the atrioventricular annulus to the insertions of the papillary muscles and need not contain a perforate atrioventricular valve. The outlet portion supports the semilunar valve, and the trabecular portion extends from the inlet and outlet portions to the ventricular apex. In the normal heart the inlet and outlet portions of the morphologic left ventricle are in fibrous continuity. In the morphologic right ventricle, these two portions are separated from one another by the crista supraventricularis. In the normal heart, each trabecular zone receives its own inlet; however, all the atrioventricular inlets can be committed to one trabecular portion, which is the classic definition of single ventricle.[40] [42]

As discussed earlier, Anderson et al then proposed that a chamber must have 50% or more of an inlet portion to be classified as a ventricle. A chamber need not have an outlet portion to be a ventricle (the left ventricle in

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Figure 39-17 Diagrammatic representation of the anatomic features used to diagnose the type of univentricular heart on two-dimensional echocardiography. The drawings represent parasternal short-axis projections. In single ventricle of the left ventricular (LV) type, the trabecular septum (stippled) and rudimentary chamber (RC) are anterior to the atrioventricular valves. The trabecular septum runs to the acute or obtuse margin of the heart and not to the crux of the heart (black circle). Thus, there is no intervening septum at the crux of the heart between the atrioventricular valves. Most often, the RC is at the left basal aspect of the heart (l-loop); however, it can also be located less frequently at the right basal aspect of the heart (d-loop). Most commonly, the ventriculoarterial connections are discordant with the aorta (AO) arising from the RC and the pulmonary artery (PA) arising from the main ventricle (depicted in the diagram); however, any ventriculoarterial connection is possible. In single ventricle of the right ventricular (RV) type, the RC and trabecular septum are posterior to the atrioventricular valves. The trabecular septum courses to the crux of the heart and there is usually left atrioventricular valve atresia (shown). Most commonly, the ventriculoarterial connections are double outlet from the main ventricle (shown); however, any ventriculoarterial connection is possible.

double-outlet right ventricle has only inlet and trabecular portions). Chambers receiving less than 50% of an inlet were termed rudimentary chambers. Rudimentary chambers possessing an outlet portion were termed outlet chambers, whereas those with only a trabecular zone were called trabecular pouches. Subsequently, Van Praagh and others argued that this definition of a ventricle was arbitrary and that the use of the term "univentricular heart" was misleading, because these hearts really possess two ventricular chambers.[18] [19] These investigators suggested that the hearts in question be described in terms of their basic embryologic abnormality (abnormal atrioventricular connection), and thus preferred the continued use of terms such as double-inlet left ventricle and tricuspid atresia. In 1984, Anderson et al[20] (in response to arguments against their definition of a ventricle) introduced the term univentricular atrioventricular connection to describe hearts in which both inlets 859

(whether patent or not) were primarily committed to one dominant ventricle. They described the small ventricular chamber that is present in almost all of these hearts as a rudimentary ventricle because it lacked the inlet portion.

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This short review of the controversy surrounding the nomenclature and classification of univentricular atrioventricular connection was undertaken not to support one point of view but to explain and clarify as many of the existing schools of thought as possible. Readers must choose their own preferred nomenclature, but it is important that they understand the meaning and derivation of all terms used in the medical literature to avoid confusion and misunderstanding. Throughout this chapter, the approach to the echocardiographic diagnosis of univentricular heart is based on the definitions and classification proposed by Anderson et al.[40] [41] [42] The distinction made in using the term "univentricular atrioventricular connection" is appreciated; however, the term "univentricular heart" often is used instead (with the realization that there are two ventricular chambers) because it is simpler and less cumbersome. Also, the terms "outlet chamber" and "trabecular pouch" continue to be used occasionally because they are in widespread use and are understood by everyone. Also, these terms, in a simple and economic use of words, convey additional information concerning the inlet and outlet connections of the chamber. Anatomic Findings

In the most common type of univentricular heart, all atrioventricular connections are committed to a chamber with a left ventricular trabecular pattern. In this case the rudimentary chamber has a right ventricular trabecular pattern and is located anterosuperiorly in the ventricular mass. This defect has been called double-inlet left ventricle, single ventricle of the left ventricular type, and univentricular heart of the left ventricular type. Conversely, all atrioventricular connections can be committed to a chamber with right ventricular trabecular pattern. In this situation the rudimentary ventricle contains a left ventricular trabecular portion and is located posteriorly in the ventricular mass. This defect is known as univentricular heart of the right ventricular type. In rare cases, neither right nor left ventricular trabecular portions are well formed and a single chamber is present with indeterminate trabecular pattern. This defect has been called univentricular heart of the indeterminate type without rudimentary chamber.[41] [42] Another important point in the morphology and echocardiographic diagnosis of univentricular heart is the nature of the septum that separates the main ventricle from the rudimentary chamber. Because the ventricles are considered to possess inlet, trabecular, and outlet portions, the septum separating them can be considered to possess inlet, trabecular, and outlet portions. Both inlets are committed to only one chamber; hence, by

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definition, the inlet septum is absent in the univentricular heart. The septum separating the ventricle from the rudimentary chamber must be the trabecular septum. The position and orientation of the trabecular septum in the ventricular mass is a key feature in the echocardiographic diagnosis of the univentricular heart.[42] Figure 39-18 Parasternal long-axis view from a patient with a univentricular heart of the left ventricular type and discordant ventriculoarterial connections. In this view the small outlet chamber (OC) can be seen anterior to the main left ventricle (LV). In this patient the pulmonary artery (PA) arose from the LV and the aorta (AO) arose from the OC. There was no pulmonary stenosis and the bulboventricular foramen was restrictive (1.4 cm2 /m2 ). LA, left atrium. Echocardiographic Diagnosis of the Type of Univentricular Heart

In univentricular heart of the left ventricular type the rudimentary chamber is located anterior to the main ventricle and is separated from this chamber by an anterior trabecular septum (Fig. 39-17) . Because the trabecular septum is an anterior structure, it is well visualized in the parasternal longand short-axis views.[43] [44] [45] In the parasternal long-axis view (Fig. 39-18) the rudimentary ventricle is seen anteriorly and separated from the main chamber by the trabecular septum. The outlet foramen or ventricular septal defect is seen connecting the main left ventricle and the rudimentary right ventricle. With this view alone it is not possible to distinguish a univentricular heart of the left ventricular type from a ventricular septal defect with a large left ventricle. This distinction is not possible because the parasternal long-axis view allows visualization of only one atrioventricular connection. Also, because the parasternal long-axis view has only anteroposterior and inferosuperior orientations, it is not possible to determine whether the rudimentary chamber is at the right or left basal aspect of the heart. When the transducer is rotated into the parasternal short-axis view, the distinction between univentricular heart of the left ventricular type and ventricular septal defect with a large left ventricle is immediately apparent. In univentricular heart of the left ventricular type, both atrioventricular valves lie posterior to the trabecular septum (Fig. 39-19) . Because these valves usually do not have the anatomic features of the normal tricuspid and mitral valves, we refer to them as the right and left atrioventricular valves. There is no intervening inlet septum between the two atrioventricular valves; therefore, these valves may actually touch one

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another when they open in diastole ("kissing" atrioventricular valves). In addition, 860

Figure 39-19 Parasternal short-axis view from a patient with a univentricular heart of the left ventricular type and ventriculoarterial discordance. The right and left atrioventricular valves are both committed to the left ventricle (LV). There is no septum intervening between the valves. Note the outlet chamber (OC) situated anteriorly. Both atrioventricular valves are posterior to the trabecular septum. The trabecular septum lies between the OC and the LV.

both atrioventricular valves are in fibrous continuity with the posterior great artery. From the parasternal short-axis view, one can determine whether the rudimentary right ventricle lies to the right or left basal aspect of the heart. Most commonly, the rudimentary right ventricle lies to the left (l-loop) and the trabecular septum courses obliquely and somewhat posteriorly from the right and anterior cardiac border to the acute margin of the heart. When the rudimentary chamber lies to the right (d-loop), the trabecular septum courses obliquely and somewhat posteriorly from the left anterior cardiac border to the obtuse margin of the heart (see Fig. 39-19) . From the parasternal short-axis views, one can easily understand why the rudimentary chamber and trabecular septum cannot be visualized in the four-chamber views in patients with univentricular heart of the left ventricular type. The four-chamber views are posterior planes that pass through both atrioventricular valve inlets and the crux of the heart; therefore, these planes lie posterior to the trabecular septum and rudimentary chamber (Fig. 39-20) . In an echocardiographic study of 57 patients with double-inlet left ventricle,[46] all patients had atrial situs solitus and normal systemic and pulmonary venous return. An l-loop was present in 63% and a d-loop in 37%. Shiraishi and Silverman[47] reported finding atrial situs inversus in 2 of 42 patients with double-inlet left ventricle and 2 atrioventricular valves. In their series, l-loop occurred in 74% and d-loop in 26%. In univentricular heart of the right ventricular type the rudimentary chamber possesses the left ventricular trabecular portion and is thus located posteriorly (see Fig. 39-17) . Likewise, the trabecular septum runs

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posteriorly to the crux of the heart. In the parasternal long- and short-axis views, visualization of the atrioventricular connections anterior to the trabecular septum is diagnostic of univentricular heart of the right ventricular type (Fig. 39-21) . The rudimentary chamber can be located posteriorly and to the right or posteriorly and to the left. Because the rudimentary chamber is posterior and the trabecular septum extends to the crux of the heart, portions of these two structures normally can be seen in the apical and subcostal four-chamber views. If a single chamber is present in the heart with no evidence of a trabecular septum or rudimentary chamber in any echocardiographic view, the diagnosis of univentricular heart of indeterminate type can be made. Echocardiographic Evaluation of Ventriculoarterial Connections

With the univentricular heart, any ventriculoarterial connection can occur, including concordant connections, Figure 39-20 Subcostal coronal views from a patient with univentricular heart of the left ventricular type and discordant ventriculoarterial connections. Top, The transducer has been tilted posteriorly to image the inlets of the heart. This view is a posterior plane passing through both atrioventricular valve inlets and the crux of the heart; therefore, this plane lies posterior to the trabecular septum and rudimentary chamber. Note the "kissing" atrioventricular valve with no intervening ventricular septum oriented to the crux of the heart. Both atrioventricular valves empty into the large posterior left ventricle (LV). Bottom, The transducer has been tilted anteriorly to image the outflow tracts. The LV is connected to a posterior pulmonary artery (PA). A small rightward and anterior outlet chamber (OC) gives rise to an anterior and rightward aorta (AO). Note that many of the echocardiographic features of transposition of the great vessels are seen. The great vessels are aligned parallel and the posterior PA has a posterior sweep. The bulboventricular foramen in this patient was of good size. LA, left atrium; RA, right atrium.

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Figure 39-21 Parasternal long-axis (top) and short-axis (bottom) views from a patient with univentricular heart of the right ventricular type. The main right ventricle (RV) is anterior to a small rudimentary left ventricle (LV). Top, Both great arteries arise from the RV, with the pulmonary artery (PA) located posterior to the aorta (AO). There is muscular subvalvular pulmonary stenosis. Bottom, Both atrioventricular valves (arrows) can be seen

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emptying into the RV anterior to the trabecular septum and rudimentary LV.

discordant connections, double outlet from the main or outlet chambers, and single outlet from the heart. Certain combinations of univentricular heart and ventriculoarterial connections, however, are commonly associated with one another and thus deserve mention. A high percentage of patients with univentricular heart of the left ventricular type have discordant ventriculoarterial connections: the aorta arises from the rudimentary right ventricle or outlet chamber and the pulmonary artery arises from the main left ventricle. In this situation the great vessels are parallel and exhibit the characteristic echocardiographic features of transposition (parallel alignment of the great arteries in long-axis views, posterior sweep of the posterior pulmonary artery in long-axis views, double circles in short-axis views) (see Fig. 39-20) . In the report of 57 patients with double-inlet left ventricle referred to previously,[46] transposition of the great arteries was present in 86% (13 with d-loop and 36 with l-loop). The great arteries were normally related in the remaining 14%, all of whom had a d-loop (so-called Holmes heart). In univentricular heart of the left ventricular type with absent right atrioventricular connection, the bulboventricular loop is usually to the right and the ventriculoarterial connections are most often concordant.[40] [41] [42] In univentricular heart of the right ventricular type, the ventriculoarterial connections are usually double outlet from the main chamber or single outlet from the heart with pulmonary atresia. In univentricular heart of indeterminate type and no outlet chamber, the connections can only be double outlet or single outlet from the main chamber.[42] Echocardiographic Evaluation of Atrioventricular Connections Double-Inlet Connections.

In the most common situation, univentricular heart exists with a doubleinlet atrioventricular connection in which both atria connect with the dominant ventricle by way of two separate atrioventricular valves or, less commonly, by way of a common atrioventricular valve. In the series of 50 patients with double-inlet ventricle reported by Shiraishi and Silverman,[47] double-inlet connection occurred with two atrioventricular valves in 88% and with a common atrioventricular valve in only 12%. It is of note that all the patients in this series with double inlet by way of a common atrioventricular valve had echocardiographic features of situs ambiguus. Also of note was the finding of a stenotic atrioventricular valve in 30% of

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patients with two separate atrioventricular valves. Most often, the stenotic valve was the left atrioventricular valve. On echocardiographic examination of patients with double-inlet left ventricle by way of two atrioventricular valves, the atrioventricular valves can be seen in short-axis and four-chamber views, both situated posterior to the trabecular septum (see Fig. 39-20) . There is no intervening inlet septum and both valves are in continuity with the posterior great artery. Univentricular hearts of the right ventricular type also can have doubleinlet connection by way of two atrioventricular valves. Usually the valves lie side by side and anterior to the trabecular septum.[42] Univentricular hearts of indeterminate type usually have a double-inlet connection, but this connection is generally via a common atrioventricular valve rather than by separate right and left atrioventricular valves. Absence of an Atrioventricular Connection.

Many hearts with atresia of an atrioventricular valve have absence of the connection rather than an imperforate valve. In absent connection the floor of the atrium is entirely muscular and is separated from the main ventricle by the atrioventricular sulcus.[42] This situation is quite distinct from those in which an imperforate membrane or connection sits above a tiny ventricular chamber. For example, in patients with univentricular heart of the left ventricular type and absent right atrioventricular connection, the apical and subcostal four-chamber views show the right and left atria above the main ventricle (Fig. 39-22A) (Figure Not Available) . There is no small chamber situated beneath the atretic right connection and no evidence of a septum oriented to the crux of the heart. The rudimentary chamber and trabecular septum are located anteriorly and have no connection to the blind-ending right atrium. [41] [42] In tricuspid atresia with an imperforate membrane and two separate ventricles, the right atrium can be seen in the four-chamber views situated directly above and connected to a small 862

Figure 39-22 (Figure Not Available) A, Apical four-chamber view from a patient with univentricular heart of the left ventricular type with an absent right atrioventricular connection. The right atrium (RA) and the left atrium (LA) both sit above the large left ventricle (LV). There is no small chamber beneath the atretic right connection and no evidence of a septum oriented to the crux of the heart. B, Apical four-chamber view from a patient with tricuspid atresia with an imperforate membrane and two separate ventricles. The connection between the RA and right ventricle (RV) is present, but the tricuspid valve is imperforate. The ventricular septum courses to the crux of the heart

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between the RV and LV, with the ventricular septal defect shown by the arrow. (From Snider AR, Bengur AR: Two-dimensional and Doppler echocardiography in the evaluation of congenital heart disease. In Marcus ML, Schelbert HR, Skorton DJ, Wolf GL [eds]: Cardiac Imaging: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1991, p 495.)

right ventricular chamber (see Fig. 39-22B) (Figure Not Available) . Here, the connection between the right atrium and right ventricle is present, but the tricuspid valve is imperforate. The ventricular septum courses to the crux of the heart between the right and left ventricles. The same diagnostic approach applies to the distinction between hypoplastic left heart with mitral atresia and univentricular heart of the right ventricular type with absent left atrioventricular connection. Straddling Valves.

In univentricular hearts an inlet portion can override or straddle the trabecular septum, whether it is located anteriorly or posteriorly. The degree of commitment of the straddling valve to its own trabecular zone or to the trabecular zone of a chamber already receiving an inlet determines whether the heart is classified as biventricular or univentricular.[42] In some instances the straddling inlet appears equally committed to both chambers on the 2D echocardiogram, and a definite diagnosis cannot be made. In these cases the position of the small chamber and septum may suggest the most likely diagnosis. Echocardiographic Evaluation of Interventricular Communication

In hearts with univentricular atrioventricular connection the communication between the main and rudimentary ventricles has been referred to by several terms, including ventricular septal defect, bulboventricular foramen, and outlet foramen. Bevilacqua et al[46] described the morphology of the ventricular septal defect in 46 patients with double-inlet left ventricle. In 24 patients the defect was separated from the semilunar valves and completely surrounded by muscle (muscular defect), and it tended to enter the rudimentary chamber inferiorly and apically. In 19 patients the defect was adjacent to the anterior semilunar valve (subaortic defect), and it was associated with hypoplasia of the infundibular septum in 5 patients and posterior malalignment of the infundibular septum (with or without hypoplasia) in 14. The remaining 3 patients had multiple muscular defects. Although further anatomic subsets of defects (e.g., midmuscular, atrioventricular canal types) can be distinguished on the pathologic examination, these subtypes were not recognized reliably on

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echocardiographic examination. The ventricular septal defect was restrictive in 47%. Only 21% of subaortic defects were restrictive, whereas 67% of muscular defects were restrictive. In patients with double-inlet left ventricle and transposition a restrictive ventricular communication resulted in an increased incidence of subaortic stenosis and/or aortic arch obstructions. The defect can be stenotic at birth or can become restrictive. In patients with transposition and pulmonary stenosis the defect was rarely stenotic; however, in transposition without pulmonary stenosis a restrictive ventricular septal defect was significantly more common. These are the same patients previously reported to develop subaortic stenosis after pulmonary artery banding.[48] [49] It is likely that subaortic stenosis develops in these patients not because of the pulmonary artery banding procedure but because the initial size of the defect places them at risk for developing a restrictive interventricular communication, and consequently subaortic stenosis. The pressure gradient across a restrictive outlet foramen can be estimated from several views using Doppler echocardiography; however, several studies suggest that direct measurement of the size of the foramen is a better indicator of obstruction.[47] [50] Situs Ambiguus The association of splenic abnormalities with complex cardiac defects and abdominal heterotaxy is well described. Traditionally, 863

these syndromes have been referred to as asplenia and polysplenia because each appears to be somewhat distinct in regard to the associated cardiac abnormalities, clinical features, and outcomes.[51] [52] [53] For example, Van Mierop et al[54] [55] described the association of right atrial isomerism with asplenia syndrome, noting the presence of bilateral sinoatrial nodes and two morphologic right atrial appendages in these hearts. Similarly, they observed left atrial isomerism with two morphologic left atrial appendages in hearts with polysplenia syndrome.[56] Noting that the status of the spleen was not always a reliable marker of these two syndromes, Van Mierop et al [57] preferred to use the bronchial branching pattern as a more consistent indicator of the diagnosis. In Phoon and Neill's[51] comprehensive review of asplenia, however, some examples of asplenia associated with bilateral bilobed lungs, interrupted inferior vena cava, and other features more

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commonly associated with polysplenia were described. These researchers concluded that although asplenia is clearly a syndrome of relative right isomerism and polysplenia a syndrome of relative left isomerism, some overlap exists between the two syndromes, making all the currently used terminology (e.g., asplenia, polysplenia, situs ambiguus, bilateral rightsidedness, bilateral left-sidedness) somewhat unsatisfactory. Although recent observations in patients with these syndromes suggest that they represent a continuum of congenital defects (both cardiac and extracardiac), there are several associated anomalies whose presence might suggest one or the other diagnosis.[4] [51] [58] [59] [60] [61] [62] [63] [64] For example, bilateral superior venae cavae, each draining to the ipsilateral atrial cavity, are commonly found in both asplenia and polysplenia; however, drainage of the left-sided superior vena cava to the coronary sinus is encountered nearly always with polysplenia. Anomalies of the systemic veins that drain the abdomen are also common.[61] In asplenia syndrome the inferior vena cava and aorta tend to be on the same side of the spine, either to the right or to the left (Fig. 39-23) (Figure Not Available) .[56] In polysplenia syndrome the inferior vena cava is frequently interrupted. In these cases, lower systemic venous return is by way of the azygous or hemiazygous vein, and the hepatic veins drain directly into one or both atria (Fig. 39-24) .[56] [61] [62] Anomalous pulmonary venous return also is common in situs ambiguus. In asplenia syndrome, total anomalous pulmonary venous return is nearly always present (in more than 80% of cases) and can be of any type. When the veins enter the cardiac atrium directly (rather than by way of a common pulmonary vein), they tend to drain to the smooth intercaval portion of the atria near the midline and are connected by a narrow confluence.[61] In polysplenia syndrome the pulmonary veins enter one atrium in a normal fashion in one third of cases. In over 50% of cases, however, the right veins enter the right-sided atrium and the left veins enter the left-sided atrium.[56] The anatomy of the cardiac chambers and great vessels is extremely variable in situs ambiguus, but a few common associations deserve mention. In asplenia syndrome, atrioventricular septal defects and single ventricle are common. Most often, the single ventricle is not the classic double-inlet left ventricle; instead, a very rudimentary septum is present between the two ventricles.[51] The great arteries Figure 39-23 (Figure Not Available) Subcostal short-axis (top) and sagittal (bottom) views from a patient with asplenia syndrome. The inferior vena cava (IVC) is on the same side of the spine as the descending aorta (DAO). Note that the IVC is anterior to

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the DAO. This abnormality of systemic venous drainage is commonly present in patients with asplenia syndrome. A, anterior; Ao, aorta; R, right; V, vertebral body. (From Snider AR, Bengur AR: Two-dimensional and Doppler echocardiography in the evaluation of congenital heart disease. In Marcus ML, Schelbert HR, Skorton DJ, Wolf GL [eds]: Cardiac Imaging: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1991, p 505.)

are frequently transposed and there is a high incidence of severe pulmonary stenosis or atresia. In polysplenia syndrome, atrial septal defects, ventricular septal defects, and double-outlet right ventricle are often encountered. Transposition of the great arteries and severe pulmonary stenosis are uncommon in polysplenia syndrome.[56] [60] Crisscross Hearts The term crisscross heart has been used to describe the rare abnormality in which the systemic and pulmonary venous streams cross at the atrioventricular level without mixing. The right-sided atrium connects to the left-sided ventricle and the left-sided atrium connects to the right-sided ventricle. This defect is believed to occur as a result of a differential rate of development of the right ventricular 864

Figure 39-24 (color plate.) Color Doppler examinations from a patient with polysplenia syndrome and an interrupted inferior vena cava. A, In the subcostal cross-sectional view, the descending aorta flow is seen in red (flow toward the transducer) because the transducer is situated in the abdomen and pointed slightly superiorly toward the patient's head. A large venous structure (blue flow area) is seen posterior and to the left of the descending aorta in the abdomen. This posterior structure represents a large hemizygous vein through which the lower body systemic venous drainage returned to a left-sided superior vena cava. Flow in the hemizygous vein is seen in blue because the flow is directed away from the transducer and toward the patient's head. B, In the subcostal long-axis view, flow in the descending aorta is again seen in red, indicating flow down the aorta toward the transducer. Flow in the hemizygous vein (located posterior to the aorta) is seen in blue, indicating flow away from the transducer toward the heart. (From Snider AR, Serwer GA, Ritter SB: Echocardiography in Pediatric Heart Disease, 2nd ed. St. Louis, Mosby–Year Book, 1997, p. 568.)

sinus and infundibulum. As a result, the ventricles appear to have rotated around their longitudinal axis (clockwise rotation when viewed from the apex in d-loop ventricles) without concomitant motion of the atria and

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atrioventricular valve annuli, producing actual crossing of the inflow tracts. The defect can be found with concordant or discordant atrioventricular connections. A ventricular septal defect is invariably present, and discordant ventriculoarterial connections are common. Associated defects can be expected.[65] On 2D echocardiography, the diagnosis should be suspected when a parallel arrangement of the atrioventricular valves and ventricular inflow regions cannot be found in the four-chamber views.[65] [66] [67] [68] [69] In the most posterior subcostal four-chamber view the left-sided atrium can be seen communicating by way of an atrioventricular valve to the right-sided ventricle. In the usual situation the left-sided atrium is a morphologic left atrium connected to a right-sided morphologic left ventricle. The left ventricle is posterior, inferior, and rightward. The posterior mitral valve is oriented from posterosuperior to anteroinferior (Fig. 39-25) .[64] As the plane of sound is tilted further anteriorly, the connection from the rightsided atrium to the left-sided ventricle can be seen. In the usual situation the right-sided morphologic right atrium is connected to a morphologic right ventricle that is anterior, superior, and leftward. The anterior and superior tricuspid valve is oriented from right to left and from posterior to anterior. Although part of the tricuspid valve and right ventricular sinus extend to the left of the mitral valve, the annulus of the tricuspid valve is to the right of the annulus of the mitral valve. In this plane a distal portion of the mitral valve leaflets can often be seen in cross section inferior to the longitudinal section through the tricuspid leaflets. With even further tilting of the plane of sound anteriorly, the entire anterior ventricle and its outflow portion can be visualized. In the usual situation this anterior and superior ventricle is a morphologic right ventricle that gives rise to a transposed aorta. Associated defects are common in crisscross hearts. Ventricular septal defects are invariably present and usually occur in the inlet septum. Subvalvular and valvular pulmonary stenosis commonly occur. In most cases of crisscross heart, there is hypoplasia of the right ventricle. The degree of underdevelopment of the right ventricular sinus is directly related to the angle between the long axes of the atrioventricular valves and the degree of ventricular rotation. Straddling mitral valve is also commonly encountered in crisscross hearts. In these cases the ventricles appear to have rotated through a greater angle, thus allowing alignment of the mitral valve and infundibulum.[12] [70]

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Although the ventricles in crisscross hearts are often arranged in a superiorinferior relationship, the terms "crisscross" heart and "superior-inferior ventricles" are not synonymous, and care should be taken not to confuse these entities on the echocardiographic examination. Superior-inferior ventricles represent a distinct entity characterized by a malpositioning of the ventricles with a horizontal ventricular septum.[71] The defect is believed to occur as a result of an abnormal tilting of the cardiac apex in the frontal plane. In a study of 17 patients with superior-inferior ventricles, Hery et al [71] found crisscross relationships of the atrioventricular valves in 41% of the patients. Most patients (59%) did not have crisscross relationships. Crisscross heart is one of the few congenital defects in which knowledge of the atrioventricular connections or alignments is wrongly predictive of the ventricular spatial position. For example, knowledge of the atrial situs and the bulboventricular loop indicates the atrioventricular connections, which in turn usually correspond to the situs or position of the ventricles. Thus, the usual form of crisscross heart (right-sided morphologic right atrium to left-sided morphologic right ventricle to left-sided aorta) can be described as atrial situs solitus, d-loop, and l-transposition of the great arteries.[67] Without further explanation, one would assume from this nomenclature that 865

Figure 39-25 Subcostal coronal views from a patient with a crisscross heart and dextrocardia. Top, The plane of sound is tilted far posteriorly. The pulmonary veins drain to the left-sided atrium, suggesting that this is a morphologic left atrium (LA). The morphologic LA is connected to a smoothwalled ventricle that has the anatomic features of a morphologic left ventricle (LV). The LV is located posteriorly, inferiorly, and rightward. The posterior mitral valve is oriented from posterosuperior to anteroinferior. Middle, The plane of sound has been tilted anteriorly so that the connections from the right-sided atrium to the left-sided ventricle can be seen. The right-sided atrium receives the drainage of the superior vena cava (SVC) and has other features suggesting that this chamber is a morphologic right atrium (RA). The anterior and superior tricuspid valve (arrows) is oriented from right to left and from posterior to anterior. A cross-section of the distal portion of the mitral valve leaflets can be seen inferior to the longitudinal section through the tricuspid valve leaflets. This view provides direct visualization of the crisscross arrangement of the atrioventricular valves. Bottom, Further tilting of the transducer shows that the left-sided ventricle has features of a morphologic right ventricle (RV) and gives rise to the leftward and anterior aorta (AO). Note that the morphologic RV is anterior, superior, and leftward.

