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Dynamic Echocardiography combines textbook, case-based, and multimedia approaches to cover the latest advances in this rapidly evolving specialty. The experts at the American Society of Echocardiography (ASE) present new developments in 3D echocardiography, aortic and mitral valve disease, interventional and intraoperative echocardiography, new technologies, and more. You’ll have everything you need to apply the latest techniques in echocardiography and get the best results…in print and online at www.expertconsult.com.

  • Stay current on aortic and mitral valve disease, prosthetic heart valve disease, interventional and intraoperative echocardiography, transesophageal echocardiography, CAD, complications of MI, pericardial disease and intracardiac masses, myocardial diseases, heart failure filling pressures, CRT, CHD, and new technologies.
  • Understand the advantages of 3D echocardiography and see how to effectively use this novel technique.
  • Appreciate the visual nuances and details of echocardiography thanks to beautiful, full-color illustrations.
  • Tap into the expertise of authorities from the American Society of Echocardiography.

Subjects

Books
Savoirs
Medicine
Médecine
Cardiac dysrhythmia
Microbubbles
Atrial fibrillation
Myocardial infarction
Hand
Transesophageal echocardiography
Surgical suture
Computed tomography angiography
Myocardial perfusion imaging
Takotsubo cardiomyopathy
Mitral valve replacement
Doppler echocardiography
Pericardiectomy
Pulmonary valve stenosis
Restrictive cardiomyopathy
Magnetic resonance angiography
Dobutamine
Valvular heart disease
Artificial heart valve
Carcinoid
Dysplasia
Revascularization
Exercise intolerance
Global Assessment of Functioning
Guideline
Cardiogenic shock
Blood culture
Neoplasm
Left ventricular hypertrophy
Aortic valve replacement
Coarctation of the aorta
Myxoma
Hypereosinophilic syndrome
Mitral regurgitation
Ventricular septal defect
Congenital heart defect
Allotransplantation
Bicuspid aortic valve
Pericarditis
Pulmonary hypertension
Atrial septal defect
Aortic insufficiency
Mitral stenosis
Stroke
Constrictive pericarditis
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Infarction
Asymptomatic
Coronary catheterization
Patent ductus arteriosus
Infective endocarditis
Chest pain
Mitral valve prolapse
Amyloidosis
Review
Cardiovascular disease
Ischemia
Vasodilation
Myocarditis
Angiography
Device
Echocardiography
Lesion
Scallop
Hemodynamics
Aortic dissection
Cardiac tamponade
Heart failure
Heart murmur
Mitral valve
Alcohol abuse
Pulmonary embolism
Dyspnea
Coronary artery bypass surgery
Aortic valve stenosis
Rare disease
Physical exercise
Embolism
Jet aircraft
Coronary circulation
Artifact
Tissue (biology)
Atherosclerosis
Artificial pacemaker
Sodium chloride
Hypertension
Electrocardiography
Prosthesis
Angina pectoris
Ischaemic heart disease
X-ray computed tomography
Cardiomyopathy
Mechanics
Magnetic resonance imaging
Endocarditis
Chagas disease
Aorta
Acoustics
Abscess
Stress
Cardiology
Palpitation
Perfusion
Testing
Viewpoint
Systole
Fenfluramine
Ablation
Diastole
Torsion
Évaluation
Syncope
Strontium
Copyright

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EAN13 9781455710034
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Dynamic Echocardiography
Roberto M. Lang, MD, FASE, FACC, FAHA, FESC, FRCP
Professor of Medicine, President, American Society of
Echocardiography, Director, Noninvasive Cardiac Imaging
Laboratories, University of Chicago Medical Center, Chicago,
Illinois
Steven A. Goldstein, MD, FACC
Director, Noninvasive Cardiology Lab, Washington Hospital
Center, Washington, District of Columbia
Itzhak Kronzon, MD, FASE, FACC, FAHA, FESC, FACP
Professor of Medicine, Director, Non Invasive Cardiology,
New York University Medical Center, New York, New York
Bijoy K. Khandheria, MD, FASE, FACC, FESC, FACP
Director, Echocardiography Services, Aurora Health Care,
Aurora Medical Group, Aurora/St. Luke Medical Center,
Aurora/Sinai Medical Center, Milwaukee, Wisconsin
S a u n d e r sFront Matter
Dynamic Echocardiography
Roberto M. Lang, MD, FASE, FACC, FAHA, FESC, FRCP Professor of Medicine
President, American Society of Echocardiography Director, Noninvasive
Cardiac Imaging Laboratories University of Chicago Medical Center
Chicago, Illinois
Steven A. Goldstein, MD, FACC Director, Noninvasive Cardiology Lab
Washington Hospital Center Washington, District of Columbia
Itzhak Kronzon, MD, FASE, FACC, FAHA, FESC, FACP Professor of Medicine
Director, Non Invasive Cardiology New York University Medical Center New
York, New York
Bijoy K. Khandheria, MD, FASE, FACC, FESC, FACP Director,
Echocardiography Services Aurora Health Care, Aurora Medical Group
Aurora/St. Luke Medical Center, Aurora/Sinai Medical Center Milwaukee,
WisconsinCopyright
3251 Riverport Lane
St. Louis, Missouri 63043
Dynamic Echocardiography
ISBN: 978-1-4377-2262-8
Copyright © 2011 by Saunders, an imprint of Elsevier Inc.