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the atrioventricular alignments or connections are concordant and that the morphologic right ventricle is to the right of the morphologic left ventricle. It is suggested, therefore, that in the rare instances in which there is disharmony between the situs and alignment information, both should be stated. The previously mentioned heart would then be referred to as atrial situs solitus, d-loop ventricles with crisscross connections, and ltransposition of the great arteries.[12] [67]

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868

Chapter 40 - Echocardiographic Evaluation of the Adult with Unoperated Congenital Heart Disease Mary Etta E. King MD

Caring for adults with congenital heart disease who have not had prior surgical intervention is a fascinating lesson in the natural history of congenital anomalies of the heart. It can also be a remarkable tribute to the tolerance, adaptation, and perseverance of the patient in the face of longstanding cardiac disability. In managing adults with unoperated congenital heart disease, three clinical subgroups emerge: patients with mild or slowly progressive defects who do not require intervention; patients who have eluded previous diagnosis and are still amenable to surgical correction; and patients with abnormalities that are deemed inoperable. It is the task of the cardiologist to evaluate each patient thoroughly to determine optimal management. Echocardiography has been a major boon to cardiologists in diagnosing and evaluating the anatomic and physiologic status of the adult with congenital heart disease. The technique is not without challenge or difficulty, however. Cardiac enlargement and hypertrophy as well as associated scoliosis cause chest wall deformities that limit transthoracic ultrasound access. Congenital or acquired pulmonary disease and cardiac malpositions lend additional

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impediment to surface echocardiographic imaging. Transesophageal echocardiography is useful in circumventing some of these difficulties and plays a major adjunctive role in evaluating and managing the adult with congenital heart disease.[1] [2] It has been said that "chance favors the prepared mind." Thus, the likelihood of an accurate diagnosis with any of these technologies requires a clear understanding of congenital heart defects and the expected sequelae and complications. This chapter includes the clinical features and echocardiographic evaluation and management of congenital heart defects that are encountered in the adult patient without the benefit of previous surgical intervention. Discussion includes valvular abnormalities, disorders affecting the left ventricular outflow tract and aorta, septal defects and shunt lesions, and complex congenital abnormalities most frequently encountered. The relative frequency of these anomalies in the unoperated adult is shown in Table 40-1 .

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Valvular Abnormalities Bicuspid Aortic Valve The congenitally bicuspid aortic valve is the most frequent of all congenital heart defects, occurring in approximately 1% to 2% of the U.S. population. [3] Morphologically, the bicuspid valve may have two equal cusps with a single central commissure, or the cusps may be disparate TABLE 40-1 -- Congenital Heart Defects in the Unoperated Adult Most Common Bicuspid aortic valve

Less Common Ventricular septal defect

Discrete subaortic stenosis Pulmonic stenosis Patent ductus arteriosus

Rare Double-outlet right ventricle Complete transposition

Ebstein's anomaly Coarctation of the Tetralogy of Fallot Truncus arteriosus aorta Coronary arteriovenous fistula Tricuspid atresia Atrial septal Sinus of Valsalva aneurysm Univentricular heart defect Corrected transposition

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Figure 40-1 Echocardiographic views from a patient with a bicuspid aortic valve and a chronic aortic dissection. The parasternal long-axis view (top) demonstrates the markedly dilated proximal ascending aorta

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with a suggestion of an intimal flap (arrow). At surgical repair, the transesophageal echocardiography showed a bicuspid aortic valve (bottom left) and confirmed an intimal tag in the dilated aortic root (bottom right). Ao, aorta; AoV, aortic valve; Asc Ao, ascending aorta; LV, left ventricle.

in size, with an eccentric commissure and the larger cusp containing a raphe. Functionally, a bicuspid valve may be nonstenotic and nonregurgitant, which is especially true in the adolescent and young adult, of whom as many as one third have no significant functional impairment.[4] Progression of stenosis is common, however, even in valves with mild dysfunction. By the age of 60 years, 53% of bicuspid valves are stenotic, and by the age of 70 years, 73% become significantly stenotic. Of individuals older than 40 years who require aortic valve replacements, about 30% have a congenitally abnormal aortic valve.[5] The mechanism of progressive valvular dysfunction appears to be a "wear and tear" process leading to fibrosis and calcification. Congenitally bicuspid aortic valves have a known association with abnormalities of the aorta. Aortic coarctation occurs in a small percentage of patients with bicuspid aortic valves. Aortic dissection is another abnormality recognized for its association with a bicuspid aortic valve (Fig. 40-1) . Reported studies have shown that 5% to 9% of patients with dissecting aneurysms of the aorta also have a bicuspid aortic valve. Pathologic study of the aorta in these patients revealed changes consistent with cystic medial necrosis. [4] [5] [6] [7] Poststenotic dilation of the ascending aorta has long been recognized in congenital aortic stenosis, presumably caused by mechanical impingement of a jet lesion eccentrically directed by the domed leaflets. The ascending aorta may be dilated, however, even in functionally normal bicuspid valves, raising the possibility of a common developmental defect affecting both the valve and the aortic root. Another group of malformations associated with a bicuspid aortic valve is Shone's complex. This complex comprises several levels of inflow or outflow obstruction to the left heart: supramitral ring, congenital mitral stenosis, discrete subaortic membrane, bicuspid aortic valve, and coarctation. Whereas most patients with this "left heart blight" have received evaluation and treatment as children, milder forms may be seen in the adult population, prompting careful assessment of the mitral valve structure and subaortic region in the adult with a bicuspid aortic valve.

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Infectious endocarditis is a significant problem for patients with congenital aortic stenosis (see Chapter 21) . Unfortunately, it may be the presenting symptom for a patient with a previously undiagnosed bicuspid aortic valve. Natural history studies of young adults with congenital aortic stenosis found a 35-fold higher incidence of endocarditis in that group than in the general population.[8] [9] A slightly higher incidence was seen in those patients with aortic regurgitation. Progression of valvular infection to the surrounding aortic root may occur if there is a delay in diagnosis and treatment or in the presence of a particularly invasive microorganism. Echocardiographic Evaluation

The distinctive echocardiographic features of the congenitally bicuspid aortic valve include systolic doming in the parasternal long-axis views and the demonstration of a single commissural line with two functional valve cusps 870

in the parasternal short-axis views. Particular care must be taken to assess the valve in systole as well as in diastole. In patients with asymmetric leaflets and a prominent raphe, the valve may appear tricuspid in diastole; however, the elliptical "football" shape of the systolic orifice indicates that the raphe is not a functional commissure. The valve leaflets often are thickened and fibrotic, more so with increasing age. When extensive calcification occurs, doming may no longer be noted and the morphology of the cusps in the short-axis views may be difficult to distinguish from calcific stenosis of a tricuspid aortic valve. Valvular stenosis should be evaluated with pulsed and continuous wave Doppler imaging exactly as one would a stenotic tricuspid aortic valve. Because of the eccentric nature of the stenotic jet in congenital aortic stenosis, Doppler sampling from the right parasternal window may detect the highest systolic velocities and should always be attempted in addition to the usual apical and suprasternal notch sampling. Serial aortic valve areas should be routinely calculated by the continuity equation in addition to peak and mean gradients. The development of left ventricular dysfunction may mask progression of stenosis if valve gradients alone are used to assess the severity of stenosis.[10] Valvular regurgitation is frequently present and may be the predominant functional abnormality in the adolescent and young adult. Careful

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echocardiographic inspection of the valve leaflets may give an indication of whether Figure 40-2 Transesophageal echocardiographic images from a patient with a bicuspid valve and severe aortic insufficiency. A, An aortic valve in cross section demonstrates the typical elliptic orifice of a bicuspid valve in systole. B, A long-axis view of the left ventricular outflow tract (Lvot) shows that prolapse and malcoaptation of the right coronary leaflet is the cause of the patient's significant aortic insufficiency, shown in C (color plate). Ao, aorta.

regurgitation is caused by fibrosis and retraction of the commissural margins of the leaflets, cusp prolapse, aneurysmal enlargement of the root and valve annulus or valvular destruction secondary to endocarditis. Color flow Doppler imaging readily detects the regurgitant flow and can be used to semiquantitate the degree of aortic insufficiency. Serial assessment of the effect of regurgitation on ventricular size and function should be performed just as described for a regurgitant trileaflet aortic valve ( see Chapter 17 and Chapter 18 ). The subvalvular left ventricular outflow tract and the mitral valve should be carefully investigated for congenital anomalies. Associated coarctation must be excluded, and the size and shape of the ascending aorta should be serially followed. Transesophageal echocardiography may be useful if valve morphology is difficult to determine transthoracically and if such information would guide a surgical attempt at valve repair (Fig. 40-2) . Additionally, more accurate aortic and pulmonary annular dimensions can be measured if a pulmonary autograft (Ross procedure) is planned or to guide the choice of a mechanical valve. Evaluation of endocarditis and aortic root abscess are also indications for a transesophageal study. Quantitative functional assessment of the valve usually is more accurate from the transthoracic approach, although transgastric views may allow adequate Doppler alignment for valve gradients. Management

871

Confirmation of the presence of a bicuspid aortic valve and echo-Doppler determination of the severity of stenosis and regurgitation assist in clinical

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management decisions. Even the patient with a functionally normal bicuspid aortic valve should receive endocarditis prophylaxis for dental work, invasive procedures, and vagin*l delivery. Periodic cardiologic follow-up is also important given the progression of valve dysfunction with age. Patients with mild to moderate degrees of stenosis or insufficiency require more regular surveillance. Development of chest pain, syncope, congestive heart failure, left ventricular hypertrophy with strain, significant arrhythmia or having a mean Doppler gradient of greater than 50 mm Hg are indications for further investigation and consideration of balloon valvuloplasty or surgical valvotomy or valve replacement. In the young adult with supple valve leaflets, balloon valvuloplasty has shown success in relieving significant aortic stenosis.[11] Aortic insufficiency, however, generally increases by at least one grade after percutaneous balloon dilation, limiting the usefulness of this procedure in a patient with combined stenosis and more than mild insufficiency.[12] With newer expertise in surgical aortic valve repair, current indications for surgical intervention in the adolescent and young adult with a bicuspid aortic valve may undergo closer scrutiny. Concerns about valve replacement and anticoagulation in young adults may be unnecessary if initial enthusiasm for aortic valve repair or the Ross procedure is maintained.[13] [14] The Ross procedure involves translocation of the patient's native pulmonary valve into the aortic position and replacement of the pulmonary valve with an aortic hom*ograft. The premature calcification and degeneration that have plagued the hom*ograft and heterologous bioprosthetic aortic valves are not a problem when the patient's own pulmonary valve is used in the aortic position. Some enlargement of the neoaortic annulus and sinuses is observed in the immediate postoperative period, which does not appear to progress with longer follow-up.[14] The long-term outcome of the aortic hom*ograft in the place of the translocated pulmonary valve is uncertain, but intermediate follow-up has shown reasonable durability, with a 9% failure rate and a 12% incidence of dysfunction in a large series of patients. The rate of freedom from dysfunction for older children and adults was 87% at 8 years. Use of a pulmonary autograft was associated with lower rates of failure and dysfunction.[15] Pulmonary Stenosis Congenital valvular pulmonary stenosis is a common anomaly that has a

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slightly higher prevalence in women. This anomaly generally follows a benign course with increasing age. Children and adolescents with mild pulmonary stenosis (peak gradient < 25 mm Hg) have less than a 5% chance of requiring valvotomy during childhood and essentially no need for intervention in adulthood. Those with more moderate degrees of stenosis (peak gradient of 25 to 50 mm Hg) have only a 20% likelihood of requiring intervention.[16] Pulmonary valve morphology in the adult usually involves a supple but thickened valve with commissural fusion or a bicuspid valve. Calcification is rarely seen even in older patients. Poststenotic dilation of the main and left pulmonary arteries is common. Pulmonary insufficiency is frequently present, but it is usually mild.[17] Valvular stenosis is usually an isolated finding; however, acquired infundibular stenosis, supravalvular stenosis, branch pulmonary stenoses, and atrial septal defect are occasionally associated. Abnormalities of the pulmonary valve and pulmonary artery are part of several genetic syndromes such as Noonan's syndrome, Williams' syndrome, trisomies 13 through 15 and 18, and congenital rubella. Because of the benign nature of this lesion, patients with pulmonary stenosis are likely to escape detection during childhood and first come to medical attention during their adult years. Echocardiographic Evaluation

Recording diagnostic two-dimensional images of the pulmonary valve in adults can be difficult because of the frequent interference of overlying lung tissue. Positioning the patient in a high left lateral decubitus position and imaging during held expiration, however, may improve the ability to visualize the valve leaflets and the pulmonary artery. Apical or subcostal views of the right ventricular outflow tract also are useful in assessing the adult with pulmonary stenosis. Leaflet thickening may actually enhance echocardiographic visualization of the valve, and the presence of poststenotic dilation of the mid or distal portion of the main pulmonary artery often is a clue to previously unsuspected valvular pathology. Classic valvular stenosis causes systolic doming of the leaflets (Fig. 40-3) (Figure Not Available) . Pulsed wave Doppler demonstrates an increase in systolic velocity that begins at the valvular level, and continuous wave Doppler allows estimation of the peak and mean transvalvular gradient. Color flow mapping distinctly delineates the turbulent jet of high-velocity flow into the main pulmonary artery. Because of the horizontal substernal course of the right ventricular outflow tract, accurate peak Doppler flow velocities sometimes are difficult to obtain from the parasternal approach. Sampling

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of the highest peak systolic velocity may be more accurate from the apical or subxiphoid approach. In older patients, long-standing valvular obstruction leads to significant right ventricular hypertrophy including the infundibular portion of the ventricle. Dynamic infundibular obstruction thus adds to the right ventricle–pulmonary artery gradient over time. Doppler flow patterns from sampling within the infundibulum typically demonstrate the dagger-shaped, late-peaking systolic signal characteristic of dynamic obstructions. Management

In general, the adult with mild valvular pulmonary stenosis (peak systolic gradient < 35 mm Hg) requires 872

Figure 40-3 (Figure Not Available) Parasternal long-axis echocardiographic view of the right ventricular outflow tract in a patient with valvular pulmonary stenosis. The valve leaflets are thickened and dome into the pulmonary artery in systole. There is poststenotic dilation of the main pulmonary artery. PA, pulmonary artery. (Modified from Liberthson RR: Congenital heart disease in the child, adolescent, and adult. In Eagle KA, Haber E, DeSanctis RW, Austen WG [eds]: The Practice of Cardiology. Boston, Little, Brown, 1989, p 1125, with permission. Copyright 1989, Little, Brown and Company.)

no specific intervention. Although bacterial endocarditis is uncommon in isolated valvular pulmonary stenosis, antibiotic prophylaxis is still recommended as appropriate for low- or intermediate-risk cardiac lesions. [18] Decisions regarding intervention in patients with peak gradients between 35 and 50 mm Hg should be individualized, but balloon or surgical valvotomy is not generally indicated for the asymptomatic individual without significant right ventricular hypertrophy. In individuals with peak gradients greater than 50 mm Hg, percutaneous balloon valvotomy or surgical valvotomy should be considered. Balloon valvotomy is rapidly becoming the treatment of choice for this group of patients. Echocardiographic evaluation is quite helpful, both for determining which patient is most likely to respond favorably and to follow the results of the dilation. A small pulmonary annulus and markedly thickened, cartilaginous leaflets predict a poor response to dilation. In addition, the patient who has acquired significant infundibular hypertrophy may demonstrate a high postprocedural gradient. Regression of hypertrophy, however, occurs in a large percentage of patients after removal of the valvular component of obstruction and thus does not constitute a contraindication to balloon

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valvuloplasty.[19] In such cases with apparent residual obstruction, reassessment of Doppler gradients is recommended over the following 6 months before proceeding to a second valvuloplasty or surgical valvotomy. Mitral Valve Anomalies Patients with congenital anomalies of the mitral valve usually present with the clinical findings of mitral insufficiency. Thus, when patients are referred for echocardiographic evaluation of the severity of mitral regurgitation and suitability for mitral valve repair, one of several congenital problems in mitral valve structure may be found. A cleft in the anterior leaflet occurs either as an isolated abnormality or as part of a complex involving defects in the atrioventricular septum. A double-orifice mitral valve results from abnormal fusion of the embryonic endocardial cushions. Patients with this anomaly may have two equal orifices or one large mitral orifice and a smaller vestigial one. Functionally, the doubleorifice mitral valve can be stenotic or regurgitant. A parachute mitral valve has abnormal attachments of the valve leaflets to the papillary muscles. Classically, one large centrally placed papillary muscle is present with all chordae from both leaflets converging on this muscle; however, a variation of this pattern occurs in which two papillary muscles are present but with all or most of the chordal attachments devoted to one papillary muscle. Although this arrangement often creates significant inflow obstruction in infancy and childhood, the coexistence of redundant leaflet tissue and chordae and strategically placed commissures and clefts may produce a valve that functions with minimal obstruction. A variety of other minor aberrant arrangements of the papillary muscles may be noted echocardiographically in adults that may contribute to inadequate coaptation of the mitral leaflets during systole. For example, it is common to find an additional posterior papillary muscle with chordal attachments creating a bifid appearance of the posterior leaflet. A papillary muscle on the high lateral or anterolateral wall (the papillary muscle of Moulaert) may have chordal attachments from the anterior leaflet, resulting in a triangular mitral valve orifice. [20] Echocardiographic Evaluation

Echocardiographic assessment of congenital mitral anomalies uses all the usual windows for evaluating the mitral valve. The parasternal short-axis view defines the number of leaflets, a single or double orifice, the presence of a cleft, and the number and location of the papillary muscles (Fig. 40-4) . Long-axis or off-axis views may be needed to follow the chordal

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attachments to their respective papillary muscles. Pulsed, continuous wave, and color Doppler all are important to assess the functional significance of these structural anomalies. Doppler quantification of the severity of mitral stenosis and regurgitation is discussed in Chapter 20 . Abnormal flow patterns created by any of the congenital mitral valve lesions predispose to the development of infectious endocarditis. Mitral anomalies are sometimes first detected when the adolescent or young adult is referred for an echocardiographic search for valvular vegetations. Management

Management of congenital mitral stenosis or regurgitation in the adolescent and adult follows the same clinical guidelines as that in acquired mitral abnormality. With the 873

Figure 40-4 Parasternal short-axis echocardiographic views of the left ventricle at the mitral valve level. Left, Parachute mitral valve with anterior and posterior leaflets inserting on the posteromedial papillary muscle. A small anterolateral papillary muscle is present (arrowhead) but does not receive any valvular attachments. Center, Double-orifice mitral valve. There is a discrepancy in orifice size, with the medial orifice (double arrows) being larger than the lateral (single arrow) orifice. Right, Cleft anterior leaflet from a patient with a partial atrioventricular canal defect. The two portions of the anterior leaflet (arrowheads) are attached to the interventricular septum.

increasing success of mitral valve repair, delaying surgical treatment in order to avoid a prosthetic valve has become less necessary. Preoperative or intraoperative transesophageal echocardiography determination of exact leaflet anatomy and the mechanism of valve dysfunction has been a key factor in predicting successful plastic repair. [21] Transesophageal echocardiography features of interest include the presence and degree of calcification or fibrosis, adequacy and mobility of individual leaflets, site and direction of the regurgitant jet, and presence of leaflet clefts and papillary muscle anomalies. Tricuspid Valve Anomalies Ebstein's malformation of the tricuspid valve is a relatively rare congenital cardiac malformation with a wide variability in natural history. The anomaly described by Ebstein consists of apical displacement of the septal

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and posterior tricuspid leaflets associated with an enlarged anterior leaflet that is variably bound to the right ventricular free wall. The septal or posterior leaflet may be rudimentary or dysplastic. Downward displacement of the functional valve orifice creates an enlarged right atrium and an atrialized portion of the right ventricle. The true right ventricle is frequently hypoplastic and functionally impaired. The infundibular portion of the right ventricle and the pulmonary artery may be mildly underdeveloped. An atrial septal defect or patent foramen ovale is present in the majority of patients.[22] The clinical presentation of this anomaly ranges from severe cyanosis in the newborn to mild tricuspid insufficiency or arrhythmia in the adult. The latter finding may be secondary to marked right atrial enlargement or to tachyarrhythmias in conjunction with Wolff-ParkinsonWhite syndrome, which is found in 10% to 15% of patients with Ebstein's anomaly.[23] The "Ebsteinoid" valve can be functionally obstructive and is variably regurgitant. Diagnosis in the adolescent or adult is commonly made during echocardiographic evaluation of clicks and murmurs heard on auscultation or as a part of clinical investigations for the cause of tachyarrhythmias. Occasionally, a patient with unexplained cyanosis or paradoxical embolization is found to have Ebstein's anomaly. Echocardiographic Evaluation

Echocardiography is ideally suited for the anatomic delineation of the tricuspid valve leaflets. The parasternal inflow view of the right heart, when properly aligned, demonstrates the apical displacement of the posterior leaflet and the elongated sail-like anterior leaflet arising normally from the tricuspid annulus. The apical four-chamber plane is optimal for defining the origin of the septal leaflet, the degree of adherence of the anterior leaflet to the free wall, and the size of the true right ventricle (Fig. 40-5) . Attention should be directed to the relative sizes and contractility of the atrialized and the true right ventricle. Color flow Doppler detects tricuspid insufficiency, which may be severe or can be present as multiple eccentric regurgitant jets through commissures in the funnel-like valve orifice. Inflow obstruction is rarely manifested as an elevated transvalvular gradient; instead, the displaced valve leaflets provide a resistance to forward flow that elevates systemic venous pressure and drives flow right to left across the atrial communication. Careful two-dimensional imaging of the interatrial septum and color Doppler interrogation should demonstrate an atrial septal communication in most patients. Agitated saline contrast injection may be necessary if imaging is suboptimal or the shunt is not apparent by color Doppler. Transesophageal echocardiography provides additional

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information about leaflet origins and chordal attachments, as well as better direct imaging of the interatrial septum in adults with difficult transthoracic studies. In some individuals with Ebstein's malformation, late development of clinical heart failure occurs as a result of left ventricular dysfunction.[24] When the left ventricular cavity is significantly distorted by the enlarged right heart chambers, calculation of left ventricular volumes and ejection fraction by the simpler echocardiographic methods is difficult. Qualitative estimation of left ventricular function or a Simpson's rule formulation, however, can provide useful clinical information regarding left ventricular performance. Management

Patients with Ebstein's malformation frequently remain asymptomatic, leading full and active lives despite marked 874

Figure 40-5 Apical four-chamber echocardiographic view in a patient with Ebstein's malformation of the tricuspid valve. The view has been modified to best demonstrate the tricuspid leaflets in diastole. There is marked enlargement of the right atrium (RA) and atrialized right ventricle (at RV), with the true right ventricle composed only of the area between the valve leaflets and the apex. The tricuspid annulus is shown (x), and the origin of the septal leaflet is displaced apically (arrowheads). The anterior leaflet is elongated but not tightly bound to the right ventricular free wall.

structural abnormality of the tricuspid valve apparatus and right atrial enlargement. Although some centers have suggested that tricuspid valve repair should be recommended in the asymptomatic patient if the cardiothoracic ratio is greater than 65%,[23] most centers would restrict intervention to those with progressive cyanosis, severe tricuspid insufficiency, left or right ventricular failure, paradoxical embolization, or intractable arrhythmias. Surgical repair of the abnormal tricuspid valve is preferred to valve replacement if the anatomy is favorable. Good results have been reported [25] [26] when there is sufficient size and mobility of the anterior leaflet to permit it to serve as a monocusp valve after plication of the right atrium and atrialized right ventricle. Echocardiographic assessment of the size and mobility of the leaflets, the degree of displacement, and the function of the right ventricle is critical for the

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selection of patients most suitable for valve repair. A numeric scoring system has been proposed for preoperative echocardiographic assessment of suitability for valve repair (Fig. 40-6) (Figure Not Available) . Patients with an echocardiographic index less than 5 are good candidates for a monocusp valve repair.[27]

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Left Ventricular Outflow Tract and Aorta Subaortic Stenosis Subaortic obstruction in the adult occurs in several forms. A discrete form, the subaortic membrane, seems to be a developmental anomaly that is rarely seen in neonates but does appear in older children and young adults. It has been postulated that turbulent flow in the left ventricular outflow tract stimulates the growth of "rest" tissue in the region of the membranous septum, creating the discrete outflow obstruction.[28] [29] [30] Discrete subaortic stenosis is usually formed by a thin fibrous membrane attached circumferentially or along a portion of the circumference of the left ventricular outflow tract. It may lie immediately adjacent to the base of the aortic leaflets or be attached more distally near the junction of the muscular and membranous portion of the interventricular septum. Occasionally the entire circumferential structure is composed of muscle, creating a muscular subaortic collar. In older patients, what began as a discrete membrane may be complicated by the development of muscular subaortic hypertrophy. The muscular hypertrophy obscures the thinner membrane, thus masking the true pathophysiology of the obstructive process. Long-segment tubular narrowing of the left ventricular outflow tract is seen more commonly in children, usually requiring surgical attention before the adult years. As previously mentioned, discrete subaortic stenosis may occur in association with other obstructive lesions affecting the left heart— supramitral ring, bicuspid aortic valve, and coarctation. In addition, aortic valve endocarditis occurs frequently because of the abnormal flow patterns created by the subaortic narrowing. Subaortic membranes also are found as part of a complex that includes a perimembranous ventricular septal defect and an obstructive muscle bundle in the right ventricle.[31] With increasing Figure 40-6 (Figure Not Available) Score of echocardiographic features in Ebstein's anomaly. Assigning the score shown for each of the features listed provides a means of estimating whether tricuspid valve repair or valve replacement is required. Scores

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of 5 or higher are highly predictive of the need for valve excision and replacement. RA, right atrium; RV, right ventricle. (Adapted from Shiina A, Seward JB, Tajik AJ, et al: Circulation 1983;68:542.)

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age, the ventricular septal defect may close spontaneously, leaving the patient with a discrete obstruction of the left ventricular outflow tract and a muscular collar in the right ventricle. Late development of discrete subaortic stenosis has been described in patients with complete or partial atrioventricular canal defects, especially after surgical repair.[32] Echocardiographic Evaluation

Echocardiographic detection of a subaortic membrane is typically made in the parasternal long-axis views of the left ventricular outflow tract where a linear structure protrudes from the left surface of the interventricular septum and the base of the anterior mitral leaflet is tented up by the tension of the circumferential membrane (Fig. 40-7) . In some cases, the membrane is difficult to visualize unless the ultrasound beam is directly incident to the plane of the obstructing membranes. Low parasternal or apical long-axis views are thus more likely to detect the fine linear structure. When the membrane originates immediately beneath the aortic valve, its detection requires appreciation of subtle abnormality in the excursion of the aortic cusps and observation of a persistent echo in systole when the aortic cusp opens into the sinus of Valsalva. Unexplained turbulence and increased flow velocities by Doppler across an apparently normal aortic valve also are a clue to the presence of a high discrete subaortic membrane. Systolic flow acceleration by pulsed or color Doppler occurs proximal to the aortic valve. Aortic insufficiency is commonly found in these patients as a result of long-standing subaortic flow disturbance or from infectious endocarditis. Initial and serial assessment of outflow tract pressure gradients by Doppler is important, because Figure 40-7 Parasternal long-axis echocardiographic view of the left ventricle (LV) from a patient with discrete subaortic stenosis, ventricular septal defect, and aortic valve prolapse. The discrete subaortic membrane is shown as a linear density protruding from the upper left septal surface (arrow). The anterior aortic sinus is distorted and has prolapsed into the perimembranous ventricular septal defect immediately below it (arrowhead). Ao, aorta; LA, left atrium.

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progression of both the severity of obstruction and the degree of aortic insufficiency is well described in younger patients.[33] As with other lesions, transesophageal echocardiography may be helpful in the patient with limited transthoracic access to delineate the exact nature of left ventricular obstruction. This approach is particularly useful in cases with mixed or multiple-level obstruction. Both midesophageal views of the subaortic area and transgastric images of the left ventricular outflow tract are useful for obtaining diagnostic information. Management

Surgical excision of the circumferential membrane is recommended for patients with symptoms, left ventricular hypertrophy with strain, or a significant outflow gradient. Controversy still exists regarding surgical intervention in the asymptomatic patient with lower gradients. Some have argued that resection of the membrane preserves the aortic valve from further trauma and reduces or prevents progressive aortic insufficiency.[34] [35] Others have found that subaortic stenosis follows a less predictable course, with stenosis and regurgitation remaining trivial over many years.[36] The frequent need for reoperation and the development of aortic insufficiency despite surgical excision[37] indicate caution in recommending surgical intervention in the asymptomatic patient with only a mild hemodynamic abnormality. Close clinical and echocardiographic follow-up is warranted, and endocarditis prophylaxis is essential. When surgical excision is indicated, intraoperative transesophageal echocardiography can be helpful to monitor the success of membrane removal and detect complications such as mitral valve perforation or iatrogenic creation of a ventricular septal defect. Percutaneous balloon dilation has been attempted in patients with discrete fibrous membranes.[38] [39] Selection criteria for optimal success include a thin discrete membrane less than 3 mm in width, a sufficient distance between the membrane and aortic valve to permit a subaortic chamber, and the absence of more than grade 2 aortic insufficiency. Intermediate followup has shown a substantial reduction in gradient that persists over 5 years in 48% of patients, with no significant change in the degree of aortic insufficiency.[40] In one series, patients older than 13 years of age had the lowest rate of recurrent stenosis after balloon dilation; however, potential damage to the mitral and aortic valves and incomplete relief of obstruction dictates a cautious approach in applying this technique. Certainly in adults with acquired secondary muscular outflow obstruction, percutaneous dilation is unlikely to produce the desired results.

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Supravalvular Aortic Stenosis Supravalvular aortic stenosis is an uncommon lesion that may not become clinically apparent until older childhood or adolescence. Obstruction occurs as either a discrete membrane at the sinotubular junction, an "hourglass" deformity, or a diffuse hypoplasia of the entire ascending aorta (Fig. 40-8) (Figure Not Available) . The hourglass deformity is 876

Figure 40-8 (Figure Not Available) The three major types of supravalvular aortic stenosis. Left, Discrete infolding of the aorta at the sinotubular junction produces an hour-glass deformity. Center, Membranous weblike obstruction. Right, Diffuse tubular hypoplasia of the ascending aortic root. (From Maizza AF, Ho SY, Anderson RH: J Heart Valve Dis 1993;2:74.)

encountered most frequently, constituting 66% of cases of supravalvular obstruction, whereas diffuse hypoplasia (20%) and discrete membranous stenosis (10%) are less common.[41] Obstruction at the supravalvular level occurs as an isolated abnormality or part of an inherited syndrome. Williams' syndrome is one such inherited abnormality associated with mild mental retardation, failure to thrive, characteristic "elfin" facies, and multiple peripheral pulmonary stenoses. A familial autosomal dominant form of supravalvular aortic stenosis also occurs unassociated with mental retardation.[42] Some supravalvular stenoses are incidental findings associated with a systolic murmur and no gradient, whereas others are progressively obstructive lesions. The aortic valve leaflets are often normal; however, in some patients the cusps are distorted by the supravalvar constriction or incorporated into the stenosing ring. When progressive obstruction and failure of normal aortic growth occurs, left ventricular hypertrophy and the typical symptoms of aortic stenosis appear. Echocardiographic Evaluation

Echocardiographic detection of supravalvular stenosis relies on careful inspection of the sinotubular junction and proximal ascending aorta, which is possible with cranial angulation in right or left parasternal windows, or from suprasternal notch views. The diameter of the normal aorta at the sinotubular junction equals or slightly exceeds that of the aortic annulus. The tubular portion of the ascending aorta should never be smaller than the aortic annulus.[43] Echo-Doppler study should determine the type of supravalvular lesion and

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the severity of stenosis. Because routine echocardiographic study in adults often does not include the ascending aorta above the sinuses of Valsalva, missing the correct diagnosis on initial study is very possible. The impetus to look specifically for this lesion may be a high-velocity turbulent flow detected by continuous wave Doppler across an otherwise normal aortic valve. Accurate assessment of the supravalvular gradient by Doppler is best determined from the right parasternal or suprasternal window rather than from the cardiac apex. Doppler estimates of the severity of stenosis may overestimate the true degree of obstruction because of the phenomenon of pressure recovery seen in tubular or long-segment stenoses. Gradients for discrete membranous forms are more likely to be accurate.[44] Imaging of the proximal branch pulmonary arteries should be attempted in patients with Williams' syndrome, although associated branch stenoses of the pulmonary arteries may be too distal for echocardiographic detection. Management

The decision for surgical intervention for supravalvular aortic stenosis is made according to the same indications as for valvular obstruction— significant outflow gradient with left ventricular hypertrophy or symptoms. The morphology of the supravalvular narrowing dictates the type of repair required, varying from patch aortoplasty to partial root replacement. A good relief of obstruction for this lesion should be possible with low mortality and without a need for reoperation.[45] [46] Abnormalities of the aortic valve leaflets may persist after repair of the root and need clinical and echocardiographic surveillance. Associated branch pulmonary stenoses may require balloon dilation or surgical arterioplasty. Sinus of Valsalva Aneurysms Congenital aneurysms of the aortic sinuses of Valsalva are thought to result from a weakness in the aortic media at its junction with the annulus fibrosus. A small diverticulum or finger-like protrusion extends most commonly from the right or noncoronary sinus. Because the aortic sinuses are almost entirely intracardiac, the aneurysms extend into regions of the heart that lie adjacent to the affected aortic sinus. For aneurysms of the right coronary sinus, the right ventricle and right atrium are common termination sites. Aneurysms of the noncoronary sinus usually enter the right atrium.[47] Over time, the aneurysm may enlarge to become a "windsock," potentially causing obstructive problems in the right ventricular outflow tract or tricuspid valve. Rarely, sinus of Valsalva

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aneurysms burrow into the interventricular septum, causing atrioventricular conduction defects. [48] Protrusion into the left ventricular outflow tract may create outflow tract obstruction.[49] Congenital sinus of Valsalva aneurysms come to clinical attention most typically in adolescence and young adulthood when the protruding structure ruptures into the receiving chamber. Acute rupture of a large aneurysm causes retrosternal or epigastric pain and severe dyspnea from congestive heart failure. By contrast, perforation of a small aneurysm may go unnoticed until a continuous murmur is heard by auscultation or chronic congestive heart failure from the long-standing volume overload brings the patient to medical attention. Coronary artery compression by a sinus of Valsalva aneurysm is an interesting though unusual mode of presentation. [50]

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Sinus of Valsalva aneurysms may be an incidental finding on echocardiographic study, but they are discovered more often during echoDoppler evaluation of a continuous murmur with the suspected diagnosis of patent ductus arteriosus or coronary artery fistula.[51] [52] Parasternal longand short-axis views of the aortic sinuses demonstrate the finger-like windsock extending from the base of the sinus toward the site of termination (Fig. 40-9) . The originating sinus may be somewhat enlarged, but the native morphology of the root and valve is usually not significantly distorted. It is important to determine that the aneurysm originates from the aortic sinus above the plane of the aortic valve in order to distinguish this lesion from the more common aneurysm of the membranous interventricular septum. Delineation of a normal coronary artery origin and lumen size distinguishes the sinus of Valsalva aneurysm from a coronary artery fistula. Acquired aortic fistulas after endocarditis can be differentiated because they lack the extended aneurysmal channel seen with a sinus of Valsalva aneurysm. Color flow Doppler demonstrates continuous turbulent flow within the aneurysm and into the receiving chamber. In patients with a significant left-to-right shunt, left atrial and left ventricular enlargement reflect the size of the volume overload, and right-sided chamber enlargement occurs when the aneurysm communicates with the right atrium. Mild aortic insufficiency is expected from distortion of the aortic cusp and root enlargement is expected from long-standing volume

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overload. Severe aortic insufficiency should raise the suspicion of aneurysm rupture into the left ventricular Figure 40-9 (color plate.) Parasternal short-axis echocardiographic images of the aorta (Ao) at the base of the heart. A, Aneurysm of the right coronary sinus of Valsalva shown as a narrow "windsock" protruding into the right atrium (RA) (arrows). B, Color flow Doppler image demonstrates turbulent flow filling the narrow channel and creating a shunt from the aorta into the right atrium.

outflow tract or secondary endocarditis affecting the aortic valve leaflets. Management

Small unruptured aneurysms found incidentally can be followed expectantly. Larger aneurysms or those that are adversely affecting surrounding structures should be electively excised. Ruptured sinus of Valsalva aneurysms require surgical closure to prevent late congestive symptoms caused by volume overload and to decrease the susceptibility to infectious endocarditis. Coarctation of the Aorta Coarctation of the aorta in the adolescent and adult is most often discovered during investigation of hypertension found in the course of routine physical examination. Weak or absent femoral pulses, left ventricular hypertrophy on the electrocardiogram, or a systolic murmur in the back or through collaterals in conjunction with the hypertension results in a referral to the echocardiographic laboratory or cardiologist's office for definitive diagnosis. The anatomic lesion found most commonly in adults is a discrete ridge or diaphragm narrowing the aortic lumen just below the left subclavian artery and opposite the ductus arteriosus or ligamentum arteriosum. Poststenotic enlargement of the descending thoracic aorta is usually present. Rarely, the coarctation lies more distally in the thoracic or abdominal aorta. Functionally, patients seen 878

as adults are usually asymptomatic, because the degree of obstruction created by the coarctation is mild or moderate, or collateral vessels bypass a

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more severe stenosis. About 50% of patients with adult coarctation have a bicuspid aortic valve. [53] Other structural defects of the left heart such as discrete subaortic membranes or mitral valve anomalies occasionally are present, and a small ventricular septal defect or residual patency of the ductus arteriosus may coexist. Cerebrovascular accidents from ruptured berry aneurysms, aortic dissection, and endocarditis or endarteritis also complicate the natural history of adult coarctation of the aorta. Echocardiographic Evaluation

Echocardiographic diagnosis of coarctation relies on two-dimensional visualization of the anatomy of the aortic arch and Doppler detection of flow disturbance in the descending aorta (Fig. 40-10) . Although the aorta can be imaged in part from a variety of parasternal views, suprasternal notch or right parasternal windows provide the best access to the region of interest. Because the site of coarctation can be difficult to visualize, patient positioning maneuvers that optimize the suprasternal view are important. In the long-axis view of the aortic arch, the brachiocephalic vessels should be identified and traced distally if possible. Just beyond the left subclavian artery, a shelf of infolded tissue narrows the aortic lumen. The thoracic aorta distal to the coarctation is often dilated from the systolic jet through the stenotic area. Color flow Doppler detects a narrowed flow stream at Figure 40-10 A, Suprasternal long-axis echocardiographic view of the aortic arch depicts tubular narrowing of the transverse arch with discrete coarctation at the isthmus (arrow). B (color plate), Doppler color flow mapping shows aliasing and turbulence beginning at the site of discrete obstruction (arrow). C, Continuous wave Doppler signal was obtained in the descending thoracic aorta and illustrates a high peak velocity in systole (3 m per second) with a gradient that persists during early diastole (arrowheads). D, Pulsed wave Doppler signal obtained from the descending abdominal aorta. There is blunting of the systolic upstroke and turbulent continuous flow during diastole (arrowheads) indicative of significant obstruction to flow located more proximally in the aorta. Asc Ao, ascending aorta.

the point of coarctation and systolic flow acceleration, with continuation of flow into diastole in cases of significant obstruction. In fact, when twodimensional imaging is indistinct, the color flow turbulence may alert the sonographer to the site of obstruction. Continuous wave Doppler in patients

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with discrete obstruction shows a typical pattern of increased systolic flow velocity and a continued gradient in diastole. Doppler gradients (∆P) estimated from the peak systolic velocity (V2 ) of the continuous wave

Doppler signal usually overestimate the catheter-measured gradient. Better correlations have been shown when the velocity proximal to the coarctation (V1 ) is included in the Bernoulli equation [∆P = 4(V2 2 − V1 2 )] or when both the peak systolic velocity and pressure half-time of the diastolic gradient are considered.[54] [55] Long-segment narrowing of the aorta without discrete obstruction causes acceleration of flow, giving high peak velocities by continuous wave Doppler. Conversion of these velocities into systolic gradients mistakenly predicts significant coarctation. The lack of a diastolic gradient helps to distinguish flow acceleration from true obstruction. Doppler flow patterns in the descending abdominal aorta are extremely useful in detecting upstream obstruction.[56] Patients with tubular narrowing but without a discrete obstruction demonstrate a normal pattern of abdominal aortic flow—rapid systolic upstroke, relatively laminar flow signal, and no continuation of flow into diastole. With coarctation, the flow profile has a delay in the systolic upstroke, turbulence in systole, and variable degrees of diastolic antegrade flow (see Fig. 40-10) . Routinely including the Doppler profile of abdominal aortic flow in the clinical examination is an excellent method to 879

screen for unsuspected coarctation. Adults with coarctation may have considerable tortuosity of the transverse arch, making both visualization and alignment for accurate Doppler detection of gradient impossible. In such cases, a high degree of suspicion is generated by abnormal flow in the abdominal aorta, directing a more diligent search from off-axis views or with a stand-alone continuous wave Doppler probe. Although Doppler flow patterns are relatively easy to obtain in most adults with coarctation, direct imaging of the anatomy of the arch and descending aorta may be limited. Alternative imaging modalities often are necessary to further define the exact details of the obstruction and to guide decisions for management. Transesophageal echocardiography can detect the site and configuration of the obstruction. Long-axis views allow quantitation of lumenal narrowing; however, Doppler gradients are difficult to obtain because the affected region of the aorta generally lies perpendicular to the interrogating Doppler beam.[57] Magnetic resonance imaging is an accurate

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noninvasive imaging tool for displaying complete arch anatomy, and newer applications allow velocity mapping as well.[58] [59] Angiography may be required in the older adult to assess the degree of collateral development as well as coronary anatomy if surgical repair is planned. Management

Hypertension, a significant pressure gradient between the upper and lower extremities, and a reduction in luminal diameter of greater than 50% are indications for intervention in the adult with coarctation. Some centers recommend percutaneous balloon dilation for discrete lesions in adolescents and young adults, finding good relief of the gradient, improvement in hypertension, and a low rate of restenosis.[60] [61] [62] Small saccular aneurysms may occur at the dilation site either acutely or on later follow-up. Although some of these aneurysms have been surgically repaired, serial follow-up of others has shown no progression in size and no rupture or dissection. The long-term outcome of these iatrogenic aneurysms is uncertain, however. Intravascular echocardiography performed immediately after dilation can demonstrate the intimal tear that routinely occurs during balloon angioplasty.[63] , [64] Transthoracic echocardiographic evaluation after angioplasty is helpful in assessing residual gradient and restenosis, but it cannot detect reliably the presence of small aneurysms. Repeat magnetic resonance imaging or angiography is needed for follow-up evaluation of this complication. The use of balloon-expandable intravascular stents has been recently applied in the treatment of aortic coarctation.[65] Early and intermediate follow-up suggests excellent relief of stenosis without a significant incidence of stent migration, fracture, restenosis or thromboembolic complications.[66] With increasing age, diminished pliability of aortic tissue increases the possibility of a more extensive aortic tear or rupture after balloon angioplasty; therefore, patients older than 30 years may be managed more safely surgically. Surgical repair of coarctation in the adult can be accomplished with low operative mortality and good intermediate outcome. [67] Attention to the degree of collateral formation is important to ensure adequate perfusion during cross-clamping and to prevent spinal cord injury. Prosthetic bypass grafts or other alternatives to mobilization and end-to-end anastomosis may be required in adults with less elastic tissue. Residual hypertension is common after late repair of coarctation.

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Septal Defects and Shunt Lesions Atrial Septal Defects After the bicuspid aortic valve, atrial septal defects are the most common congenital lesion found in adolescents and adults, constituting nearly 22% of adult congenital heart defects.[68] The ostium secundum defect is the most frequent (75%) followed by the ostium primum type (20%) and the sinus venosus defect (5%).[68] A very rare form of atrial septal communication is the coronary sinus septal defect in which the roof of the coronary sinus is partially or completely absent, allowing left-to-right shunt from the left atrium into the coronary sinus and thence into the right atrium. A patent foramen ovale, the fetal communication between the overlapping layers of the primum and secundum portions of the atrial septum, persists in 10% to 18% of adults as determined by echocardiographic contrast injection and as many as 25% to 30% of patients in autopsy series.[69] [70] Because of failure of fusion of the two septal layers, the flap of septum primum covering the fossa ovalis may open transiently with changes in the transatrial pressure gradient, allowing the passage of flow in either direction. Additionally, this thin membranous layer may have multiple small perforations or develop into a septal aneurysm with or without an atrial shunt. Improved detection of atrial defects and more aggressive investigation in patients with cerebrovascular events has generated great interest regarding the association of patent foramen ovale, atrial septal aneurysm, and cryptogenic stroke.[71] [72] [73] A large multicenter trial is currently under way to examine prospectively the exact nature of the relationship between patent foramen ovale and stroke. It is clear, however, that the potential for a right-to-left embolus exists when there is any form of communication in the interatrial septum (see Chapter 37) . Patients with shunting at the atrial level are usually asymptomatic until middle to late adult years. If their cardiac anomaly has not been diagnosed

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during childhood by the physical findings of a widely split second heart sound and pulmonic flow murmur, detection may occur by routine chest xray findings of cardiomegaly and pulmonary plethora. Beginning in the fourth or fifth decades of life, symptoms of fatigue, dyspnea on exertion, and atrial arrhythmia develop. Right or left ventricular failure and paradoxical embolization also may be the mode of presentation in older patients with atrial septal defects. Endocarditis is quite rare, most often seen in patients with accompanying mitral valve anomalies.