No part of this publication may be reproduced or transmitted in any form or
by any means, electronic or mechanical, including photocopying, recording, or
any information storage and retrieval system, without permission in writing from
the publisher. Details on how to seek permission, further information about the
Publisher’s permissions policies and our arrangements with organizations such as
the Copyright Clearance Center and the Copyright Licensing Agency, can be found
at our website: www.elsevier.com/permissions.
This book and the individual contributions contained in it are protected under
copyright by the Publisher (other than as may be noted herein).
Notices
Knowledge and best practice in this 9eld are constantly changing. As new
research and experience broaden our understanding, changes in research
methods, professional practices, or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and
knowledge in evaluating and using any information, methods, compounds, or
experiments described herein. In using such information or methods they should
be mindful of their own safety and the safety of others, including parties for
whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identi9ed, readers are
advised to check the most current information provided (i) on procedures
featured or (ii) by the manufacturer of each product to be administered, to verify
the recommended dose or formula, the method and duration of administration,
and contraindications. It is the responsibility of practitioners, relying on their
own experience and knowledge of their patients, to make diagnoses, to determine
dosages and the best treatment for each individual patient, and to take all
appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the author assumesany liability for any injury and/or damage to persons or property as a matter of
products liability, negligence or otherwise, or from any use or operation of any
methods, products, instructions, or ideas contained in the material herein.
Library of Congress Cataloging-in-Publication Data
Dynamic echocardiography / American Society of Echocardiography ; [edited
by] Roberto M. Lang.—1st ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4377-2262-8 (hardcover : alk. paper)
1. Echocardiography. I. Lang, Roberto M. II. American Society of
Echocardiography.
[DNLM: 1. Cardiovascular Diseases—ultrasonography. 2. Echocardiography—
methods. WG 141.5.E2 D997 2010]
RC683.5.U5D96 2010
616.1′207543—dc22
2010017586
Vice President and Publisher: Linda Belfus
Executive Editor: Natasha Andjelkovic
Editorial Assistant: Bradley McIlwain
Publishing Services Manager: Patricia Tannian
Project Manager: Carrie Stetz
Design Direction: Steven Stave
Printed in the United States of America
Last digit is the print number: 9 8 7 6 5 4 3 2 Preface
For more than a quarter of a century, echocardiography has made unparalleled
contributions to clinical cardiology as a major tool for real-time imaging of cardiac
dynamics. Echocardiography is currently widely used every day in hospitals and
clinics around the world for assessing cardiac function while simultaneously
providing invaluable noninvasive information for the diagnosis of multiple disease
states.
The American Society of Echocardiography (ASE) is an organization of
professionals committed to excellence in cardiovascular ultrasound and its
application to patient care through education, advocacy, research, innovation,
and service to our members and public. ASE’s goal is to be its members’ primary
resource for education, knowledge exchange, and professional development. This
comprehensive textbook on echocardiography constitutes a major step toward the
achievement of this goal.