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Figure 40-11 (Figure Not Available) (color plate.) Series of apical four-chamber echocardiographic views from a patient with a large ostium primum atrial septal defect. A, Large defect in the inferior portion of the atrial septum (arrow). B, Doppler color flow mapping readily detects the passage of flow through the defect (arrow and arrowhead). C, After IV injection of agitated saline, a positive contrast effect is observed as opacified blood from the right atrium (RA) crosses from right to left (arrows). D, Shunting of unopacified blood from the left atrium (LA) creates a negative contrast effect in the right atrium (arrows). LV, left ventricle; RV, right ventricle. (From Levine RA, et al: Echocardiography: Principles and clinical application. In Eagle KA, Haber E, DeSanctis RW, Austen WG [eds]: The Practice of Cardiology. Boston, Little, Brown, 1989, p 1555. Copyright 1989, Little, Brown and Company.) Echocardiographic Evaluation

Patients with atrial septal defects require echocardiographic assessment of the anatomic abnormality of the atrial septum, the hemodynamic effect of shunt flow, and the presence of any associated defects. Imaging of the interatrial septum is best performed with subxiphoid views when these are available. The true apical four-chamber view is unreliable because falsepositive septal dropout often occurs in the midatrial septum. An off-axis four-chamber view obtained by sliding midway between the apical and subxiphoid views, however, yields a more perpendicular interface between the interrogating ultrasound beam and the interatrial septum. Parasternal short-axis and right parasternal views are supplemental windows for imaging the atrial septum. The septum primum covering the fossa ovalis is thinner than either the superior portions of the septum or the region near the crux of the heart. Mobility of the septum primum or aneurysmal deformity (>1-cm deviation from the plane of the basal septum) raises the suspicion of a patent foramen ovale. True atrial septal defects should have a distinct edge visible at the blood-tissue interface. All aspects of the atrial septum

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should be inspected, including the superior rim, with visualization of the superior vena caval entry. Right parasternal views are especially helpful for imaging this area. When the atrial defect can be imaged directly, measurement of its dimensions in orthogonal planes and its size relative to the entire atrial septal length should be made. Pulsed and color flow Doppler add additional diagnostic power to the transthoracic examination. In any of the views mentioned earlier, the passage of flow across an apparent atrial defect further confirms the presence of an interatrial communication (Fig. 40-11) (Figure Not Available) . When right heart pressures are normal, a clear stream of flow occurs in late systole with accentuation in diastole. Elevation of right heart pressures decreases the trans-septal pressure gradient, and shunt flow then may be difficult to distinguish from other low-velocity atrial flows. Contrast echocardiography plays an important diagnostic role in cases in which the imaging and Doppler findings are equivocal. With rapid IV injection of 5 mL of agitated saline (or saline mixed with a small amount of the patient's blood), highly reflective microbubbles appear in the right atrium and right ventricle. Contrast passes into the left atrium and left ventricle within three to five cardiac cycles in the presence of an interatrial communication (see Fig. 40-11) (Figure Not Available) . Even when leftto-right shunting is predominant, there is a period of transient right-to-left shunting during which contrast can pass into the left atrium. The right-toleft pressure gradient can be augmented by having the patient cough or perform a Valsalva maneuver. A negative contrast effect occurs with leftto-right shunts when unopacified blood enters the densely opacified right atrium. Negative contrast is a less reliable diagnostic feature, however, because flow from the inferior vena cava or coronary sinus may create the same appearance. Sensitivities of 92% to 100% have been reported for detection of atrial septal defects by transthoracic contrast echocardiography.[74] [75] It has been suggested 881

that injection from the leg improves the sensitivity of the contrast technique, because the eustachian valve tends to direct inferior vena caval flow across the fossa ovalis. [76] Transthoracic echocardiographic study also helps to define the hemodynamic effects of shunt flow. Right atrial and right ventricular

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enlargement and dilation of the main pulmonary artery are expected with shunts of 1.5:1 or greater. The pulmonary veins are prominent, but the left atrium is usually normal in size unless there is associated mitral regurgitation or left ventricular failure. The interventricular septum in the cross-sectional views of the left ventricle is flattened in diastole and moves paradoxically toward the right ventricle in systole. Specific quantification of shunt volume by echo-Doppler techniques has been attempted by several methods, all of which remain semiquantitative in clinical use. Pulsed Doppler determination of cardiac output has been validated with a high degree of accuracy in the experimental setting.[77] The ratio of pulsed Doppler cardiac output across the pulmonary and aortic valves gives an estimate of the pulmonary-to-systemic flow ratio (Qp /Qs ). This technique is not accurate if the flow across either valve is influenced by something other than the intracardiac shunt, such as valvular stenosis, subvalvular obstruction, or significant valvular regurgitation. Application of this method to the clinical arena has been less successful, partly because of the difficulty of obtaining accurate dimensions of the pulmonary annulus in adults. When color flow mapping became a part of the echocardiographic diagnostic armamentarium, there was initial enthusiasm for its quantitative potential. Planimetry of the area of the flow stream within the right atrium has been compared with shunt volumes but with poor correlations.[78] Better correlation has been shown when the diameter of the color flow stream at the atrial defect is compared with shunt ratios,[79] but this remains semiquantitative with considerable overlap between patients with small, moderate, and large shunts. This result might be expected because the color flow diameter simply reflects the anatomic dimension of the atrial defect, and although it bears a gross relationship to the size of the shunt, factors such as right ventricular compliance and pulmonary artery pressures cause variation in the volume of shunt for a given atrial septal defect size. The development of new intravenous contrast agents that pass through the pulmonary bed to the left-sided circulation has led to the possibility of an echocardiographic indicator dilution technique for quantifying shunts.[80] With videodensitometry, the concentration of sonicated albumin can be determined serially in the right ventricle during the initial appearance of contrast and then during the recirculation phase. An indicator dilution curve then can be constructed and the shunt ratio calculated in a manner similar to that used for radionuclide shunt calculation. This method requires that the

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sonicated albumin remain stable during the period of observation. Because the rate of disappearance of sonicated contrast has been shown to be pressure sensitive, shunt ratios in patients with higher pulmonary artery pressures might be underestimated.[81] Estimation of pulmonary artery pressure is an important part of the echocardiographic assessment of atrial shunts. The pulmonary artery pressure is easily and reliably determined by applying the simplified Bernoulli equation to the peak velocity of the tricuspid regurgitation jet to obtain the pressure gradient between right ventricle and right atrium.[82] Adding an assumed or actual right atrial pressure to the pressure gradient yields an estimated right ventricular systolic pressure (RVSP): RVSP = 4(TR jet velocity)2 + RA pressure where TR is tricuspid regurgitation and RA is right atrial. Right ventricular systolic pressure equals pulmonary artery pressure in the absence of pulmonary stenosis. If the patient does not have tricuspid insufficiency, other subjective signs of pulmonary hypertension may be present. For example, the interventricular septum is flattened in systole if right ventricular systolic pressure is greater than half the systemic pressure. Systolic notching on the pulmonic valve M-mode or the pulmonary artery Doppler flow profile also indicates significant elevation of pulmonary artery pressure. Applying the modified Bernoulli equation to the enddiastolic velocity of the pulmonary insufficiency jet provides quantitative information about pulmonary artery diastolic pressure as well. Associated abnormalities should be sought as part of the complete transthoracic examination. Mitral valve prolapse occurs with large right ventricular volume overload, usually from geometric distortion of the left ventricle but occasionally from a myxomatous mitral valve. A cleft in the anterior mitral leaflet is usually present with ostium primum atrial septal defects. Significant mitral regurgitation occurs with increasing age.[83] Valvular pulmonic stenosis is present in a small number of patients, and when it is significant it can promote right-to-left shunting across the atrial septal defect with resultant cyanosis. The drainage of all four pulmonary veins should be established if possible in any patient with an atrial septal defect. Anomalous return of the right upper and middle lobe veins is found in the majority of patients with superior sinus venosus atrial septal defects and in a small percentage of

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patients with ostium secundum atrial septal defects. The right veins drain to the superior vena cava either at the junction with the right atrium or more distally along the course of the superior vena cava. Echo-Doppler detection of this anomaly is difficult in adults, but it can be attempted with long- and short-axis right parasternal views of the superior vena cava and occasionally can be appreciated in subcostal views of the superior vena cava. A turbulent flow stream entering the superior vena cava laterally and posteriorly represents the pulmonary vein inflow. Anomalous drainage of the right lower vein to the inferior vena cava occurs with the "scimitar syndrome." Right parasternal views that focus on the inferior vena caval entry to the right atrium are most useful to search for the anomalous pulmonary venous inflow. Transesophageal echocardiography has proved to be superior to transthoracic study in adult patients for detecting patency of the foramen ovale, small secundum atrial septal defects, sinus venosus defects, and anomalous pulmonary venous return.[84] [85] [86] Although the presence of an interatrial shunt and an estimate of its hemodynamic 882

Figure 40-12 Transesophageal echocardiographic images of the interatrial septum in a patient with a secundum atrial septal defect undergoing transcatheter device closure with a Sideris device. A (color plate), The shunt across the defect is apparent by color flow Doppler. B, Measurement of defect size in the vertical plane image. C, Balloon sizing is performed by measuring the diameter of an inflated balloon (arrowheads) as it is pulled across the defect. D, The occluder of the Sideris device is demonstrated (arrowheads) being deployed along the left atrial surface. E, The counteroccluder (arrowheads) is positioned parallel to the right atrial septal surface. F, After removal of the guiding catheter and wire, the device (arrowheads) lies snugly against the interatrial septum. LA, left atrium; RA, right atrium.

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significance can be determined adequately by transthoracic echocardiography, defect sizing and specific anatomic detail are much more accurately obtained from the transesophageal window (Fig. 40-12) . The interatrial septum is easily imaged with the probe in the midesophageal position. In the transverse plane, the crux of the heart is well seen, and

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ostium primum or secundum atrial defects are most apparent. From the longitudinal plane, the superior vena caval entry to the right atrium is clearly defined and superior sinus venosus defects with anomalous pulmonary venous entry can be detected. The flaplike opening of the patent foramen ovale also can be appreciated in this view. Color flow mapping confirms the presence of shunting, and saline contrast injection may be useful if proof of right-to-left shunting is needed. Atrial septal defects vary in shape, making measurements of the defect in two orthogonal views important. The pulmonary veins can be identified from both the transverse and the longitudinal planes. Management

Patients with an isolated atrial septal defect with a significant left-to-right shunt should have elective closure of the defect because of the possibility of progressive pulmonary hypertension and the late development of right ventricular failure and atrial arrhythmias. Closure may be appropriate even for patients with smaller shunts because of the tendency for shunt size to increase with age, because of alterations in left ventricular compliance and the ever-present risk of paradoxical embolization. Surgical mortality for this lesion is quite low, and long-term follow-up shows improvement in symptoms, decrease or stabilization of pulmonary hypertension, and nearnormal long-term survival rates in patients repaired before the age of 25 years.[87] [88] [89] Patients with elevation of pulmonary arteriolar resistance greater than 15 U/m2 are not good surgical candidates and are better managed medically.[90] There is some divergence of opinion regarding closure of atrial defects in the older adult. One natural history study[91] found no difference in survival or symptoms and no difference in the incidence of new arrhythmias, stroke, emboli, cardiac failure, or progressive pulmonary hypertension between medically and surgically managed patients over the age of 25 years. A subsequent large series of adults over the age of 40 years, however, demonstrated a significant reduction in mortality and dramatic improvement in functional class after atrial septal defect closure compared with a similar group managed medically. The risk of atrial arrhythmias and attendant embolic complications was not altered by atrial septal defect closure.[92] Thus, with low surgical morbidity and mortality and with the availability of transcatheter closure devices, closure of atrial septal defects with a significant shunt without severe pulmonary hypertension is recommended regardless of age.

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At the present time, patients with an incidentally detected patent foramen ovale do not require intervention. The occurrence of an embolic stroke or peripheral embolus in the patient with a patent foramen ovale and no other obvious embolic source can be considered justification for surgical or device closure, particularly in the younger adult. Controlled studies are needed to determine if anticoagulation alone is an equally effective alternative to patent foramen ovale closure after an embolic event (see Chapter 37) . [93] For patients with contraindications to surgery or complex lesions requiring multiple surgical procedures, a non-surgical method of closing an atrial communication is particularly desirable. Several different transcatheter closure devices have been designed for this purpose, but most are currently still in the investigative stage in the United States.[93] [94] [95] The basic device is a flexible wire framework covered with fabric or foam that folds inside a catheter delivery system. One portion of the device is extruded on the left atrial side of the atrial septal defect, the sheath is withdrawn across the defect, and the other portion of the device is deployed along the right atrial side. Newer generation devices have a thicker central core that allows the device to be self-centering within the defect (Fig. 40-13) . This characteristic permits closure of larger atrial defects because less overlap is required to ensure that the device remains well-seated. For any of the current devices, the best results are achieved when the atrial defect is relatively centrally located in the interatrial septum because the extension of the device beyond the edges of the defect may impinge on the atrioventricular valves or extend into the superior vena cava, right upper pulmonary vein, or coronary sinus. Thus, most sinus venosus and ostium primum atrial septal defects would be excluded from consideration for device closure. Echocardiography plays an essential role in the selection of patients most suitable for device closure. Assessment of the defect size, the overall length of the interatrial septum, the amount of septal rim around the defect, and the degree of mobility or aneurysm of the septum primum are all important in evaluating a patient for device closure.[96] Although transthoracic echocardiography can provide some of this information, transesophageal echocardiography generally is more accurate in adults.[84] [85] [86] Because some traction is applied to the atrial septum in the process of placing the occluding device, the balloon-stretched diameter is the measurement that is most reliable in selecting a device that will not slip through the atrial septal defect. Thus, in clinical practice, transthoracic echocardiography is used to

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diagnose the shunt at the atrial level, categorize the location of the atrial defect and its approximate size, determine the shunt size, and detect any associated defects. If device closure is considered, transesophageal echocardiography before or during catheterization can further define the anatomy, and the balloon-stretched diameter can be measured. Transesophageal guidance in the catheterization laboratory has greatly facilitated the optimal placement of the closure device parallel to the plane of the interatrial septum and centered across the defect. Additionally, deployment in the atrial appendage or within the mitral valve orifice can be avoided under direct observation by transesophageal echocardiography. The fully deployed device can then be observed for a period of time before the procedure is completed to ensure that it remains in a good position. Color flow Doppler and contrast echocardiography determine residual 884

Figure 40-13 Current generation transcatheter closure devices for septal defects. A, The Das self-centering device. The edges of the left atrial disc are retracted to show the central collar, which promotes centering of this device within the septal defect. B, The Amplatzer septal occluder is a doubledisc device with a nitinol wire frame and a broad waist that centers the device. C, The Gore Helex device, which is extruded as a single helical disc with a narrow waist. D, The STARFlex version of the CardioSEAL septal occluder. Hinges midway along each leg promote retroflexion of the legs back toward the septum. Microsprings assist in centering the device in the defect. E, The Sideris button device modified with centering wires attached to the occluder (OCC), which is introduced with a pushing catheter (PUSH). (A, From Das GS, Voss G, Jarvis G, et al: Circulation 1993;88(part I):1756; B, From Sharafuddin MJ, Gu X, Titus JL, et al: Circulation 1997;95:2162. Reproduced with permission. Copyright American Heart Association. C, Courtesy of N. Wilson, MD; D, From Hausdorf G, Kaulitz R, Paul T, et al: Am J Cardiol 1999;84:1113. Reproduced with permission. Copyright Elsevier, Ltd.; E, From Sideris EB, Sideris SE, Fowlkes JP, et al: Circulation 1990;81:314.)

patency immediately after deployment (see Fig. 40-12) . Follow-up studies of device closure of atrial septal defects have shown a high rate of successful placement. Residual patency rates are moderate but trivial in degree, with a continued decrease in shunting over time. A small incidence of device embolization or unacceptable deployment is reported with all of the devices. Endothelialization of the device is thought to occur within 6 months when properly aligned flush with the native septum.[94] [95] [97] [98] [99]

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Ventricular Septal Defects Ventricular septal defects are the most common congenital anomaly recognized at birth, but they account for only about 10% of cases of congenital heart disease in the adult. This decrement in prevalence is due in part to a high rate of spontaneous closure during the first few years of life. In addition, moderate and large lesions generally cause symptoms of congestive heart failure, dyspnea, and failure to thrive in childhood, requiring medical and surgical intervention long before adulthood. The ventricular septal defects that persist in adult years are either small defects, larger defects that have diminished in size by one of several natural processes, or very large defects with irreversible pulmonary vascular disease. Spontaneous closure does occur in later years but is uncommon. The incidence of infectious endocarditis for patients with ventricular septal defects is low in the current antibiotic era; however, the risk is higher for adults than children, and it is higher for patients with associated aortic insufficiency.[8] The most common location for adult ventricular septal defects is the membranous ventricular septum. Shunt flow passes from the left ventricular outflow tract to the right ventricle just beneath the septal leaflet of the tricuspid valve. Membranous septal aneurysm formation may occur by fibrous tissue proliferation and incorporation of the septal tricuspid valve leaflet. The aneurysm limits shunt flow and occasionally closes the defect entirely. Aneurysms may become quite large and have been noted to cause turbulence and obstruction in the right ventricular outflow tract (Fig. 40-14) . Distortion of the septal leaflet from incorporation into the septal aneurysm may create a communication from the left ventricular outflow tract into the right atrium, a Gerbode defect. Over time, this defect leads to a right ventricular volume overload, right atrial enlargement, and atrial arrhythmias. In some membranous ventricular septal defects, the support of the right aortic cusp is undermined, leading to prolapse of this cusp into the defect (see Fig. 40-7) . Progressive aortic insufficiency often becomes a more important hemodynamic issue than the ventricular shunt. Subaortic membranes also may develop in association with membranous ventricular septal defects during adolescence or early adulthood.

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Figure 40-14 Apical four-chamber echocardiographic image from a

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patient with a perimembranous ventricular septal defect (closed arrowheads) and a large membranous septal aneurysm (open arrowheads). The aneurysm protrudes into the right ventricle (RV) and has incorporated tricuspid septal leaflet tissue. LV, left ventricle; RA, right atrium.

Muscular ventricular septal defects are the next most common. Because smaller defects of this type often close spontaneously, the ones that persist in adulthood are generally quite large, sometimes multiple, and associated with pulmonary vascular obstructive disease (Eisenmenger's syndrome). These patients may present with cyanosis from reversal of shunt flow. Pulmonary hypertension is avoided in a few individuals by the development of muscular hypertrophy of the right ventricular outflow tract, a sort of natural pulmonary banding referred to as the Gasul phenomenon. [100] Hypertrophy of the moderator band also can restrict shunt flow across sizable apical muscular defects, and when this occurs, the left ventricular and the right ventricular apex become one chamber, giving the cardiac apex an aneurysmal appearance. Defects of the supracristal or subpulmonary septum are found more commonly in patients of Asian background and are associated with a high incidence of aortic insufficiency.[101] Prolapse of the right or left coronary cusp into the ventricular septal defect actually may decrease the ventricular septal defect shunt while creating more severe aortic insufficiency. Occasionally the aortic sinus is extruded through the defect and ruptures, causing a fistula from the aorta to right ventricular outflow tract. Defects in the inlet septum are usually the result of a defect in the formation of the atrioventricular septum. Because the formation of this portion of the septum is intimately associated with the development of the atrioventricular valves and the crux of the heart, associated atrioventricular valve anomalies and a primum atrial septal defect are common (Fig. 4015) . Clefts in either the mitral or tricuspid valves or a common atrioventricular valve may occur. The tricuspid valve occasionally straddles the inlet ventricular septal defect, with chordal insertions that cross the defect into the left ventricle. When the ventricular septal defect is small, dense chordal tissue crossing the defect may effectively obstruct flow, limiting the shunt size. Fibrous aneurysms also occur with atrioventricular septal defects, decreasing or closing the ventricular septal communication. In most cases, however, an inlet ventricular septal defect is large and rarely closes spontaneously. Adults with this lesion develop pulmonary vascular obstructive disease early in life. Atrioventricular septal defects are frequently seen in adults with Down's syndrome, in whom surgery may

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have been avoided because of the patient's neurologic and functional limitations. Echocardiographic Evaluation

The interventricular septum is a complex fibrous and muscular structure requiring careful interrogation of all aspects by two-dimensional imaging and color Doppler to detect ventricular septal defects (Fig. 40-16) (Figure Not Available) . Membranous ventricular septal defects are best seen in the parasternal long- and short-axis views as echo dropout beneath the aortic valve and near the attachment of the septal leaflet of the tricuspid valve. Apical or subcostal five-chamber views also demonstrate the position of the defect in relation to the left ventricular outflow tract and tricuspid valve. Associated abnormalities of the right aortic cusp, subaortic region, and septal aneurysm formation should be delineated. The supracristal ventricular septal defect can be appreciated in the parasternal long-axis view of the right ventricular outflow tract or the parasternal short-axis view at the base of the heart, located immediately proximal to the pulmonic valve. If the right aortic cusp has become distorted and prolapses into the ventricular Figure 40-15 Apical four-chamber echocardiographic image of a type C complete atrioventricular canal defect. The large-inlet ventricular septal defect (arrowhead) and primum atrial septal defect (arrow) are crossed by a central bridging leaflet that has no chordal attachments to the crest of the interventricular septum. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

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Figure 40-16 (Figure Not Available) (color plate.) Standard two-dimensional echocardiographic views with color coding of the location of the common types of ventricular septal defects. The membranous septum is coded in red, the supracristal or infundibular septum in orange, the inlet septum in green, and the muscular septum in blue. Ao, aorta; LA, left atrium; LV, left ventricle; PA, pulmonary artery; PV, pulmonary valve; RA, right atrium; RV, right ventricle; RVOT, right ventricular outflow tract. (From Levine RA, et al: Echocardiography: Principles and clinical application. In Eagle KA, Haber E, DeSanctis RW, Austen WG [eds]: The Practice of Cardiology. Boston, Little, Brown, 1989, p 1554. Copyright 1989, Little, Brown, and Company.)

septal defect, the defect itself may not be detectable without color or pulsed

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Doppler. Muscular septal defects may be located anywhere within the trabecular septum. Careful scrutiny of parasternal short-axis sweeps as well as apical, off-axis apical, and subcostal views is required to detect muscular defects. Inlet ventricular septal defects are most apparent in apical or subcostal four-chamber views directed posteriorly toward the crux of the heart. Associated abnormalities of the atrial septum and the atrioventricular valves also can be appreciated from this vantage point. Assessment of left atrial and left ventricular chamber size and left ventricular function is important. Long-standing volume overload is associated with enlargement of left heart structures and may cause left ventricular failure in the older adult. In the clinical setting of endocarditis, vegetations can be detected on the aortic valve, the membranous septal aneurysm, or the tricuspid septal leaflet. Endarteritis at the site of the jet lesion within the right ventricle or right ventricular outflow tract is usually not detectable by two-dimensional imaging unless vegetations are extensive. Color flow mapping greatly enhances the sensitivity of detection of all forms of ventricular septal defects. Left-to-right shunts are readily detected as turbulent jets crossing the septum into the right ventricle when the pulmonary pressures are normal. Ambiguity may occur when there is little difference between left and right heart pressures, because shunt flow is low in velocity and difficult to distinguish from other low-velocity flow within the right heart.[102] [103] Pulsed and continuous wave Doppler studies are helpful to confirm the timing and velocity of shunt flow. With small membranous and supracristal ventricular septal defects, low-velocity diastolic shunt flow may precede the high-velocity systolic jet, presumably owing to slight differences in late diastolic pressures between left and right ventricles (Fig. 40-17) . This diastolic flow is sometimes mistaken clinically for aortic insufficiency or another aortic runoff lesion such as a sinus of Valsalva fistula or coronary artery fistula. Continuous wave Doppler measurement of the ventricular septal defect peak jet velocity allows estimation of right ventricular systolic pressures, and consequently pulmonary artery systolic pressures. By applying the modified Bernoulli equation, one can calculate the pressure gradient between the left and the right ventricle from the ventricular septal defect peak velocity. Subtracting this gradient from the cuff systolic blood pressure yields the right ventricular systolic pressure (Fig. 40-18) . Alignment as parallel as possible to the direction of the ventricular septal

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defect jet prevents underestimation of the gradient between the ventricles. Sampling from multiple windows or off-axis views may be required to achieve the best alignment. Shunt quantification by pulsed Doppler is performed in the same way as with atrial septal defects. Measurement of cardiac output across pulmonic and aortic valves is made, and the pulmonic-to-systemic flow ratio (Qp /Qs ) is computed. The turbulence created in the pulmonary artery by shunt flow from nearby membranous and supracristal defects may make measurement of the pulmonary flow velocity integral inaccurate. An alternative method for deriving shunt ratios involves calculating the volumetric shunt flow across the ventricular septal defect (VSD) and adding it to the systemic cardiac output to get pulmonary flow: Qp = Qs + VSD shunt The ventricular septal defect shunt volume is the product of the crosssectional area of the color flow jet at the Figure 40-17 Pulsed Doppler spectral tracing from the right ventricular aspect of the ventricular septum in a patient with a small perimembranous ventricular septal defect. A low-velocity left-to-right shunt is present in mid-diastole and late diastole (arrowheads) preceding the high-velocity shunt flow in systole.

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Figure 40-18 (color plate.) A, Shunt flow through a small perimembranous ventricular septal defect (VSD). d is the diameter of the flowstream at the septal surface. B, Continuous wave Doppler spectral tracing of the VSD shunt flow. The peak systolic velocity is 3.5 m per second. Dotted lines trace the flow velocity integral of the shunt flow. Estimation of right ventricular systolic pressure (RVSP) can be made by the formula on the lower left, using four times the square of the peak velocity. Calculation of the VSD shunt is possible using the formula on the lower right, including the diameter of the VSD and the flow velocity integral of the continuous wave Doppler tracing. Ao, aorta; LA, left atrium; LV, left ventricle; P, pressure; SBP, systolic blood pressure; VTI, velocity time integral.

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defect and the flow velocity integral of the continuous wave Doppler systolic flow signal (see Fig. 40-18) . In one study, this method had better correlation with shunt ratios determined by the Fick method than the standard pulsed Doppler calculation of Qp /Qs . [104] It may prove particularly useful in patients with pulmonary stenosis or in whom the pulmonary annulus or pulmonary flow profile is difficult to measure. Management

Surgical intervention for the adult with a small ventricular septal defect and normal pulmonary artery pressures is not necessary. Periodic follow-up is important to reinforce endocarditis prophylaxis, to reassess ventricular size and function, and to follow pulmonary artery pressures. Closure of a small ventricular septal defect may be indicated when intervention is needed for associated abnormalities such as significant aortic insufficiency or right ventricular outflow tract obstruction. Patients with large ventricular septal defects and irreversible pulmonary hypertension should be managed medically. Device closure of ventricular septal defects has been accomplished in selected cases when surgery was contraindicated, and it is now approved by the Food and Drug Administration for clinical application.[105] Appropriate placement requires a sufficient distance from the aortic valve or the atrioventricular valves to avoid damaging these structures. The eventual fate of devices in the actively contracting ventricle is unknown; however, with further development and modifications of transcatheter devices, this procedure may have wider application in the future. Patent Ductus Arteriosus The patent ductus arteriosus is a fetal necessity to allow diversion of flow from the nonfunctioning pulmonary circuit into the aorta and back to the placenta. The ductal channel arises from the pulmonary artery bifurcation near the origin of the left pulmonary artery and passes to the lesser curvature of the aorta just opposite the left subclavian artery. Ductal shape is quite variable, sometimes being a long, tortuous channel or a conical connection or even a very short window-like communication (Fig. 40-19) . The ductus arteriosus normally closes spontaneously within the first 24 to 48 hours of life. Persistence Figure 40-19 The various shapes of a patent ductus arteriosus as seen

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angiographically. The ductus is shown arising from the lesser curvature of the aortic arch. Its configuration varies from a window-like communication to a long tortuous channel (A to E). Knowledge of the ductal shape is important in choosing the best method of transcatheter closure. (Modified from Krichenko A, et al: Am J Cardiol 1989;63:878. Reprinted by permission of the publisher. Copyright 1989 by Excerpta Medica Inc.)

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beyond the neonatal period is abnormal, and spontaneous closure after the first year of life is distinctly uncommon. This lesion is found in only about 2% of adults with congenital heart disease. It is usually an isolated anomaly, but it can occur in association with complex lesions, ventricular septal defect, or coarctation. After 30 years of age, the ductal tissue becomes calcified and more friable. Aneurysms of the ductus arteriosus or the closed ductal diverticulum also occur and may rupture. Infectious endocarditis is more common in the second and third decades of life, affecting the pulmonary end of the ductal channel. The clinical presentation of an adult with a patent ductus arteriosus depends on the size of the shunt. Trivial shunts may be clinically silent, detected by an echo-Doppler study that was requested for an unrelated lesion. Small ductal shunts produce a continuous murmur at the upper left sternal border, which can be confused with the murmur of a coronary artery fistula, combined aortic stenosis and insufficiency, or a ventricular septal defect plus aortic regurgitation. Patients with moderate or large shunts develop congestive heart failure and atrial arrhythmias from the long-standing left ventricular volume overload. With the onset of pulmonary hypertension and reversal of the shunt, the murmur decreases in intensity or disappears and differential cyanosis of the lower extremities may be noticed. Echocardiographic Evaluation

Two-dimensional imaging of the ductus arteriosus is accomplished with ease in the neonate and young child, but it becomes progressively more difficult in adolescents and adults. The direct view of the ductal channel is best obtained in a high left parasternal window at the pulmonary artery bifurcation where the left pulmonary artery crosses the descending thoracic aorta. The main pulmonary artery appears to "trifurcate," with the third channel being the ductus. Visualization is possible also in suprasternal notch views of the aorta focused on the lesser curvature opposite the left subclavian artery. Diagnosis of a patent ductus arteriosus in the adult

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usually is made with color flow Doppler imaging rather than direct twodimensional imaging. The left-to-right flow stream appears as a red jet in diastole entering the main pulmonary artery near the left pulmonary artery origin (Fig. 40-20) . Although patent ductus arteriosus shunt flow is continuous, the systolic component is usually washed along with systolic flow in the main pulmonary artery. If flow can be visualized within the ductus itself, however, a continuous Doppler signal is present. As the pulmonary artery pressures rise, the velocity of the patent ductus arteriosus shunt decreases and it becomes more difficult to distinguish a discrete patent ductus arteriosus jet from other low-velocity flows within the dilated pulmonary vessel. Adults with a dilated main pulmonary artery often have a low-velocity retrograde flow in late systole from swirling of flow within the enlarged vessel. Pulsed Doppler can distinguish this from ductal flow by the difference in timing. Continuous flow into the pulmonary artery also is seen with coronary artery fistulas and with an aortopulmonary Figure 40-20 (color plate.) Parasternal short-axis echocardiographic view of the heart at the base, demonstrating a small patent ductus arteriosus. The stream of left-to-right shunt flow is shown in color as it passes from the descending thoracic aorta (DAo) to the pulmonary artery (PA). Ao, aorta.

window. Demonstration of the color Doppler flow stream emanating from the bifurcation and originating within the descending thoracic aorta should confirm that the shunt comes from a patent ductus arteriosus. Continuous wave Doppler sampling of ductal shunt flow is important for estimation of pulmonary artery pressure. When the ultrasound beam is aligned from the high left parasternal window directly into the mouth of the patent ductus arteriosus, systolic and diastolic flow velocity can be recorded. Applying the modified Bernoulli equation, the peak systolic velocity of the patent ductus arteriosus jet can be used to calculate the systolic gradient between the aorta and pulmonary artery. Subtracting this gradient from the cuff systolic aortic blood pressure yields the pulmonary artery systolic pressure. Shunt quantitation for a patent ductus arteriosus is performed in the same way as for atrial and ventricular shunts, measuring cardiac output across aortic and pulmonary valves. In the case of a patent ductus arteriosus, however, the shunt occurs after the flow crosses the pulmonary valve. Hence, the transpulmonary flow represents systemic flow, whereas the transaortic flow includes the shunt. The shunt ratio is computed by putting transaortic flow in the numerator and transpulmonary

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flow in the denominator.[106] Management

Closure of a patent ductus arteriosus is recommended for all but the clinically silent or the severely hypertensive ductus. Angiographic or magnetic resonance imaging delineation of the ductal shape is still necessary for surgical planning and for decisions regarding device closure in the 889

adult. Surgical mortality in repairing this lesion is low, but calcification of the ductus or a short, wide ductal shape complicates the procedure. Transcatheter closure of the ductus arteriosus is becoming the treatment of choice for children and adults. Several types of devices are currently in use, including a pluglike occluder within the ductus, umbrella devices that occlude the orifices at each end of the ductus, and coils that are extruded within the ductus and thrombose the channel. [107] [108] [109] Transesophageal echocardiographic guidance of device placement has not played as critical a role for the ductus arteriosus as for atrial septal defects. The difficulty in imaging the anatomic details of the ductus arteriosus by transesophageal echocardiography limits the usefulness of the modality, and fluoroscopic monitoring alone is sufficient for accurate placement. Transthoracic echo-Doppler assessment after device closure is quite helpful to ensure appropriate device position and assess residual shunting. [110] The highly reflective device can be appreciated by two-dimensional imaging at the pulmonary bifurcation and along the lesser curvature of the aorta. Malpositioning of the umbrella devices results in protrusion of a portion of the occluder into the aortic lumen or into the main pulmonary artery (Fig. 40-21) .[111] Residual shunt flow can be expected in about half of patients 24 hours after umbrella device placement, but this diminishes significantly over time. In one long-term follow-up study, 38% had detectable shunting at 1 year, and at late follow-up (3 to 4 years) about 10% of patients still manifested a small residual shunt by Doppler study.[110] Long-term results after coil occlusion are limited, but 1-year follow-up indicates that about one third have Doppler evidence of small clinically silent residual shunts. [109]

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Coronary Fistulas A coronary fistula is an abnormal communication of a coronary artery with a cardiac chamber, great vessel, or Figure 40-21 Echocardiographic images from a patient after patent ductus arteriosus closure with a Sideris device. Left, In the parasternal short-axis view the counteroccluder (arrow) is seen near the origin of the left pulmonary artery (PA). Right, The occluder protrudes into the aortic lumen (double arrows) in the suprasternal notch view. Ao, aorta.

other vascular structure without passing through the myocardial capillary bed. Most coronary fistulas are congenital, resulting either from persistence of embryonic channels between the cardiac chambers and the developing coronary circulation or from aberrant connection of some of the coalescing coronary channels to the pulmonary artery. Coronary fistulas have been reported in 0.2% of coronary angiograms, usually as incidental findings.[112] The clinical presentation depends on the site of termination of the fistula and the degree of shunting. Over 90% of fistulas terminate in the right heart—right ventricle, right atrium, pulmonary artery, coronary sinus, or superior vena cava. A continuous murmur is caused by shunting from the aorta to the right heart. When the fistula communicates with the left ventricle, the murmur is audible only in diastole. Shunting is usually modest (Qp /Qs of 1.5:1), but it may progress over time by gradual enlargement of the fistulous tract or from the development of systemic hypertension. Signs of right ventricular volume overload and congestive heart failure may appear later in life from the long-standing left-to-right shunt. The shunt is rarely large enough to cause severe pulmonary hypertension. Angina, and rarely myocardial infarction, occurs in a small percentage of patients from "coronary steal" as the fistula diverts flow from the normal coronary circulation.[113] Echocardiographic Evaluation

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Echo-Doppler diagnosis of coronary artery fistulas begins with the detection of enlargement of the proximal coronary artery involved in the abnormal communication. The affected coronary vessel is diffusely enlarged (>0.6 cm) and can often be traced to the site of termination with knowledge of the expected coronary course and the usual sites of fistulous communication. Aneurysmal lakes may develop near the communication with the receiving chamber or vessel, appearing as large sonolucent regions (Fig. 40-22) . Enlargement of the right or left heart chambers 890

Figure 40-22 Echocardiographic images from a patient with a coronary artery fistula from right coronary artery (RCA) to right atrium (RA). A, In the parasternal short-axis view the RCA is markedly dilated and tortuous, feeding a large venous lake adjacent to the interatrial septum (arrowheads). B, Apical fourchamber view demonstrates the venous lake along the right atrial septal surface (arrowheads). Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

gives an indication of the significance of left-to-right shunting. Color flow Doppler demonstrates continuous flow within the involved coronary artery and helps to localize the exit site.[114] [115] When a small fistula from the left coronary artery to the pulmonary artery is present, a tiny stream of continuous flow may be found incidentally in the proximal main pulmonary artery. Larger fistulas are diagnosed by scanning the right atrium, right ventricle, and left ventricle for a continuous turbulent flow signal (Fig. 40-23) . Transesophageal echocardiography also can detect coronary enlargement and visualize the enlarged and aneurysmal channels of the fistula. It is particularly helpful intraoperatively to assess residual fistulous flow and segmental wall motion after ligation of the feeding coronary vessel.[115] Figure 40-23 (color plate.) Apical echocardiographic images from a patient with a coronary artery fistula terminating in the right ventricular apex. A, A small venous lake (arrowheads) is apparent along the right septal surface. B, Entry of flow into the right ventricle from the fistula is clearly demonstrated by color flow Doppler. LV, left ventricle; RV, right ventricle.

Contrast echocardiography has been used in conjunction with angiography to detect fistulous communication when there are multiple entry sites of a

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coronary fistula.[116] [117] If the fistula terminates in both the right and the left ventricles, angiographic contrast may stream preferentially to the lowerpressure chamber. Faint opacification of the left ventricle easily may be overlooked. With injection of agitated saline into the arterial catheter, however, even a trace appearance of contrast in the left ventricle is obvious echocardiographically. Management Small, clinically silent coronary fistulas do not require closure. Patients with fistulas that are large enough to cause coronary dilation should be followed clinically for 891

the development of symptoms or significant right or left ventricular volume overload. Coronary angiography is generally necessary to completely evaluate the coronary circulation for coexistent atherosclerotic disease as well as for complete anatomic delineation of the fistula. Closure of large fistulas may be approached surgically or with transcatheter coil occlusion, depending on the specific anatomy of the lesion.

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Complex Congenital Heart Disease Adults who survive with complex congenital heart defects represent a very small but intriguing fraction of an adult cardiology practice. In the current surgical era, most patients with complex lesions have had the benefit of either palliative or corrective surgery during childhood (see Chapter 41) . The occasional patient reaches adulthood and seeks medical attention for symptoms more typical of acquired heart disease—congestive failure, angina, valvular disease, arrhythmia, endocarditis—only to be found to have complex congenital heart disease, once a echocardiographic study is performed. A brief consideration is given to some of the complex lesions that permit natural survival into adulthood. Tetralogy of Fallot The tetralogy originally described by Fallot in 1888 consisted of a large ventricular septal defect, an overriding aorta, pulmonary stenosis, and right ventricular hypertrophy. About 15% of patients have an atrial septal communication (pentalogy of Fallot), and 25% have a right aortic arch. Anomalous origin of the left anterior descending coronary artery from the right coronary artery or bilateral left anterior descending vessels occurs in 5% to 9% of patients, complicating patch repair of the right ventricular Figure 40-24 Echocardiographic images from a patient with tetralogy of Fallot. A, Parasternal long-axis view of the left ventricle (LV) illustrates a large malalignment ventricular septal defect with aortic overriding of the interventricular septum (arrowheads). B, Anterior deviation of the parietal band (arrow) is apparent in the parasternal short-axis image, creating obstruction in the right ventricular outflow tract. Ao, aorta; PA, pulmonary artery; RV, right ventricle.

outflow tract because the anomalous vessel passes over the right ventricular outflow tract.[118] [119]

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Physiologically, the clinical picture with tetralogy of Fallot is that of a ventricular septal defect with right ventricular outflow obstruction of variable severity. Most patients develop severe cyanosis either at birth or within the first year of life, requiring surgical palliation or correction. Only 3% to 5% of patients survive beyond 25 years of age without intervention. [120] With only a modest degree of pulmonary stenosis, patients can survive with few symptoms into adult years. Paradoxically, the other group of late survivors without surgery includes patients with complete obstruction to right ventricular outflow. This subgroup—having pulmonary atresia with ventricular septal defect—has multiple congenital aortic-to-pulmonary collaterals capable of supplying the pulmonary circulation so as to produce only modest clinical desaturation. Cerebrovascular accidents or brain abscess, bacterial endocarditis, acquired aortic valve disease, and arrhythmias account for much of the morbidity and mortality in the adult with uncorrected tetralogy of Fallot. Echocardiographic Evaluation

Echo-Doppler evaluation can accurately define the characteristic features of tetralogy of Fallot. The malalignment ventricular septal defect usually is large and lies immediately beneath the dilated overriding aortic root (Fig. 40-24) . In parasternal views of the left ventricle, the size of the ventricular septal defect can be appreciated. The direction and velocity of shunt flow across the defect are easily determined in these planes by color flow and pulsed Doppler imaging. Unless the ventricular septal defect has become restrictive over time, the shunt is very low velocity and predominantly right to left. Parasternal short-axis views of the right ventricular outflow tract and aorta demonstrate the typical anterior deviation of the conal septum, narrowing the right ventricular outflow 892

tract (see Fig. 40-24) . A small pulmonary annulus, valvular pulmonary stenosis, and hypoplasia of the main and branch pulmonary arteries also are visible in this view. The systolic gradient across the stenotic outflow tract should be measured by continuous wave Doppler imaging. In patients with native or acquired pulmonary atresia, the right ventricular outflow tract is filled with muscle and ends blindly with no visible pulmonary valve leaflets and no detectable flow by pulsed Doppler. When the parasternal views are not able to visualize the pulmonary artery because of chest wall or lung interference, scanning from the suprasternal notch or high left subclavicular

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area may provide the necessary access to the branch pulmonary arteries. The proximal right pulmonary artery is measurable in nearly all patients with confluent pulmonary arteries. Suprasternal or high parasternal views of the ascending aorta are most accurate for measuring the right pulmonary artery, which passes behind the aorta as a small cross-sectional lumen in the long-axis plane, or a small linear vessel in the short-axis plane. Aortopulmonary collaterals can be detected, but they are not fully delineated by either magnetic resonance imaging or two-dimensional echocardiography.[121] [122] Apical and subcostal five-chamber views depict the large subaortic ventricular septal defect and the overriding aorta. Acquired aortic valve stenosis and insufficiency also can be further evaluated at this point in the examination. Moving the scan plane even more anteriorly from the five-chamber view brings the right ventricular outflow tract into view. This approach may provide better alignment of the Doppler cursor for sampling the right ventricular outflow tract gradient. In the cross-sectional views of the aortic root at the base of the heart, attempts should be made to visualize the coronary arteries. Enlargement of the right coronary orifice hints at a larger blood supply through this vessel, perhaps caused by the anomalous origin of the left anterior descending coronary artery. Careful attention should be directed to cross-sectional lumina seen anterior to the right ventricular outflow tract in high parasternal views and to anteriorly coursing vessels arising from the proximal right coronary artery. Although some success has been reported with transthoracic study of the coronary arteries in adults with tetralogy of Fallot,[123] coronary arteriography is still needed as part of the preoperative assessment in the adult. Transesophageal imaging in tetralogy of Fallot can provide nearly all the important diagnostic information, particularly with multiplane imaging probes. Malalignment of the conal septum is apparent in midesophageal longitudinal views of the right ventricular outflow tract or from the transgastric approach. The pulmonary valve anatomy and the size of the main and right pulmonary artery can be determined from transverse views in the midesophagus or high esophagus. The left pulmonary artery is often more difficult to image. The ventricular septal defect and overriding aorta can be appreciated in transverse views from the midesophagus and from transgastric views. Management

The majority of adults with tetralogy of Fallot should be candidates for

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complete repair. Surgery for this lesion can be accomplished in the adult with a reasonably low mortality (2000 echocardiographic studies per year under a level 3 director with recognized expertise in TEE. TEE studies are to include intraoperative, critical care, and ambulatory settings. Type of Cases Esophageal Recommended intubation to learn TEE probe insertion. Supervised TEE examinations and interpretations. Maintenance Annual TEE studies

Conditions of Training

Postfellowship Training Level 2 training or equivalent to 6 months of echocardiographic training Laboratory performing >2000 echocardiographic studies per year under a level 3 director with recognized expertise in TEE. TEE studies are to include intraoperative, critical care and ambulatory settings. Esophageal intubation to learn TEE probe insertion. Supervised TEE examinations and interpretations. Annual TEE studies

Number of Studies to Complete 300 complete transthoracic studies

Not applicable

50–75

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of Skills Modified from Pearlman AS, Gardin JM, Martin RP, et al: J Am Soc Echocardiogr 1992;5:187–194. for competence in training includes active participation and performance with image acquisition in at least 50 studies, with interpretation of at least 100 studies. Careful attention to refinements in test performance as well as review of digital images and videotape should be part of the training curriculum.[45] [46] [47] [48] Ongoing maintenance of skill in interpretation should be sought with at least 15 studies per month after training. The clinical setting of training in stress echocardiography also deserves emphasis. The training stress echocardiography laboratory should perform more than 40 studies per month and be led by a level 3–trained cardiologist with experience in more than 200 stress echocardiographic studies. Given the ample availability of corroborative testing in ischemic coronary disease with nuclear perfusion imaging and coronary angiography, these data should be sought out by the trainee in stress echocardiography to gain further insight into his or her interpretive 929

TABLE 42-5 -- Training Requirements for Performance and Interpretation of Stress Echocardiography Fellows in Training Qualifications Level 2 training for Training and ability to interpret resting wall motion Conditions of Laboratory Training performing ≥40 stress echocardiographic studies per month Supervisor with level 3 training, and experience

Postfellowship Training Level 2 training or equivalent current active practice of echocardiography Laboratory performing ≥40 stress echocardiographic studies per month Supervisor with level 3 training, and experience

Maintenance of Skills Not applicable

Not applicable

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with >200 stress with >200 stress echocardiographic echocardiographic studies studies Number of Participation and Participation and Interpretation of Cases performance of at performance of at at least 15 stress echocardiographic least 50 exercise Recommended least 50 exercise echocardiographic echocardiographic studies per month and/or and/or pharmacologic pharmacologic stress stress echocardiographic echocardiographic studies. studies. Interpretation of at Interpretation of at least 100 stress least 100 stress echocardiographic echocardiographic studies with studies with supervision as supervision as above. above. Modified from Popp R, Agatson A, Armstrong W, et al: J Am Soc Echocardiogr 1998;11:95–96. ability. Also, given the small but measurable serious complication rates of stress and pharmacologic echocardiography, the trainee should also master the skills necessary to detect the beginnings of such complications early in their development.[49] [50] [51] [52] [53] Pediatric and Fetal Echocardiography In most clinical practices and academic centers, the discipline of pediatric echocardiography is a separate service performed by pediatric cardiologists, and the discipline of fetal echocardiography is a service provided by a highrisk pregnancy team of pediatricians, radiologists, and pediatric cardiologists. In smaller medical centers and in rural communities, these functions may fall to a general adult echocardiographer. With limited experience, an adult echocardiographer may only be able to function in a triage capacity, referring to more specialized care centers once cardiac pathology is discovered.[54] [55] [56] [57] [58] To define the levels of expertise needed for a practitioner to be competent in these areas, the consensus guidelines for pediatric echocardiography,

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pediatric TEE, and fetal echocardiography have been published or supplemented[59] [60] [61] [62] [63] and are summarized in Table 42-6 . Parallel to adult echocardiography, these guidelines emphasize both the setting of training and the case mix number recommended for achieving competence. Furthermore, pediatric cardiologists who have achieved level 2 training are strongly urged, as are adult cardiologists, to ally themselves with a level 3 laboratory once in practice to ensure the availability of collaboration and more specialized diagnostic capacity. Emerging Technologies It appears certain that new echocardiography technologies will develop that will require new credentials. The skill required for some of these techniques may be mastered "on the job," after a review course or workshop, as for contrast echocardiography.[64] [65] [66] More complex or invasive emerging technologies, such as three-dimensional and intravascular echocardiography await both a repertoire of clinical applications and a set of guidelines to foster their application. The principles of technical and cognitive competence already outlined should serve as a template for future guidelines.

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Echocardiography Training for Noncardiologist Physicians Perioperative Echocardiography The consensus guidelines for training in intraoperative and perioperative echocardiography have necessarily been a product of interdisciplinary collaboration (Table 42-7) (Table Not Available) . Inpatient and ambulatory TEE requires considerable training, but perioperative echocardiography requires on-the-spot diagnosis and decision making and collaboration with surgical management and implications for surgical outcome and, in general, a lack of opportunity to repeat the study or obtain leisurely consultation with a colleague in complex decision making. To the extent that the guideline[38] has been a collaboration of members of the Society of Cardiovascular Anesthesiologists, American College of Cardiology, and the American Society of Echocardiography, each discipline can learn from that collaboration. The cognitive and technical skills required for perioperative echocardiography are at once similar to those for TEE in general and specific to the operative setting. Cardiologists should note well that the basic skills of equipment handling, infection control, electrical safety recommendations, and recognition of hemodynamic manifestations of general anesthesia, air embolism, and anaphylaxis are listed as requirements, as these are not skills commonly taught in TEE training. The development of the guidelines has been contentious in some areas, because of the apparent "short-track" to basic skills in echocardiography outlined for anesthesiologists. Those of us who trained ourselves in TEE and stress echocardiography can both sympathize with the anesthesiologists' desire to apply a very useful 930

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TABLE 42-6 -- Training Guidelines for Performance of Pediatric and Feta Echocardiography Duration and Objectives Conditions Physicians in a Cardiology Training Program Level 1 Introductory 3 months experience

Level 2

Sufficient experience to take independent responsibility for echocardiographic studies

Level 3

Sufficient expertise to direct a pediatric echocardiography laboratory

Special Pediatric general Procedures and intraoperative TEE

Number of Cases/Level

Total Numb of Cas

150 200 twodimensional/Mmode and Doppler exams; one half done on patients younger than 1 year 400 6 months 200 twoincluding level 1 dimensional/Mmode and Doppler exams; one half done on patients younger than 1 year 350 two12 months 750 including levels 1 dimensional/Mand 2 mode and Doppler examinations and special procedures Level 2 or 25–30 equivalent transesophageal intubations, most in patients younger than 2 years 30–50 supervised complete pediatric TEE studies

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TEE continued competence Fetal Level 2 or echocardiography equivalent 3 months in formal fetal echocardiography laboratory Independent 6 months interpretation and direction of fetal echocardiographic program

50 complete studies per year 50 supervised complete fetal echocardiographic studies, including high-risk pregnancies 100 general fetal echocardiographic studies

100 fetal studies of high-risk patients, with serial study Fetal Continued echocardiography membership in continued fetal-maternal competence management team Adapted from Meyer RA, et al: J Am Soc Echocardiogr 1988;1:285–286; Fyfe DA, et al: J Am Soc Echocardiogr 1992;5:640–644; and Meyer RA, et al: J Am Soc Echocardiogr 1990;3:1–3. technology and also agree that rigorous application of credentialing be applied within the medical community. The practitioners at the Cleveland Clinic[36] have outlined a comprehensive, year-long perioperative echocardiographic training curriculum available to cardiologists, anesthesiologists, and surgeons. Additional skills in epicardial echocardiography and valve repair assessment are included and constitute a level of even more advanced training. More specifically, optimal goals of examinations done are listed in the curriculum and are in the range of experience dictated by a cardiology fellow's level 2 training, in-training TEE experience, plus an additional 75 perioperative TEE or epicardial echocardiographic procedures. As in general echocardiography, the principle of an experience hierarchy is implied in these guidelines. That is, anesthesiologists who have mastered

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the basic skills (level 1) are encouraged in training either to master advanced skills (level 2) or to ally themselves with an advanced practitioner in the postgraduate setting (level 3, including valve repair assessment). There is substantial merit to having TEE be an anesthesiologist skill, but there is also justification for adhering to training guidelines to provide the best clinical outcomes.[35] [67] [68] [69] [70] [71] [72] [73] [74] Given the multiple tasks an anesthesiologist must pursue, it seems desirable that TEE collaboration with fellow anesthesiologists and cardiologists should take place. The training pathway chosen by a given practitioner may be as limited or as demanding as his or her practice and research interests dictate (Fig. 42-2) . A comprehensive echocardiography laboratory is defined especially by the level of training of its physicians and sonographers, and only in a subordinate sense by its technologic armamentarium. Thus, a level 3 echocardiography laboratory is defined by its leadership experience, not by how many new machines it has. A deeply experienced level 3 echocardiography laboratory is competent in all pathways of training illustrated. Emergency Department It is a further testament to the broad usefulness of echocardiography that emergency room physicians have begun performing "limited" echocardiographic studies to answer "focused" questions in critically ill patients presenting to the emergency department.[75] The proposed training standard for physicians performing echocardiography in the emergency department[76] recommends a minimum of 25 to 50 echocardiograms. The American Society of Echocardiography has issued a Position Statement on the use of echocardiography in the Emergency Department, [77] expressing the conviction that the proposed number of cardiac echograms for emergency department physicians' training is inadequate to assess the multitude of causes of "acute hemodynamic instability." The authors of the statement further argue that the emergency department "community has posed an eminently testable hypothesis: that [emergency department physicians] after a very modest amount of training, can use ultrasound to correctly diagnose acute and life-threatening conditions, in a time frame too short for a cardiologist or an echocardiography lab extender to arrive."[78] Thus far, this hypothesis 931

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TABLE 42-7 -- Skills Needed to Perform Intraoperative Transesophageal Echocardiography (TEE) (Not Available) Adapted from Savage RM, et al: Anesth Analg 1995;81:399–403; and Thys DM, et al: Anesthesiology 1996;84:986–1006.