Dynamic Echocardiography is a comprehensive project several years in the
making. This text and the companion online library of cases together comprise a
state-of-the-art publication on all aspects of clinical echocardiography written by
more than 100 medical experts a) liated with ASE. The book consists of 111
chapters divided into 14 sections: Native Valvular Heart Disease: Aortic
Stenosis/Aortic Regurgitation; Native Valvular Heart Disease: Mitral
Stenosis/Mitral Regurgitation; Prosthetic Heart Valve Disease;
Interventional/Intraoperative Echocardiography; Transesophageal
Echocardiography; Coronary Artery Disease; Mechanical Complications of
Myocardial Infarction; Pericardial Disease and Intracardiac Masses; Myocardial
Diseases; Heart Failure Filling Pressures/Diastology; Cardiac Resynchronization
Therapy; New Technology; Cases From Around the World; and Congenital Heart
Disease. Most sections include a commentary chapter written by a leading
authority summarizing the current knowledge on each topic as well as a chapter
written by a sonographer describing the technical aspects required for optimal
data acquisition and display.
Each of the 111 chapters has a companion online library of didactic slides that
include multiple cases. Once readers have completed review of the written
chapter, we encourage them to review the accompanying slides and case
presentations. This exercise will allow the reader to visualize dynamic9
>
9
9
9
echocardiographic clips of multiple cardiac pathologies. We believe that this
combined approach is the most e ective way of learning clinical
echocardiography. Our hope is that physicians and cardiac sonographers will use
this text and the companion online materials as a reference and self-assessment
tool.
The editors and the authors wish to thank the sonographers with whom we have
had the privilege of working throughout the years. Without their daily pursuit of
quality, hard work, and desire to continuously learn, this project would never have
been completed.
We also especially want to thank each of the section editors: Randolph Martin,
Patricia Pellikka, Fausto Pinto, Mani Vannan, Neil Weissman, Malissa Wood, and
William Zoghbi for their time and expertise in bringing this product to fruition.
We owe a great debt to our ASE sta , who has collaborated with us closely in
every aspect of this project, including Chelsea Flowers, who helped obtain the
required permissions; Hilary Lamb, who assisted us with all aspects of the artwork;
and Anita Hu man and Debra Fincham, who assembled the list of contributors. In
particular, we would like to acknowledge the tireless and invaluable help of
Andrea Van Hoever and Robin Wiegerink, who helped us complete this project in
a timely and e ective manner. We would like to also thank Dr. Harry Rakowski,
who has provided us with practical, positive encouragement and advice.
We also wish to thank our families for their continuous support while we worked
on this project—our wives Lili, Simoy, Ziva, and Priti; our children Daniella,
Gabriel, Lauren, Derek, Iris, Ra , Shira, Vishal, and Trishala; and our
grandchildren Ella, Adam, Lucy, and Eli.
Roberto M. Lang, MD, FASE, Steven Goldstein, MD,
Itzhak Kronzon, MD, FASE, Bijoy Khandheria, MD, FASE
Foreword
It is di cult for contemporary cardiology fellows to imagine a day when
echocardiography was not the focal point for patient diagnosis and management,
but cardiovascular ultrasound is still a relatively young discipline. It has been less
than 60 years since Inge Edler and Helmuth Hertz rst directed a shipyard
re! ectoscope toward their own hearts and noted moving echoes on an oscilloscope
screen, a development that the normally clairvoyant Paul Dudley White termed
“ingenious” but of little clinical value. Even by the 1980s, when two-dimensional
echocardiography and continuous wave Doppler were well established, one of the
factors in! uencing me to choose an echo fellowship over electrophysiology was
that echocardiography was so little regarded clinically that echo fellows were
never called in at night or on the weekends! I recall the day in 1988 when this all
changed for me. I was attending the weekly catheterization laboratory conference
at Massachusetts General Hospital, traditionally a setting for pointing out the
perceived failings of the echo lab. On that fateful day, however, Peter Block,
director of the cath lab, announced that in his mind echo was the gold standard
for quanti cation of aortic stenosis, leading to Ned Weyman nearly falling out of
his chair! Flash forward to 2010. At the Cleveland Clinic, we now do
approximately 100,000 cardiovascular ultrasound studies, more than ve times
the combined total of nuclear, magnetic resonance, and computed tomographic
studies. The echo lab is the hub of decision making in valvular heart disease, adult
and pediatric congenital abnormalities, congestive heart failure, arrhythmia
management, aortic and vascular disease, and cardiac ischemia. And, in a cruel
irony, it is now the echo lab that is far more likely to be called in after hours than
electrophysiology!