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Figure 42-2 Pathways of training in echocardiography. Proficiency in multiple pathways requires additional training. A, Anesthesiologist training pathway; C, cardiologist training pathways; P, pediatric cardiologist training pathway.

has not been tested, and emergency department physician credentialing in echocardiography remains unvalidated, although the potential for echocardiography services in the emergency department remains significant.[79] , [80] Rural Medicine Geographic as well as temporal separation from a level 2 or 3 echocardiography laboratory poses similar restrictions on the availability of echocardiography services in rural areas. General internists and radiologists not uncommonly provide echocardiography interpretation in these settings. Formal alliance with a level 3 echocardiography laboratory is to be encouraged for technical support to rural echocardiography. Soon, ready access to telemedicine consultation via the Internet or broadband transmission of digital echocardiographic studies will make near real-time consultation with a level 3 laboratory a reality and sustain the local imaging prerogative. [58] Integrated Echocardiography Services Comprehensive echocardiography services involve multiple service lines in a medical center and must extend to noncardiology and remote sites. A fully integrated tertiary referral echocardiography laboratory (Fig. 42-3) should function centrally for level 3 training and level 2 and level 1 support, with ongoing training, learning, and mutual benefits present at

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Evaluating and Maintaining Competence The American Board of Internal Medicine has, since 1983, required that medical residents be assessed in procedural skills as a requirement for board certification. This assessment has been of such skills as thoracentesis, cardiopulmonary resuscitation, lumbar puncture, and sigmoidoscopy. The evaluation and documentation of competence in these procedures has been left to individual training program directors. Despite the level of sophistication and potential risk of cardiac procedures, no such standard exists for cardiology fellows. Individual training programs are left to define and have reported success in Figure 42-3 Oversight responsibilities of a comprehensive tertiary care referral echocardiography laboratory.

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measuring competence,[81] achieved through programmatic goals (procedures done) and the in-house training examination. Formal fellowship training provides multiple opportunities for senior observation and mentorship of cardiology fellows in diagnostic and technical skills. The Echocardiography Specialized Examinations The cardiology fellow should ideally be measured by a national competence standard, both as an affirmation of training adequacy and to ensure that a national professional standard is being maintained. For these reasons, the Examination of Special Competence in Adult Echocardiography was developed and is now administered by the National Board of Examiners. The person who has successfully taken this examination has a credential in echocardiography that parallels other

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cardiac subspecialties such as electrophysiology and interventional cardiology. In addition, a separate Certification Examination in Perioperative Transesophageal Echocardiography is offered by the NBE to credential special competency in this discipline. These examinations are open to cardiologists, sonographers, anesthesiologists, surgeons, and internists who have an interest in testing their skills in a written examination. Although technical skill is not directly measured in these examinations, it appears optimal that a passing grade be associated with at least level 2 training in adult echocardiography or advanced training in perioperative echocardiography. Successful passage of these examinations seems to be a prudent goal for those individuals who wish to practice echocardiography. Additional means for measuring and maintaining competence include workshops, national and regional meetings, continuing medical education (CME) accredited videotapes, CD-ROM courses, and specialty textbooks. Accreditation under the Intersocietal Commission for Accreditation of Echocardiography Laboratories (ICAEL) includes the recommendation that physicians maintain at least 30 category 1 CME credit hours in echocardiography every 3 years.[82] Governmental Regulation and the Echocardiography Laboratory Thus far, there is no national governmental policy requiring specific credentialing, certification, or accreditation of echocardiography laboratories or their personnel. However, state legislatures, under whose jurisdiction such prerogatives lie, have begun to make such demands. Four states—New York, Ohio, Wisconsin, and Louisiana—have enacted laws requiring that, in part or whole, laboratory functions and personnel be ICAEL accredited or be associated with an ICAEL-accredited lab.[83] This trend is expected to spread to other states. The implications for laboratories include the need to document personnel training and to meet the essentials and standards of ICAEL (see Chapter 43) . If enforced, these regulations will have an immediate impact on regional HCFA reimbursem*nt for echocardiography services.

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Sonographer Training in Echocardiography The complexity of echocardiography has been magnified many-fold from the days of simple imaging and M-mode measurements to routine quantitative measurements of left ventricular systolic performance, diastolic relaxation, and complex Doppler evaluation of valvular and congenital heart disease. The demands of exercise and pharmacologic stress studies, transesophageal echocardiography, and intravenous contrast examinations have also been introduced to the field in the past 20 years (Table 42-8) . Training The cardiac sonographer can no longer be adequately trained in an "on the job" fashion, as was once acceptable. It is clear that the sonographer must possess extensive cognitive ability to adequately perform diagnostic examinations on increasingly more sophisticated equipment. As outlined previously in Table 42-1 , the cognitive and technical skills needed to obtain a diagnostic echocardiogram are demanding and apply to both physician and sonographer. It would be a disservice to the profession of cardiac sonography to underestimate the responsibilities that have been assigned to and accepted by this sophisticated group of practitioners. Echocardiography is a very "operator-dependent" modality, relying heavily on the skills and knowledge of the individual acquiring the diagnostic images. In most cases, it is the cardiac sonographer, not the physician, who makes basic decisions as to which images, Doppler patterns, and manifestations of pathology are recorded to represent the diagnostic examination.[84] [85] [86] The cardiac sonographer often has the responsibility for the decision to use an echocardiographic contrast agent, for left ventricular opacification, or agitated saline to evaluate intracardiac shunts. It is imperative TABLE 42-8 -- Developments in the Field of Echocardiography

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Echocardiography in 1980 M-mode tracings and measurements Two-dimensional imaging with limited two-dimensional measurements available Limited pulsed and continuous wave Doppler capabilities Intravenous agitated saline contrast Echocardiography in 2000 M-mode tracings and measurements Two-dimensional imaging with advanced two-dimensional measurement capabilities including volumes, ejection fraction, and cardiac output Pulsed and continuous wave Doppler with advanced calculation measurements of valve area, peak gradients, mean gradients, stroke volume/cardiac output, shunt ratios, regurgitant fractions, diastolic relaxation, and compliance Color Doppler echocardiography Exercise stress echocardiography Pharmacologic stress echocardiography Transesophageal echocardiography Intraoperative echocardiography Contrast echocardiography

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that the cardiac sonographer have the ability to analyze data continually during a procedure and integrate these data with information obtained from other diagnostic testing to provide an accurate impression of the cardiac status for the interpreting physician. It is only through rigorous education and training that one acquires these skills. The American Society of Echocardiographers has revised the recommended educational curriculum for cardiac sonographers and sonography students.[87] [88] The guideline addresses many concerns involved not only in training new sonographers but also in defining the skills needed by practicing adult sonographers to obtain stress echocardiograms and transesophageal echocardiograms. The didactic courses that must be

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included during clinical training are quite specific (Table 42-9) . The recommendations include curriculum in cardiac anatomy, physiology and pathophysiology, medical ethics, and pharmacology. Important ancillary patient care skills in the recommendations include cardiopulmonary resuscitation, sterile technique, and universal precautions. One of the most important recommendations is that of a clinical internship of supervised full-time instruction for at least 6 months. During this internship, the student intern should be involved with at least four echocardiographic TABLE 42-9 -- 12-Month Didactic Curriculum for Cardiac Ultrasonography A Course include: Anatomy and physiology Pathophysiology Algebra and trigonometry Basic sciences (e.g., biology, chemistry, and physics) ASE Recommended Educational Curriculum for Cardiac Sonographers Cardiac anatomy and physiology Physical principles of ultrasound Cardiac pathology and pathophysiology Medical ethics and legal issues Professionalism, health care delivery Pharmacology Special Procedures Cardiopulmonary resuscitation Isolation techniques Universal precaution technique Sterile technique Basic history-taking and cardiac physical examination Electrocardiography interpretation Echocardiography modalities: techniques and applications Echocardiography quantitative methods

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Determinants of echocardiographic image quality Basic interpretation and understanding of other cardiac diagnostic methods Understanding of cardiovascular therapeutic techniques and intervention: echocardiographic evaluation Research techniques and statistical analysis 6-Month Clinical Internship Full-time supervised instruction should include: Hands-on scanning incorporating two-dimensional, M-mode, spectral, and colorflow Doppler with measurement and preliminary impressions on 40 patients per month (2 per day) Additional 240 echocardiograms observed and reviewed (2 per day) Perform hands-on imaging on 10 stress echocardiograms (recommended that these be performed on patients undergoing stress electrocardiography procedure only) Adapted from Ehler D, Carney DK, Dempsey AL et al: J Am Soc Echocardiogr 2001;14:77–84. Assumes college-level prerequisites have been met.

graphic procedures per day with the expectation of making all measurements and calculations and giving preliminary impressions with at least half of those. The recommendations of the new guideline comprise the repertoire for entry-level competence in cardiac sonography. There are many pathways by which a sonographer can obtain proficiency in the field of echocardiography. There are certificate programs only months in length that are unlikely to meet all of the recommendations of the ASE. Two-year programs offer the participant an associate's degree in ultrasonography or cardiovascular technology with an emphasis on either pathway. Four-year programs offer a baccalaureate degree in medical ultrasonography. Not all of these programs are accredited. Credentialing The two certifying bodies that currently offer testing in echocardiography are the American Registry of Diagnostic Medical Sonographers and

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Cardiovascular Credentialing International. They both require minimum standards of education and experience to sit for examination, typically met by matriculants of accredited educational programs. The accreditation process for training programs is rigorous, and it is recommended that students attend programs that are accredited by the Joint Review Committee for Diagnostic Medical Sonography (JRC-DMS), the Commission on Accreditation of Allied Health Programs (CAAHEP), or the Joint Review Committee for Cardiovascular Technology (JRC-CVT). These credentialing organizations, as well as ICAEL, require a minimum of 30 hours of echocardiography-related continuing medical education over a 3-year period. It should be the joint responsibility of the individual sonographer and his or her clinical institution to meet or exceed continuing education goals. Career Promotion Sonographer skill level continues to be defined in a somewhat simplistic fashion as either entry-level or experienced. Little heed is paid to the duration or breadth of education the sonographer has achieved in assigning job classification. The scope of practice for sonographers has lately received more intense scrutiny[89] the Society of Diagnostic Medical Sonography will soon publish its summary recommendations for scope of practice. Hospital and state legislatures have, until only recently, required demonstration of basic skills to grant a credential or a license to practice cardiac sonography. Now, the formalization of accreditation of echocardiography services through ICAEL has directed attention back to defining credentialing through involvement of the profession[84] [89] [90] rather than through mere state licensing. This trend should allow the experienced sonographer to be recognized for professional achievement and acquisition of new skills and to open pathways toward advanced practice in ultrasonography.[91] [92] Sonographers, through their professional organizations, are beginning to define 935

career pathways for echocardiography practice as "physician assistants" or "echocardiography practitioners" working more independently but in association with a level 3 laboratory. Such forward-thinking approaches to providing service have been successful in electrophysiology and invasive

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cardiology. It may be possible to meet echocardiography needs in rural medicine, emergency departments, and noncardiology areas through such programs.

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Future Directions The guidelines outlined in this chapter have been put forth by our professional organizations as optimal levels of training. Individuals and training programs should apply these guidelines to develop specific curricula of study and develop tools to measure competence.[93] [94] [95] [96] Certainly, not all physicians who interpret echocardiograms independently or perform TEE have achieved level 2 competence[97] and, in particular, may not have developed or maintained the technical skill to perform complete examinations independently. Their sonographers are the most immediate resource available to redevelop these skills, along with a level 3 laboratory alliance. Training of noncardiology professionals in echocardiography remains a formidable challenge, one likely to be met at a local institution level with strong central echocardiography laboratory leadership. Optimal practice may be difficult to achieve, but it appears that regional government has recognized laboratory accreditation as a measure of competence and will at some level link the definition of professional achievement with reimbursem*nt.

MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26082022/1031/361.html/top

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Chapter 43 - Maintaining Quality in the Echocardiography Laboratory Benjamin F. Byrd III MD

Echocardiography is the most rapidly proliferating, frequently performed major diagnostic test in the United States. Well over 10 million echocardiograms were performed in 2000, at an average cost of $500 per study. Doppler echocardiographic studies are the most operator-dependent of noninvasive cardiac studies. Thorough training of the operator in image acquisition is essential to both reliable demonstration of cardiac structures and interrogation of intracardiac blood flow. An understanding of cardiac pathophysiology is necessary to determine which imaging and flow information is critical to diagnosis in a given patient. Even assuming a high-quality work environment (adequate space, few disturbances, and excellent instrumentation), performance of high-quality studies demands sonographers who are not only well trained but also continually educated, who perform an adequate volume of studies annually, and who are stimulated to excellence by their peers and physicians in the laboratory. Interpretation of echocardiographic studies is for the most part subjective (with the exception of a few M-mode and Doppler measurements) and extremely dependent on the proficiency level of the interpreting physician. The American College of Cardiology (ACC) and the American Society of Echocardiography (ASE) have established training guidelines for cardiologists in surface, transesophageal, and stress echocardiography, [1] [2]

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[3]

but there are no true board examinations as in electrophysiology. In a parallel fashion, there are sonographer organizations that provide voluntary testing and registration (e.g., the American Registry of Diagnostic Medical Sonographers), but competing organizations exist, and there is no unanimity on training requirements. Until recently, therefore, recommendations for the initial training, continuing education, and annual procedure volumes of sonographers and physicians were provided,[4] as were guidelines for the clinical use of echocardiography,[5] but no laboratory accreditation organization existed to confirm that established, across-the-board standards of quality were being met by an echocardiography laboratory. Establishment of quality standards for all aspects of laboratory performance (Fig. 43-1) is actually highly useful to the patients, workers, and payers whose paths cross in the echocardiography laboratory. Patients are assured a high-quality study and interpretation, with reports generated in a timely fashion. Sonographers are assured adequate instrumentation, education, and time to perform optimal studies. Physicians in the laboratory are assured that the best quality study that can be performed will be performed on each patient, and the Medical Director is provided with a vehicle for assuring consistent performance and commitment to excellence from all physicians working in the laboratory. Finally, payers are assured that study performance and interpretation are up to a nationwide standard. In the next few years, digital image storage and transfer under the DICOM standard will facilitate the electronic transfer of echocardiographic studies when patients move between hospitals. The need to repeat studies could fall dramatically, with great cost savings, but only if a consistent level of performance is assured by widespread laboratory accreditation. The Intersocietal Commission for the Accreditation of Echocardiography Laboratories (ICAEL) was established by collaboration between the ACC, the ASE, and several other interested organizations, including the Society of Pediatric Echocardiography. ICAEL has established standards for the practice of echocardiography based on the guidelines of these professional organizations.[6] It accredits laboratories based on these standards in all three major areas of echocardiography: transthoracic, stress, and transesophageal. In addition to documentation of adequate facilities and instrumentation, adequate initial and continuing education, adequate procedure volumes for sonographers and physicians, and a quality assurance (QA) process in the laboratory, videotapes of studies from each laboratory are reviewed by ICAEL sonographer and physician volunteers.

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To date, more than 500 laboratories have been accredited by ICAEL. The major stimulus to applying for ICAEL accreditation has previously been a simple commitment to excellence on the part of each laboratory's sonographers, physicians, and administrators. However, an external stimulus is now being applied, as Medicare carriers in several states Figure 43-1 Elements of echocardiography laboratory accreditation.

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now stipulate that billing echocardiography laboratories be ICAELaccredited. As previously occurred with vascular ultrasonography, Medicare carriers nationwide will likely soon require accreditation of echocardiography laboratories for reimbursem*nt. Thus, the ICAEL guidelines for maintaining quality in the adult echocardiography laboratory, summarized in Table 43-1 Table 43-2 Table 43-3 , assume ever-increasing importance. TABLE 43-1 -- Adult Laboratory Organization Category Description Personnel and Supervision Medical Director training and Completion of a 12-month formal training program. experience or Completion of a 6-month formal training program with at least 600 echocardiogram interpretations. or Three years of echocardiography practice experience with at least 1800 echocardiogram interpretations. responsibilities Responsible for all clinical services provided and for the determination of the quality and appropriateness of care provided.

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CME

Technical Director training and experience

responsibilities

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May supervise or delegate the entire operation of the laboratory. Responsible for ensuring the medical and technical staffs' adherence to the standards and the supervision of their work. Thirty hours of category I CME credits continuing education in echocardiography over a period of 3 years. At least 20 of the continuing education hours must be category I AMA. An appropriate credential in echocardiography. or Successful completion of an ultrasonography or cardiovascular technology program that includes verified didactic and supervised clinical experience in echocardiography. or Completion of 12 months full-time (35 hours/week) clinical echocardiography experience performing echocardiograms plus one of the following: completion of a formal 2-year program in another allied health profession completion of an unrelated bachelors degree possession of an MD or DO degree or equivalent or Three years of echocardiography practice experience with the performance of at least 1800 echocardiogram/Doppler examinations. All laboratory duties delegated by the Medical Director. General supervision of the technical and ancillary staff. The delegation, when warranted, of specific responsibilities to the technical staff and/or the

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CME Medical staff experience and training

responsibilities CME

Technical staff experience and training

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ancillary staff. Daily technical operation of the laboratory (e.g., staff scheduling, patient scheduling, laboratory record keeping). Operation and maintenance of laboratory equipment. Ensuring the technical and ancillary staffs' adherence to the standards. Working with the Medical Director, medical staff, and technical staff to ensure quality patient care. Technical training. At least 30 hours of echocardiography-related continuing education over a period of 3 years. Completion of a 6-month training program in echocardiography that includes interpretation of at least 300 echocardiographic examinations. or Three years of echocardiography practice experience with interpretation of at least 900 echocardiographic examinations. To perform and/or interpret clinical studies. Fifteen hours of AMA category I CME credits continuing education in echocardiography over a period of 3 years. An appropriate credential in echocardiography. or Successful completion of an ultrasonography or cardiovascular technology program that includes verified didactic and supervised clinical experience in echocardiography. or Completion of 12 months full-time (35 hours/week)

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clinical echocardiography experience performing echocardiograms plus one of the following: completion of a formal 2-year program in another allied health profession completion of an unrelated bachelors degree possession of an MD or DO degree or equivalent or Twelve months of echocardiography practice experience with the performance of at least 600 echocardiogram/Doppler examinations. responsibilities Responsible for the performance of clinical examinations and other tasks as assigned. CME At least 15 hours of echocardiography-related continuing education over a period of 3 years. Trainees Training, if conducted, does not compromise patient care and benefits the trainee. Ancillary personnel Ancillary personnel (e.g., clerical, nursing, transport) necessary for safe and efficient patient care should be provided. Physical Facilities Examination areas Examinations shall be performed in a setting providing reasonable patient comfort and privacy. Interpretation and Adequate designated space shall be provided for the storage space interpretation of the echocardiogram and the preparation of reports. Examination Data Archiving, Examination Interpretation, Examination Reports, and Laboratory Records Echocardiographic A system for recording and archiving examination data echocardiographic data (images, measurements, and final reports) obtained for diagnostic purposes must be in place. A permanent record of the images and interpretation must be made and retained in accordance with applicable state or federal guidelines for medical records, generally for 5 to 7 years.

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Echocardiographic data should be readily retrievable for comparison with new studies. Recorded data should consist of real-time (or its digital equivalent) systolic and diastolic images of all cardiac valves, chambers, and great vessels, plus pertinent images that document the presence of pathology. Archiving media include, but are not limited to, videotape, paper strip chart recordings, and digital storage. A log documenting all echocardiographic procedures performed and interpreted by each member of the medical and technical staff should be maintained on an ongoing basis. The log should contain patient, sonographer, and physician identification information sufficient to allow for the review of staff procedure volumes and for the retrieval of previous studies on the same patient. Examinations are interpreted and reported by the Medical Director or a member of the medical staff of the laboratory. Echocardiography reporting must be standardized in the laboratory. All physicians interpreting echocardiograms in the laboratory should agree on uniform diagnostic criteria and a standardized report format. The report should accurately reflect the content and results of the study. The report should include, but not be limited to, a report header, a table of twodimensional and M-mode numeric data, which includes the measurements performed in the course of the examination and/or interpretation, Doppler evaluation and hemodynamic data, and report text that includes an overview of the results of the examination, including any pertinent positive and negative findings. Reports must be typewritten, include a physician signature line (including the name of the interpreting physician), and be signed by the interpreting

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physician. Quality Assurance Instrument maintenance

Echocardiography conferences

Case review

Instrumentation Cardiac ultrasonographic systems

Instrumentation is maintained in good operating condition; this includes recording of method and frequency of maintenance, policy for routine safety inspections and electrical safety and routine instrument cleaning. Four quality assurance conferences per year to review results of comparative studies and address discrepancies, difficult cases, and lab issues. Twice-monthly echocardiographic departmental conferences are recommended. Peer review of performance and interpretation of selected studies to determine quality, accuracy, and appropriateness of the examination. M-mode imaging.

Two-dimensional imaging. Spectral display for pulsed wave and continuous wave Doppler studies. Color flow imaging. Video screen or other display method of suitable size and quality for observation and interpretation of all modalities. Where data are derived from a given line of interrogation (e.g., M-mode or pulsed wave Doppler), a reference line should be available on the screen within a frozen two-dimensional image, except for nonimaging continuous wave Doppler. Range or depth markers should be available on all displays. Capabilities to measure the distance between two points, an area on a two-dimensional image, blood flow velocities, time intervals, and peak and mean

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gradients from spectral Doppler studies. At least two imaging transducers, one of low frequency (2–2.5 MHz) and one of high frequency (3.5 MHz or higher), or a multifrequency transducer that includes these frequencies, plus a transducer dedicated to the performance of continuous wave Doppler studies should be available for each study. Indications, Ordering Process, and Scheduling Indications Echocardiographic testing is performed for appropriate indications. Verification of the A process should be in place in the laboratory for indication obtaining and recording the indication. Ordering process Echocardiography testing is appropriately ordered and scheduled. Definition of Complete imaging study: examines all of the cardiac procedure types and chambers and valves and the great vessels from protocols multiple views, then uses the available information to completely define any recognized abnormalities. Complete Doppler study: examines every cardiac valve and the atrial and ventricular septi for antegrade and/or retrograde flow. In addition, a complete Doppler study provides functional hemodynamic data. Limited study: generally performed only when the patient has undergone a complete recent examination and there is no clinical reason to suspect any changes outside the specific area of interest. A limited study generally examines a single area of the heart or answers a single clinical question. Scheduling Sufficient time is allotted for each study according to the procedure type. The performance time of an uncomplicated complete (imaging and Doppler) transthoracic examination is 45 to 60 minutes (from patient encounter to departure). An additional 15 to 30 minutes may be required for complicated studies. Elements and Components of Examination Performance Examination performance should include proper technique.

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Elements of study performance

Elements of study quality

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Proper patient positioning. Transducer selection and placement. Optimization of equipment gain and display settings. Performance of a two-dimensional/M-mode/Doppler examination according to the laboratory-specific and appropriate protocol. Utilization of appropriate Doppler technique (including proper Doppler alignment) and measurements. Definition of endocardium. Display of standard (on-axis) imaging planes (e.g., avoidance of foreshortening). Delineation of the details of valvular anatomy. Measurements of left ventricular dimensions from standard orthogonal imaging planes. Optimal recording and evaluation of Doppler flows (which should include alignment of the Doppler beam parallel to flow). Accurate spectral Doppler recording and recording of abnormal Doppler flow signals in multiple views. Adherence to the laboratory-specific and appropriate protocol. A protocol must be in place that defines the components of the standard examination.

Components of the transthoracic echocardiogram Complete M-mode Standard views from multiple planes including and two-dimensional views of all cardiac structures and selected examination extracardiac structures. These include, but are not limited to left ventricle right ventricle left atrium right atrium

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aortic valve pulmonic valve mitral valve and tricuspid valve proximal ascending aorta yransverse aorta proximal descending aorta main pulmonary artery and proximal branches inferior vena cava hepatic vein pericardium Complete Doppler Includes spectral Doppler and/or color flow study interrogation of all normal and abnormal flows within the heart, including the valves, the great vessels, and the atrial and ventricular septa. Limited examination A limited study is generally performed only when the patient has undergone a recent complete examination and there is no clinical reason to suspect any changes outside the specific area of interest. A limited study generally examines a single area of the heart or answers a single clinical question. Standard twoParasternal long-axis view. dimensional views Parasternal short-axis views (basal, mitral valve, left ventricle at the mid-papillary muscle level, left ventricular apex). Right ventricular inflow view. Parasternal long-axis view of the pulmonary artery. Apical four-chamber view. Apical two-chamber view. Apical five-chamber view. Apical long-axis view. Subcostal four-chamber view.

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Subcostal short-axis view (when indicated). Subcostal IVC/hepatic vein view. Suprasternal notch view (when indicated). Two-dimensional or The left ventricular internal dimension at endM-mode diastole. measurements of The left ventricular internal dimension at endthe left heart systole. The left ventricular posterobasal free wall thickness at end-diastole. The ventricular septal thickness at end-diastole. The left atrial dimension at end-systole. The aortic root dimension at end-diastole. The four cardiac valves—forward flow spectra for Doppler flow evaluations each valve, and any regurgitation, shown in at least two imaging planes with color Doppler. For aortic stenosis, the highest systolic velocity must be evaluated from multiple transducer positions (e.g., apical, suprasternal, and right parasternal). The tricuspid regurgitation spectrum should always be sought for estimation of systolic right ventricular pressure. Atrial and ventricular septa—color Doppler screening for defects. Left ventricular outflow tract velocity. Use of nonimaging transducer in appropriate views such as apical, right parasternal, and suprasternal notch to assess valvular abnormalities (such as AS, MS, or TR) is strongly encouraged. Velocity-time integrals and hepatic and pulmonary vein flow spectra are optional. Procedure Volumes The annual procedure volume must be sufficient to maintain proficiency in examination performance and interpretation. Maintenance of A laboratory should perform a minimum of 600

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proficiency

echocardiograms annually. Each member of the medical staff should interpret a minimum of 300 studies annually. Each member of the technical staff should perform a minimum of 300 studies annually. The total volume of studies interpreted and performed by each staff member may be combined from sources other than the applicant laboratory.

Results Comparison and confirmation of results

Results of transthoracic echocardiography laboratory examinations should be regularly correlated and compared with operative findings and results of available diagnostic procedures such as cardiac catheterization, angiography, MRI/CT, nuclear studies and PET scans. AMA; American Medical Association; CME, continuing medical education; CT, computed tomography; ECG, electrocardiography; MRI, magnetic resonance imaging; PET, positron emission tomography; TEE, transesophageal electrocardiography.

TABLE 43-2 -- Adult Transesophageal Echocardiography Category Instrumentation Cardiac ultrasonography systems

Description M-mode imaging.

Two-dimensional imaging. Spectral display for pulsed wave and continuous wave. Doppler studies. Color flow imaging. Video screen or other display method of suitable size and quality for observation and interpretation of all modalities. Where data are derived from a given line

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of interrogation (e.g., M-mode or pulsed wave Doppler), a reference line should be available on the screen within a frozen two-dimensional image, except for non-imaging continuous wave Doppler. Range or depth markers should be available on all displays. Capabilities to measure the distance between two points, an area on a two-dimensional image, blood flow velocities, time intervals, and peak and mean gradients from spectral Doppler studies. Transesophageal Transesophageal ultrasound transducers should be ultrasonography those manufactured for the ultrasonography system transducer of the laboratory. Transesophageal ultrasound transducers should incorporate biplane or multiplane imaging capabilities. Indications, Ordering Process, and Scheduling Indications Transesophageal echocardiographic testing is performed for appropriate indications. Verification of the A process should be in place in the laboratory for indication obtaining and recording the indication. Ordering process The TEE order and/or requisition should clearly indicate the type of study to be performed, reason(s) for the study, and the clinical question(s) to be answered. Definition of In general, TEE should be performed to answer procedure types and clinical questions that cannot be answered by protocols transthoracic imaging. A TEE study is one that examines all of the cardiac chambers, valves, and great vessels from multiple imaging planes, then uses the information to completely define any recognized abnormalities. The study should include appropriate Doppler interrogation of all cardiac valves and structures (e.g., pulmonary veins and atrial appendage) and provide any hemodynamic data felt to be of importance for patient care.

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Scheduling

Sufficient time should be allotted for each study according to the procedure type. The performance time for an uncomplicated complete study (outside of the operating room) is estimated to be 45 to 60 minutes (from patient encounter to departure), with an additional 15 to 30 minutes for complicated studies. Sufficient time must be included in the scheduling process for the adequate post-procedure monitoring of the patient, especially if conscious anesthesia is utilized. Elements and Components of Examination Performance Examination performance should include proper technique. Training Transesophageal echocardiography is a semi-invasive test that, if performed incorrectly, can lead to serious harm to patients and therefore should be performed by appropriately trained personnel. Elements of study Include, but not limited to performance transducer insertion optimization of equipment gain and display settings utilization of appropriate Doppler technique and measurements optimization of image orientation to enhance Doppler display performance of a two-dimensional/Doppler transesophageal examination according to the laboratory-specific and appropriate protocol Elements of study Demonstration of cardiac structure and function. quality Evaluation of atrial-septal integrity. Evaluation of left and right atria and appendices. Delineation of the details of valvular anatomy. Optimal recording and evaluation of Doppler flows.

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Adherence to the laboratory-specific and appropriate protocol. Technical personnel Due to the complexity of the TEE study, appropriate technical personnel should be available to assist the performing physician. These personnel may include a sonographer and a nurse. The duties of these individuals include, but are not limited to, preparing the patient for the test, assisting the physician with the ultrasonographic equipment, monitoring the patient during and after the examination, and administering anesthetic medication as allowed by law. Preparation of the To perform TEE studies safely, appropriate safety patient guidelines must be in place. Patients should have a functioning intravenous access in place. Cardiac monitoring with standard telemetry leads should be utilized. Instrumentation to monitor the oxygen saturation of the patient before, during, and after the examination should be available, as well as oxygen with appropriate delivery devices, if needed. All procedures must be explained to the patient and/or the parents or guardians of those unable to give informed consent. Consent should be obtained in a manner consistent with the rules and regulations required by the hospital or facility. Monitoring of the During the procedure, the vital signs and medical patient stability of the patient should be periodically evaluated and recorded by the performing physician or the technical assistant. The development of instability in either the vital signs or comfort of the patient should be addressed by the performing physician. Laboratory guidelines for the monitoring of patients who receive intravenous anesthesic agents are

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required. A list of periprocedural complications should be maintained. Recovery of the Prior to discharge from the TEE laboratory, the patient patient should be monitored for a sufficient amount of time to ensure that no complications have arisen either from the procedure or the medication administered. The patient and/or the family should be instructed on any postprocedure care that the physician feels is necessary. Information should be given to outpatients that will allow them to contact the performing physician should complications arise after patient discharge. A list of post-procedural complications should be maintained. Components of the A protocol must be in place that defines the standard examination components of the TEE examination. A complete TEE and TEE-Doppler examination includes standard views from multiple planes, including views of all cardiac structures and selected extracardiac structures. Standard views in Gastric short-axis and long-axis views. complete examination Standard two- and four-chamber views. Short- and long-axis views of the aortic valve with appropriate Doppler. Multiple imaging planes of the mitral valve with appropriate Doppler. Multiple imaging planes of the tricuspid valve with appropriate Doppler. Longitudinal view of the pulmonic valve with appropriate Doppler. Multiple imaging planes of the left and right atria and appendices with appropriate Doppler.

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In cases of suspected cardiac source of emboli, appropriate use of contrast methods to evaluate for the presence of intracardiac shunting. Multiple imaging planes of the atrial septum and foramen ovale with appropriate Doppler. Imaging of the pulmonary veins with appropriate Doppler. Short- and long-axis views of the ascending, descending, and transverse arches of the aorta. Short- and long-axis views of the main pulmonary artery and proximal portions of the right and left pulmonary arteries. Images of the proximal inferior and superior vena cava. Imaging of the pericardial space and pericardium. Evaluation of extracardiac structures visualized by TEE ultrasonography. Published guidelines exist for the appropriate care and cleansing of the TEE transducer. These guidelines should be followed, except in circ*mstances in which the recommendations of the manufacturer differ but are equivalent.

Procedure Volumes The annual procedure volume must be sufficient to maintain proficiency in examination performance and interpretation. Maintenance of A laboratory should perform a minimum of 50 TEEs proficiency annually. It is recommended that each member of the medical staff who performs or interprets TEEs should perform a minimum of 50 studies annually. The total volume of studies interpreted and performed by each medical staff member may be combined from sources other than the applicant laboratory. Results

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Comparison and confirmation of results

Results of TEE laboratory examinations should be regularly correlated and compared with operative findings and results of available diagnostic procedures such as cardiac catheterization, angiography, and MRI/CT. AMA; American Medical Association; CME, continuing medical education; CT, computed tomography; ECG, electrocardiography; MRI, magnetic resonance imaging; PET, positron emission tomography; TEE, transesophageal electrocardiography.

TABLE 43-3 -- Adult Stress Echocardiography Category Instrumentation Cardiac ultrasonography systems

Digital acquisition systems

Description Hardware and software to perform two-dimensional imaging. Image display device (monitor) that identifies the parent institution, the name of the patient, the date and time of the study, the ECG, and range or depth markers. Measuring capabilities including the ability to measure the distance between two points and an area on a two-dimensional image. A minimum of two imaging transducers, one of low frequency and one of high frequency, or a multifrequency transducer. Image recording device, videotape recorder, and digital recording device. Digital acquisition of the echocardiographic image must be available and utilized for the performance and interpretation of stress echocardiography. The digital acquisition system may be either integrated (part of the ultrasonography system) or nonintegrated (a separate digitizing unit that is connected to the ultrasonography system). This system should allow for accurate "triggered"

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acquisition of images and side-by-side image display. The digitizing system should have adequate memory to allow performance of multistage stress echocardiographic studies and should have a digital recording device capable of recording the resultant side-by-side images. Indications, Ordering Process, and Scheduling Indications Stress echocardiography is performed for appropriate indications. Verification of the A process should be in place in the laboratory for indication obtaining and recording the indication. Ordering process Echocardiography testing is appropriately ordered and scheduled. Definition of Two phase examines and compares left ventricular procedure types wall segments before stress and after stress and is usually accomplished using treadmill exercise (and is sometimes accomplished using pacing methods). Three phase examines and compares left ventricular wall segments before, during, and after stress and is usually accomplished using bicycle exercise ergometry (and is sometimes accomplished using pacing methods). Four phase examines and compares left ventricular wall segments before, during, and/or after stress and is usually accomplished using pharmacologic stress agents or supine bicycle ergometry (and is sometimes accomplished using pacing methods). Doppler compares antegrade and retrograde flow (if present) before, during, and/or after stress. Doppler stress echocardiography may be performed alone or in conjunction with a two-phase, three-phase, or fourphase stress echocardiography examination (and is sometimes accomplished using pacing methods). Contrast examines and compares left ventricular wall segments before stress and after stress following the injection of a contrast agent that is used to enhance endocardial border definition. Contrast may also be

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used to enhance the Doppler signal when performing Doppler stress echocardiography. Contrast stress echocardiography may be used in conjunction with two-phase, three-phase, four-phase, and Doppler stress echocardiography. Scheduling Sufficient time is allotted for each study according to the procedure type. The performance time for a two-phase or three-phase stress echocardiogram is 45 to 60 minutes from patient encounter to departure. An additional 15 to 30 minutes per study may be needed for the performance of a pharmacologic stress echocardiogram, since these procedures require that intravenous access be obtained. Additional time will also be required when adding Doppler to any standard stress echocardiography. Elements and Components of Examination Performance Examination performance should include proper technique. Training Stress echocardiography is a diagnostic test that, if performed and/or interpreted incorrectly, can lead to serious consequences for the patient. Accurate performance of stress echocardiography requires that the performing sonographer and interpreting physician be adequately trained and experienced to perform and interpret stress echocardiograms. Elements of study Proper patient positioning during image acquisition. performance Appropriate transducer selection and placement. Achievement of optimal heart rate. Optimization of the ultrasonographic equipment gain and display settings. Appropriate and consistent scan depth selection for each phase of image acquisition. Rapid post-stress image acquisition (ideally, all post-

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Elements of study quality

Stress echocardiography laboratory arrangement

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stress images should be obtained within 60 seconds of stress cessation). Optimization of digitized images for side-by-side comparison. Utilization of artifact-free ECG for digital triggering purposes. Appropriate ECG lead placement. Utilization of appropriate Doppler technique (including proper alignment) and measurements. Performance of a stress echocardiogram according to the laboratory-specific and appropriate protocol. Definition of endocardium. Display of standard, on-axis imaging planes (e.g., avoidance of foreshortening). Measurements of left ventricular dimensions (when performed) obtained from standard orthogonal imaging planes. Accurate digital triggering (from ECG R wave). Appropriate side-by-side image display. Adherence to the laboratory-specific and appropriate protocol. Stress echocardiograms should be performed in a laboratory designed to ensure patient safety and to facilitate rapid acquisition of post-stress images. Elements of the stress echocardiography laboratory arrangement include Proper placement of the examination table next to the treadmill. Proper placement of the ultrasonographic equipment next to the examination table. Proper placement of the examination table to allow access to both sides of the table. Proper placement of emergency equipment (crash

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Stress echocardiography standard components

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cart and oxygen) such that they are easily accessible. A protocol must be in place that defines the components of the various types of stress echocardiograms. Indications for the performance of a pharmacologic stress echocardiogram and/or a standard exercise stress echocardiogram should be included. Alternative views may be obtained if contrast is used. A two-phase stress echocardiogram includes the following views, obtained both before and immediately following stress: parasternal long-axis view, parasternal short-axis view (mid-papillary muscle level), apical four-chamber view, and apical two-chamber view. Timers are recommended and should be activated when exercise stops. It is also recommended that post-stress images be obtained within 60 seconds. A three-phase stress echocardiogram includes the following views, obtained before, during, and immediately following stress: parasternal long-axis view, parasternal short-axis view (mid-papillary muscle level), apical four-chamber view, and apical two-chamber view. A four-phase stress echocardiogram includes the following views, obtained before, during, and immediately following stress: parasternal long-axis view, parasternal short-axis view (mid-papillary muscle level), apical four-chamber view, and apical two-chamber view. Additional images obtained during a four-phase stress echocardiogram may include low-level stress images, mid-level stress images, and/or peak-level stress images, depending on the clinical question that is being answered with the stress echocardiogram. A Doppler stress echocardiogram includes interrogations of flow velocities (from the same site) before, during, and/or immediately following stress.

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Doppler stress echocardiography may be used to document gradient changes that occur with stress or to evaluate diastolic filling pattern changes that occur with stress. Patient preparation To adequately perform stress echocardiographic studies, appropriate safety guidelines must be in place. All stress echocardiographic procedures must be explained to the patient and/or the guardian of those unable to give informed consent. Consent should be obtained in a manner consistent with the rules and regulations outlined by the hospital or facility. Patients undergoing pharmacologic or contrast echocardiography must have a functioning intravenous access in place. Emergency equipment (standard crash cart) with additional medications utilized for reversing the effect of the pharmacologic stress agent(s) must be readily available at all times. Adequate personnel (a minimum of two individuals) should be present during all stress echocardiographic procedures. Personnel should be certified in Basic Cardiac Life Support (BCLS). Patient monitoring During the image acquisition phase and during the recovery phase of the examination, the vital signs of the patient should be periodically evaluated in accordance with the stress testing protocol. Cardiac monitoring with standard stress testing leads should be used. A list of procedural complications should be maintained. Procedure Volumes The annual procedure volume must be sufficient to maintain proficiency in examination performance and interpretation. Maintenance of A laboratory should perform a minimum of 100

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stress echocardiographic examinations annually. Each member of the medical staff who interprets stress echocardiograms should interpret a minimum of 100 stress echocardiograms annually. Each member of the technical staff who performs stress echocardiograms should perform a minimum of 100 stress echocardiograms annually. The total volume of studies interpreted and performed by each member may be combined from sources other than the applicant laboratory.

Results Comparison and confirmation of results

Results of transthoracic echocardiography laboratory examinations should be regularly correlated and compared with operative findings and results of available diagnostic procedures such as cardiac catheterization, angiography, and MRI/CT. AMA; American Medical Association; CME, continuing medical education; CT, computed tomography; ECG, electrocardiography; MRI, magnetic resonance imaging; PET, positron emission tomography; TEE, transesophageal electrocardiography.

References 1. Stewart WJ, Aurigemma GP, Bierman FZ, et al: Guidelines for training in adult

cardiovascular medicine. Core Cardiology Training Symposium (COCATS). Task Force IV: Training in echocardiography. J Am Coll Cardiol 1995;25:16–19. 2. Pearlman AS, Gardin JM, Martin RP, et al: Guidelines for physician training in

transesophageal echocardiography: Recommendations of the American Society of Echocardiography Committee for Physician Training in Echocardiography. J Am Soc Echocardiogr 1992;5:187–194. 3. Popp R, Agatston A, Armstrong W, et al: Recommendations for training and

performance and interpretation of stress echocardiography. J Am Soc Echocardiogr 1998;11:95–96. 4. Kisslo J, Byrd BF III, Geiser EA, et al: Recommendations for continuous quality

improvement in echocardiography. J Am Soc Echocardiogr 1995;8:S1–S28.

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5. Cheitlin MD, Alpert JS, Armstrong WF, et al: ACC/AHA guidelines for the clinical

application of echocardiography. Circulation 1997;95:1686–1744. 6. ICAEL Essentials and Standards for Adult Transthoracic Echocardiography Testing,

Parts I–IV. Intersocietal Commission for Accreditation of Echocardiography Laboratories, 8840 Stanford Boulevard, Suite 4900, Columbia, Maryland 21045.

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947

Chapter 44 - The Digital Echocardiography Laboratory Douglas S. Segar MD

Although not new, the concept of the digital echocardiography laboratory is rapidly expanding and evolving. Some laboratories have embraced the digital echocardiography laboratory in part or in total for more than a decade.[1] [2] [3] It is only within the past few years, however, that a digital echocardiography laboratory has become a practical and embraceable reality for the majority of laboratories. The concept encompasses a single echocardiography used as a reading station to a far-reaching network with potentially worldwide accessibility. The major impetus for the digital echocardiography laboratory was the advent of stress echocardiography. It was under that modality that the first images were digitized and the advantages of a digital approach realized. The pioneer of digital echocardiography, Dr. Harvey Feigenbaum, has been quoted as saying that it was only digital echocardiographic systems that allowed stress echocardiography to become a clinical and not just a research tool.[4] [5] [6] [7] Understanding the digital echocardiography laboratory requires a basic understanding of computer networking vocabulary and principles. A glossary of terms is provided for assistance (Table 44-1) . The basic

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premise of a digital echocardiography laboratory is that the information is acquired, processed, interpreted, and stored in a digital modality. All echocardiographs convert the ultrasound information into a digital format at some point in the imaging chain. Traditionally, the output has been converted into an analog signal for display and storage (videotape). A digital approach avoids at least part of the analog step by recording and storing the image in a digital file format. Newer instrumentation allows for recording of the actual digital image rather than the older method of digitizing (through a frame grabber) the analog video output. The advantages of digital versus digitized output have been described. For research purposes, a true digital output may have significant utility for the analysis of color Doppler signals[8] [9] [10] and multicenter trials.[11]

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Setting Up the Digital Echocardiography Laboratory One of the most difficult problems in establishing a digital echocardiography laboratory is the initial design and implementation of the digital echocardiography networking and hardware components. It is important early on in the process that the various personnel (equipment manufacturer, computer support, hardware engineer, software applications, and information systems) involved be included in the design process so that areas of overlap can be avoided and communication enhanced.[12] [13] [14] [15] Of paramount importance early on in the process is determining who is responsible for the various components of the laboratory. This requires that the network, echocardiography, and information system directors determine who is going to service and be responsible for questions on each component on the digital echocardiography laboratory. One of the primary determinants of the scope of the digital laboratory is the volume of studies being performed and the number of echocardiographs and users that will be involved. Determining a digital laboratory solution requires knowing how many machines will be involved, the type of machine, the digital output of each machine, and how the digital output will be interfaced with the computer interpretation and recording systems. One must determine whether the users will be all within one network system or whether there will be both internal and external users. Obviously, the complexity of stringing fiberoptic cable or Ethernet line is quite different if one is dealing with one machine and one computer on one floor versus trying to interface numerous points of service on different floors, different buildings, or even different cities. The location of the echocardiographs and the location of reading stations for sonographers as well as for interpreting physicians will need to be determined at the outset. It 948

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TABLE 44-1 -- Terms Used in Digital Echocardiography Term access

access time

analog

A/D Converter

ATM

bandwidth

baud (rate)

bit

Definition To send or retrieve data from a disc drive or from another computer. Usually refers to discs and network entry. The amount of time that elapses between a request and a response. An example is the time between when one requests data from a disc drive and when it appears on the monitor's display. Continuous signals; data presented or collected in continuous form. These data are shown on an instrument that can change constantly. For example, speedometers or thermometers are analog devices. Analog signals can represent many different realworld things, such as video, audio (voice, music), and physiologic waveforms (electrocardiogram, heartsounds, respiration). A device that converts an analog signal into a digital signal. Complex waveforms are converted into simple strings of numbers. Acronym for "Asynchronous Transfer Mode," an emerging technology for high-speed networking, with transmission capacity ranging from 1.544 Mbps (T1) to 2 Gbps (SONET OC 48), but typically in the 150 Mbps range (OC-3c). 1. The difference in Hertz (Hz) between the highest and lowest frequencies of a transmission channel. 2. The amount of data that can be sent through a given communications circuit per second, usually expressed in Kbps or Mbps. A unit of data transmission equal to the number of discrete conditions per second. In a system of binary states, represents the number of bits per second. The unit of information; the amount of information obtained by asking a yes-or-no question; a computational quantity that can take on one of two

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broadband

bridge

byte (B)

CD-R

CD-ROM

client/server

clinical data compression

compression

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values, such as true and false or 0 and 1; the smallest unit of storage sufficient to hold 1 bit. Loosely defined physical medium specification for analog signals for multiple data channels (video, audio). A device and software that links similar-to-similar network environments (e.g., Ethernet and Token Ring). LAN bridges are used to create a single logical LAN from multiple physical ones, including remote LANs. A bridge typically separates at the upper half of the data link layer. One of the bridge standards is IEEE 802.1 A component in the machine; now most often 8 bits. A byte typically holds one character or for the Primer discussions, one pixel. Acronym for "Compact Disc-Recordable." This form of CD media allows user-defined data to be recorded onto the disc. It is different from audio CDs and other forms of CD-ROMs, which are typically massproduced from a master disc. Acronym for "Compact Disc-Read Only Memory." The digital information on the disc is created by mass production pressing techniques. A client sends requests to a server, according to some protocol, asking for information or action, and the server responds. There may be either one centralized server or several distributed ones. This model allows clients and servers to be placed independently on nodes in a network, possibly on different hardware and operating systems appropriate to their function. All data with clinical content; includes images, waveforms, measurements, findings, and reports. A general description for a family of mathematical techniques that can reduce the amount of data and therefore improve digital storage efficiency and retrieval rates. A description for the amount of reduction in the

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factor/compression amount of data from the original, expressed as a ratio. ratio Conformance A document provided by manufacturers of DICOMStatement compatible equipment that identifies the subset(s) of the DICOM standards that individual products actually support. database A collection of related information about a subject, arranged in a useful manner. The information in a database provides a base for understanding information, drawing conclusions, and making decisions. DICOM Acronym for "Digital Imaging and Communications in Medicine." A communications standard for the exchange of medical information developed by the National Electrical Manufacturers Association and the American College of Radiology. DICOMDIR A file reserved to store DICOM file information stored on the same media where the file resides. digital image An image that has been discretized both in the spatial coordinates and in brightness. dpi Acronym for "Dots Per Inch." A measure of resolution for printers, scanners, and displays. DVD Acronym for "Digital Video Disc." Ethernet The term used to refer to several different physical types of computer networks. Different types of wire and speeds are available under the term Ethernet. Refer to the IEEE 802.3/ISO8802.3 standards. file set A collection of files that share a common naming spacing, where File ID(s) are unique within the file set. DICOM File sets must contain a single file with the File ID of DICOMDIR. DICOMDIR contains information on the other files contained in the DICOM file set. File Set Creator A system that can produce DICOM media under a (FSC) specific Application Profile as described in the system's Conformance Statement.

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File Set Reader (FSR) File Set Updater (FSU) Gbps

GByte gray scale resolution HIS HL7

hub

Hz icon interchange

internet IP

ISO

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A system that can read DICOM media under a specific Application Profile as described in the system's Conformance Statement. A system that can add information to a DICOM media under a specific Application Profile as described in the system's Conformance Statement. Abbreviation for "Gigabits per Second." A measurement of the data transfer capacity of a system. Gigabit stands for 1 billion bits. Abbreviation for "GigaByte." Gigabyte stands for 1 billion bytes. Sometimes called gray scale. The resolution of image brightness expressed by the number of bits used to represent the light intensity of a pixel. Acronym for "Hospital Information System." Acronym for "Health Level 7," a common protocol for communicating with hospital and radiologic information systems. A device that connects several nodes to a network. Hubs are used in conjunction with routers to produce subnetworks. Abbreviation for "Hertz," a unit of frequency equal to one occurrence per second. A small picture intended to represent something (a file, directory, or action) in a graphic user interface. Generally refers to the exchange of diagnostic imaging studies between institutions. Sometimes it is also used in the context of exchange within an institution. Any set of networks interconnected with routers. The Internet is the biggest example of an internet. Acronym for "Internet Protocol." The network layer for the TCP/IP protocol suite widely used on Ethernet networks. A prefix for "International Organization for Standardization."

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ISDN

Acronym for "Integrated Services Digital Network," a twin 64 Kbps digital phone line for high speed data communication at a lower cost than a T1 line. Widely available in Europe and gaining popularity in the United States. JPEG Acronym for "Joint Photographic Experts Group." JPEG-DCT Acronym for "Joint Photographic Experts Group – Discrete Cosine Transform." It is the lossy compression algorithm used to store echocardiograms in DICOM. jukebox A storage device that contains an automatic media changer. When a computer asks for data not stored on the loaded media, the jukebox automatically loads the correct media. Kbps Abbreviation for "Kilobits per Second." A measurement of the data transfer capacity of a system. Kilobit stands for 1000 bits. LAN Acronym for "Local Area Network." lossless A category of digital image compression types that compression possess the following characteristics: (1) The original digital images can be exactly (bit for bit) reproduced as originally acquired. (2) It does not affect postdecompression digital image processing. (3) It can achieve only relatively low levels of data reduction. lossy compression A category of digital image compression types that possess the following characteristics: (1) The original digital images cannot be exactly reproduced as originally acquired, but the changes may not be visually apparent. (2) The compression algorithms can introduce artifacts into the images and affect postdecompression digital image processing. (3) The prevalence of artifacts increases as the amount of compression increases or as the image detail content increases. (4) Much higher degrees of compression are possible than with lossless compression. MB Abbreviation for "MegaByte." MegaByte stands for 1 million bytes of information.

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Mbps

Mbytes/sec

Media

network

node

optical disc pixel POTS RAID

repeater

router

spatial resolution

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Abbreviation for "Megabits per Second." A measurement of the data transfer capacity of a system. Megabit stands for 1 million bits. Abbreviation for "MegaBytes per Second." A measurement of the data transfer capacity of a system. MegaByte stands for 1 million bytes. Used in DICOM to describe any one of the physical data storage devices approved in the DICOM standard in part 12. The currently approved media are 120 mm CD-R, 90 mm magneto-optical disc, 130 mm 650 MB magneto-optical disc, 130 mm 1.2 GB magneto-optical disc, 1.44 MB discette. Application profiles define which specific media is required for interchange. The connection between two or more computers to create a communications and data exchange system. See LAN and WAN. A connection for a device to be attached to the network. Nodes could also refer to the number of computer systems on the network. A group of media products that use a magneto-optical media for storage of information. The elements of a digital image array. The smallest element a monitor can display. Acronym for "Plain Old Telephone System." Acronym for "Redundant Array of Inexpensive Discs," any of six arrangements of conventional disc drives to increase speed and/or reliability. A device that repeats the signal or bit by bit from one physical segment to the next. Used to effectively extend the distance covered by the LAN. Links multiple networks. It selects the best path for data between networks based on link speed and number of hops (from one network into the next one). Sometimes called resolution. The resolution of image in the horizontal and vertical directions, expressed by the number of pixels used to make up the image.

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TCP

The most common transport layer protocol used on Ethernet and the Internet. It was developed by U.S. Department of Defense. TCP is built on top of Internet Protocol (IP) and is nearly always seen in the combination TCP/IP (TCP over IP). TCP/IP Acronym for "Transmission Control Protocol over Internet Protocol." The de facto standard Ethernet protocols. TCP/IP was developed by US Department of Defense for internetworking, encompassing both network layer and transport layer protocols. While TCP and IP specify two protocols at specific layers, TCP/IP is often used to refer to the entire protocol suite. temporal The resolution of images in time, expressed by the resolution number of images per second. T-1 A specialized digital phone line with a maximum speed of 1.544 Mbps. ThickNet Ethernet see 10Base5 ThinNet Ethernet see 10Base2 UID Acronym for "Unique Identifier." Used throughout DICOM to identify information uniquely throughout the world. It uses the structure defined by ISO 8824 for OSI Object Identifiers. WAN Acronym for "Wide Area Network." 10Base5 A term referring to Ethernet using a thick coaxial cable ("yellow cable"), maximum length 500 m, maximum 100 nodes per segment. The "10" means 10 Mbps, "base" means "baseband" as opposed to RF and "5" means a maximum single cable length of 500 m. Also called ThickNet Ethernet. 10Base2 A term referring to Ethernet using RG-58 cable or similar, maximum length 185 m, maximum 30 nodes per segment. If BNC connectors are used, T-connector must be on interface card. The "10" means 10 Mbps, "base" means "baseband" as opposed to RF, and "2" means a maximum single cable length of 200 m. Also called ThinNet Ethernet.

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10BaseT

A term referring to Ethernet using twisted-pair cable, maximum length 100 m; hubs are required to connect nodes. Also called Twisted-Pair Ethernet. Modified from Leong D, Adams DB. In Kennedy TE, Nissen SE, Simon R, et al (eds): Digital Cardiac Imaging in the 21st Century: A Primer. Bethesda, MD, American College of Cardiology, 1997, pp 224–231.

is important to keep in mind the anticipated growth of an echocardiography service so that one leaves room for expansion. In some cases, it may be more cost-effective to place network ports into potential echocardiography examination rooms initially, rather than adding on in the future. Careful consultation with contractors is necessary to determine whether existing wiring can be used or new wiring will need to be strung. If one is using existing wiring, it is extremely important that the added traffic required for a digital echocardiography system will not exceed the available bandwidth in existing cabling. In some circ*mstances, it may be worth the extra cost to string dedicated lines serving only the echocardiography computer network to avoid sharing bandwidth with hospital or office systems. In all aspects of the decision making process, one must trade off concerns of capital with concerns of speed and accessibility. As briefly mentioned earlier, one also needs to determine who will be responsible for the maintenance of all the systems, including wiring, routers, nodes, servers, storage devices, computers, and software. When determining the structure of the network system, leaving room for expansion is clearly important. Keep in mind that computer systems typically outdate themselves within a relatively short period of time and when one is buying a network one is buying essentially only a few years worth of service. Additional options to consider would be remote interpretation of echocardiographic studies via Internet access, modem, cable modem, or even satellite transmission. Block diagrams representing two different digital laboratory solutions are displayed in Figure 44-1 and Figure 44-2 . The first figure demonstrates a digital laboratory solution in an office practice between two different floors. This system has the advantage of using the same echograph and digital output in all systems. In this example, all wiring, servers, switches,

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and nodes are dedicated to the echocardiographic system, requiring no sharing of resources. The advantages of this solution are an increase in speed, a decrease in access time, and the avoidance of traffic-related issues. Relatively speaking, this type of solution is perhaps more expensive to implement, with the trade-off being the advantages just listed. The system represented in Figure 44-2 is a more extensive approach using existing connections between multiple hospitals and points of service. In this particular system, network access is shared by existing lines, although there are dedicated servers and reading stations for the echocardiography laboratory. Stringing fiberoptic cable between different hospitals solely for the purpose of an echocardiography laboratory is in most circ*mstances cost-prohibitive. This particular system is a hybrid. Although bandwidth is shared, access time is kept to a minimum by the use of dedicated servers, storage devices, and reading stations for echocardiography. Another potential advantage of this system is that the computer and network access can be used for nonechocardiography laboratory applications, improving multitasking of each computer unit. Numerous other set-ups and variations are possible. One is limited only by the scope of the problem and the resources and finances available.

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DICOM DICOM (Digital Imaging and Communications in Medicine) is a formatting standard constructed by the National Electrical Manufacturers Association (NEMA). [16] [17] [18] The most recent version (3.0) incorporates a wide variety of image types, including ultrasonograms. The DICOM document encompasses 12 parts, each of which can be updated without updating the entire document. DICOM specifies a hierarchical organization standard that should allow for communication between different systems. When utilizing an echograph that can export a study in a DICOMcompatible format, a digital echocardiogram reader should be able to view the demographic information, individual images, and loops and have access to regional and pixel calibrations. A manufacturer may elect to adhere to all or part of the DICOM standard. This is documented in the DICOM conformance statement. When evaluating a digital echocardiography laboratory system as well as echograph, it is important that the degree of adherence to the DICOM standard be defined. For example, an echograph manufacturer may elect not to put all of the calibration information into the digital download, making it impossible to read calibrations.

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Acquisition of Signal Output Digital versus Digitized One of the earliest steps in the digital laboratory process is acquiring the signal output from the echograph. The majority of contemporary machines have the option 951

Figure 44-1 Depiction of the layout for a digital echocardiography laboratory using a separate series of network connections—an intranet. Abbreviations and terms are given in Table 44-1 . The intranet is wired between two separate floors within one building. A centralized server and optical jukebox is used, with switches on each floor. There is highspeed connectivity between switches and server. The physician reading stations are served by 400 megabit lines. The inset box in the upper left is a separate office that operates in a similar fashion but is not linked to the other floors.

952

Figure 44-2 Depiction of the layout for a digital echocardiography laboratory network between four different institutions that are physically separate by several blocks. The systems do not use one vendor (as shown in Figure 44-1 ) but allow for the connectivity of several different types of echographs and computer workstations. The systems use a fiberoptic backbone provided by the University; therefore, bandwidth is shared with other applications. The connections between each local institution and the backbone involve a dedicated 10 Mbps switch. All images are stored on one 200 GB RAID array. This arrangement is a hybrid, with components of dedicated and shared resources.

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of a true digital output via a network card, Ethernet card, or some other modality. Older machines will have only an analog signal output, which then must be digitized via a frame grabber system. Once the image has been placed in a digital format, either digital or digitized, the remainder of the process remains essentially the same. The advantages of a true digital signal have been reported. With time, it is anticipated that the echographs requiring digitizing will be phased out, allowing implementation of a true digital signal and all the benefits inherent to it. For systems that do require digitization, several additional steps must be considered. The entire analog signal cannot be concisely digitized, so compromises must be made. These compromises include the length of time that is digitized, the interval between each digitized segment or frame, and the length of time encoded. The playback speed of the digitized signal must be determined. In the early days of echocardiography, it was customary to use an eightframe loop, which was formed by creating frames in increments of 50 to 67 msec. This interval was shown to be reasonable for two-dimensional recordings. When diastolic features needed to be emphasized, it was necessary to either increase the digital interval to 83 to 100 msec or to add a built-in start delay of 30 to 50 msec after the initial R wave before the digital triggering process was begun. It was customary to trigger on the R wave, as it was an easily recognizable signal from the echograph. The original eight-frame loop was chosen mostly out of necessity because of limited memory. As the field progressed, memory became less of an issue and cycle lengths of any dimension could be included. With the advent of a true digital output, it became apparent that one was limited more by memory available in the system than by any other determinant. Typically, 953

one can elect to acquire a digital image stream beginning at the R wave from the electrocardiographic signal, or one can determine to acquire a signal based solely on a length of time one wishes to review. The advantage of triggering from the R wave is that the cardiac cycle has an easily recognized start point and end point. One may elect to trigger off the R wave and acquire one, three, five, or even 10 continuous cycles for review. In practice, this tends to be a more effective solution than simply grabbing

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a preset length of time with cardiac cycles. With use of the latter scheme, the image may begin somewhere in systole or diastole and tends to be disorienting, unless the image can be trimmed to a recognizable start point. The latter approach has the advantage in cases with significant arrhythmias or artifactual electrocardiographic signals that may cause problems in R wave triggering. Loop versus Streaming One of the advantages of a digital system is the ability to determine whether one is going to replay a loop of cardiac cycles in an endless fashion or whether one wants to instead try to do a form of digital streaming. The advantage of a loop is that it allows endless access to the same view, providing for meticulous attention and interpretation. Digital streaming is more of a real-time interpretation modality. It is beyond the resources of most systems to allow a typical 20-minute examination to be entirely encoded in a digital format and stored without using immense amounts of memory. One of the goals of a digital echocardiography system is not to simply replace videotape with digital and have the examiner try to fast-forward through a digital file as one would fast-forward through a videotape. Streaming may have more applicability to teleconferencing or remote telemedicine than it does for a routine application in a digital echocardiography laboratory. Exceptions are obviously possible. One may elect to stream a limited subset of information into an acquisition and storage system. Intertwined into all discussions of acquisition, display, storage, and transmission of images is the complexity of computer memory. Increasing image resolution, shades of color, and rate of digitization all increase the size of a file and the memory required to store that file. The more memory that is required, the more difficult it is to store and transmit the image. Therefore, a compromise must always be inherent in any digital echocardiography laboratory between the amount of information that one wishes to acquire and the ability of one to deal with that information in an effective fashion. Although a 512 × 512 pixel display may be a "standard," a 256 × 256 display essentially carries the same information with very little, if any, loss in resolution. The actual resolution of the signal exiting the echograph has a typical resolution of 256 × 256; thus, there is little to be gained by increasing the display resolution or the exported signal resolution in most circ*mstances. The advantages of some existing systems are in the

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Sonographer Training A digital acquisition approach is believed to place more of a burden on the sonographer. The sonographer must decide whether to digitally acquire an image and if the acquired image is representative and of diagnostic quality. Rather than taping 10 to 20 minutes of a study, the study is represented by a series of 10 to 30 loops or frames of images. This requires that the sonographer actively review each image and determine whether to save or delete it from the image set. The mechanics of digital acquisition are quickly learned. This process may be facilitated by visiting an established laboratory or by training with an applications specialist. Initially, this process will lengthen the echocardiography examination until the sonographer becomes comfortable with the process. Once the initial training is completed, sonographers will find that the digital approach improves the quality of the study by ensuring that the information needed is displayed. Arguments have been made that if the sonographer does not recognize an abnormality, he or she will not acquire the proper view. The same argument could be made of videotape (the sonographer would not have pushed the record button). Guidelines are being formulated by the American Society of Echocardiography that will suggest a set of "standard" views that should be obtained on all patients. The purpose of the guidelines is to avoid the problem that could potentially arise from not acquiring enough information during a digital examination. During the implementation of a digital examination, close collaboration between the sonographer and echocardiographer is essential. One of the advantages of the digital laboratory is the facility for careful review of selected images so that questions can be addressed. One can quickly review a study to determine whether additional images or Doppler is needed.

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Storage Devices The field of computer memory storage is always in evolution. In the early days of digital echocardiography, studies were stored on 5¼-inch floppy discs. Within a few years, 3½-inch discs became standard, with a small increase in memory. More recently, the field has evolved to include optical discs, compact discs, digital tape, and a RAID array. The newer devices all share common features of being able to store massive amounts of digital data in a format that allows for relatively fast accessibility and retrieval. Intertwined with the access time of the storage devices are the ever-present issues of networking traffic, server traffic, and available bandwidth. When one is choosing a long-term storage device, all of these factors must be kept in mind and discussed with an information system specialist. Currently, the most common options include a CD jukebox, RAID array, DVD jukebox, or MOD system. Long-term Data Archiving and Back-up Keeping medical records for 7 years appears to be the norm at most institutions. Obviously, a massive disc failure, 954

fire, or other natural disaster could potentially destroy thousands if not hundreds of thousands of patients' data quickly. It is recommended that all information be backed up and stored at a separate site. A back-up system need not have the rapid accessibility, flexibility, or portability of the primary system. Storage of back-up information should be in a separate site, fireproof safe, or similar location. One of the advantages of the digital echocardiography laboratory is that information can be copied, and each copy remains the exact duplicate of the primary source. This clearly separates the digital modality from videotape,

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Display Many options exist for the monitor display of the digital echocardiographic image. The majority of current systems use a series of thumbnail images, which may be either static or dynamic (Fig. 44-3) . By placing the mouse cursor over the thumbnail image and clicking, the examiner can get an enlarged view, which allows for interpretation (Fig. 44-4) . The number of views arranged on the screen is usually a user-definable option. For example, when comparing serial studies, one may elect to compare two or four views at once. In other cases, one may choose the same screen size for only one view, allowing for increased image size. Offline measurements would typically be performed on a full-screen image to maximize accuracy. Other examples of multiple views playing simultaneously would be for stress echocardiography, in which case such a display is essential. How the information is displayed is a software-definable option within the parameters of the monitor hardware. As such, the user should have the choice in determining which set-up is most effective.

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Interpretation of the Digital Echocardiographic Image One of the key questions in the interpretation of a digital echocardiographic image is whether such interpretation is comparable to interpretation that would be made from the same images recorded on videotape. This question has been addressed and answered in several studies. Several authors have reported their results comparing videotape to digital interpretation of echocardiograms using a variety of different digital techniques. The majority of the digital techniques have compared different forms of compression algorithm (JPEG, MPEG) or lossless compression. Digital interpretation of images was supported by Segar et al,[19] in whose study 110 echocardiographic examinations were recorded simultaneously on videotape and with a commercially available digitized frame grabber. Studies were stored using a lossless compression algorithm. In this study, exact agreement of interpretation between the videotape and digital image was found for 83% of patients. A major discrepancy in the interpretation was found in only 2% and a minor discrepancy in 15%. Most discrepancies occurred in the setting of valvular heart disease. When compared with a consensus interpretation, there were an equal number of errors between the digital and the videotape interpretation. Interestingly, in this study, it was shown that there were findings noted in the digital interpretation that were not found in the videotape. When reviewed, the videotape revealed in each case that the finding was present but had been overlooked in the initial interpretation. This was believed to reflect the thought that during interpretation of a videotape one may be subjected to information overload. The cine loop format of a digital recording allows for repeated visual exposure to an image. This potentially allows for increased recognition of abnormalities. Similar results were reported by Mobarek et al.[20] Among 1156 parameters or measurements assessed, there was a 99% concordance rate for normal versus abnormal. Karson et al[21] [22] reported that JPEG compression of up to 20:1 is possible

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without any interpretation errors being introduced by the compression algorithm. Although JPEG does result in some loss of information, image quality is not adversely affected unless very high ratios are used. JPEG ratios of 20:1 are similar to s-VHS images. Ratios of 40:1 have been used for M-mode or spectral Doppler, and 65:1 for color images.[10] [21] [22] MPEG compression has also been used. It was designed for moving images and clearly is necessary for any live transmission or telemedicine type applications. It currently is not supported by the DICOM 3.0 standards.[23] [24] [25] Spencer et al[25] reported that compression ratios of up to 200:1 demonstrated no degradation in endocardial visualization quality or diagnostic content. Compression to this degree can markedly decrease the size of image files. The advantages of compression algorithms have been well documented. By allowing compression, one is able to allow the digital echocardiographic information to be condensed into a format that allows for easier storage, transmission, and access. Essentially one is allowing for the information to be stored in a fraction of the space that would be needed had it not been compressed. Advantages of a digital approach include access to old studies, not just to the old reports. In the past, it was commonplace to compare a current study to an old report. The virtue of the digital approach is that it allows the actual old images to be compared to the new images in a side-by-side fashion. Measurements can be repeated and the interpretation can be checked and rechecked. The digital approach also allows for easy review by clinicians, house staff, medical students, and echocardiographers. It is no longer necessary for a videotape to be pulled out of an echograph, rewound to the correct study, and then shown. Such accessibility increases the utility of echocardiography for patient care. Interpretation of digital echocardiograms from a physician's standpoint appears to be rather straightforward. One new feature of a digital echocardiographic study is that the physician has the option and in fact the requirement to check and remeasure the images and Doppler information. This capability has been difficult to implement in the past with a videotape system. It not only 955

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Figure 44-3 Still frame image from a commercially available software program used for digital echocardiography. Depicted at the bottom is a series of thumbnail images representing a series of quad-screen loops and still frame Doppler images. The demographic information for the patient is shown on the left, and the upper portion contains the toolbar commands.

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Figure 44-4 Depiction of how thumbnail images can be clicked on with a mouse cursor, bringing up a quad-screen display. The thumbnail images of the remaining views are displayed to the left.

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requires that the physician be able to perform the measurements but also allows for an excellent method of feedback to the sonographer. It enhances communication between the physician and sonographer. DICOM allows for image calibration information to be stored in an appropriate file format, which can be read by a majority of DICOM readers. This allows for measurement packages to incorporate the calibration information so that accurate measurements can be made. Other advantages of a digital approach include the ability to perform stat interpretations for echocardiograms obtained in the operating, intensive care unit, emergency room, clinic, or outreach center. The ability to interpret these images may exist at home if there is a connection between the echocardiography network and the physician's home computer. With the advent of satellite and cable modem capabilities, these connections should be more prevalent. Not all digital echocardiography laboratories rely solely on the digital image. For stress echocardiography, arguments exist that a digital interpretation may not be as good as a combined digital and videotape review.[26] Other investigators have reported the reproducibility in interpretation with digital stress echocardiographs to be quite good.[27]

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Reporting of Information Once a digital echocardiographic study is interpreted, the digital report can be placed on the hospital information system platform, printed out, faxed, or even e-mailed to physicians' offices. As in any computer-based information system, adequate security and passwording is essential. Different encryption algorithms have been developed to protect patient confidentiality and the security of the medical information. Systems exist for Internet browser access to patient reports. In the future, it is anticipated that both reports and image clips will be readily available on the Web.

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Changes in Practice Patterns One of the common limitations of the traditional videotape-driven echocardiography laboratory was the problem of the videotape always residing within the echocardiographic instrument. This commonly resulted in a number of current studies on one tape, which could not be interpreted until late in the day after all the patients were seen. For the physician, this meant that results were not available on the same day that the study was performed. For the echocardiographer, this meant late nights in the echocardiography laboratory interpreting studies. Clinicians, surgeons, and other medical personnel would not have easy access to the echocardiographic images, resulting in clinical decision making from dictated reports or, all too commonly, from sonographer interpretations. The ability of an echocardiographer to almost instantly interpret a digital study allows the patient to leave the echocardiography laboratory with a completed and final report. Not only can patients know the result of their study, their treating physician can have a timely, completed report in hand. The physician may also have unlimited access to the echocardiographic study through any reading station. Reading stations may be located not only in the echocardiography laboratory, but also in the cardiac catheterization laboratory, the critical care unit, the intensive care unit, the operating room, and outpatient offices. With a digital echocardiography laboratory, rapid interpretation of echocardiograms is limited only by the availability of the echocardiographer, not by the logistical limitations of the laboratory. In large practices with dedicated echocardiographers, it may be reasonable to assign an echocardiographer to the laboratory throughout the day so that studies can be interpreted as they are completed. This would also allow the echocardiographer to review every study, ensuring that all necessary information and views are obtained before the patient leaves the laboratory.

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Remote interpretation of echocardiograms from sites physically removed from the echocardiography laboratory may become routine. Use of a digital approach in the operating room has been described and compared to more traditional formats.[28] Telemedicine applications have been reported for pediatrics[29] and for interpretation of echocardiograms[30] [31] and dobutamine stress echocardiograms from the emergency room.[32] For example, at Indiana University it is routine for a physician to be asked to interpret a study from the VA hospital or Krannert Institute of Cardiology on an urgent basis. This can be easily accomplished from one's office computer, since all echocardiograms performed on campus are accessible from one network. As the field of telemedicine grows, it is anticipated that remote interpretation of studies from different states or outer space will become common.[33] The digital echocardiography laboratory is no longer a concept, it is a reality. There is sufficient experience to justify the implementation of a digital echocardiography laboratory in every functioning laboratory today.

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The Practice of Clinical Echocardiography - PDF Free Download (2024)