As the utility of echocardiography has expanded, the technical and clinical
knowledge base required to apply this technique to its fullest potential has grown
exponentially. Learning the many nuances of echocardiography must be a lifelong
commitment. With this goal in mind, the American Society of Echocardiography
has published Dynamic Echocardiography, a comprehensive text and atlas of
echocardiography. Conceived and executed by editor in chief Roberto Lang,
2009/2010 President of ASE, and senior editors Steven Goldstein, Itzhak Kronzon,
and Bijoy Khandheria, this book provides a comprehensive and practical approach
to the basic principles and clinical application of echocardiography. This really is
two educational products in one. First is an expansive book with more than 100chapters that detail the myriad ways that echocardiography can be used to solve
clinical problems. Complementing this book is the accompanying online library
that provides a wealth of classic examples of the various pathologies likely to be
encountered clinically. Combined, the book and online library provide the perfect
study guide for fellows initially learning echocardiography, those studying for the
echocardiography boards, and practicing cardiologists looking for a refresher and
update to improve their clinical echo skills.
In this era of multimodality imaging, many have predicted the decline of
echocardiography. Those of us who have spent our careers in the eld, however,
have long marveled at the capacity of echo for reinvention, most obviously in its
technical capabilities but even more impressively in its expanded clinical
applications. By publishing Dynamic Echocardiography, the American Society of
Echocardiography continues its commitment to educational excellence. I
commend this resource to you with great enthusiasm.
James D. Thomas, MD, FACC, FAHA, FESC, Cleveland,
OhioContributors
Theodore P. Abraham, MD, FASE, FACC, Director,
Hypertrophic Cardiomyopathy Clinic
Division of Cardiology
Johns Hopkins University
Baltimore, Maryland
Harry Acquatella, MD, FASE, FACC, FAHA, Professor of
Medicine
Universidad Central de Venezuela, Caracas
Department of Echocardiography
Centro Medico de Caracas
Caracas, Venezuela
David Adams, RCS, RDCS, FASE, Cardiac Sonographer
Duke Echocardiography Laboratory
Duke University Hospital
Durham, North Carolina
Deborah A. Agler, RCT, RDCS, FASE, Coordinator of
Education and Training
Cardiovascular Imaging
Cleveland Clinic
Cleveland, Ohio
Josef Aichinger, MD, Senior Cardiologist
Cardiology, Angiology, Intensive Care
Elisabethinen Hospital Linz
Linz, Austria
Bilal Shaukat Ali, MD, Fellow in Advanced Cardiac
Imaging
Division of Cardiology
Brigham and Women’s Hospital
Boston, MassachusettsSamuel J. Asirvatham, MD, FACC, FHRS, Consultant,
Division of Cardiovascular Diseases and Internal
Medicine
Division of Pediatric Cardiology
Professor of Medicine
Mayo Clinic College of Medicine
Vice Chair, Cardiovascular Division—Innovations
Program Director, EP Fellowship Program
Mayo Clinic
Rochester, Minnesota
David S. Bach, MD, FASE, Professor
Department of Internal Medicine, Division of
Cardiovascular Medicine
University of Michigan
Ann Arbor, Michigan
Sripal Bangalore, MD, MHA, Division of Cardiology
Brigham and Women’s Hospital
Harvard Medical School
Boston, Massachusetts
Manish Bansal, MD, DNB, Consultant Cardiologist
Indraprastha Apollo Hospital
New Delhi, India
Helmut Baumgartner, MD, FACC, FESC, Professor of
Cardiology
Adult Congenital and Valvular Heart Disease Center
University Hospital Muenster
Muenster, Germany
Jeroen J. Bax, MD, PhD, Professor of Cardiology
Department of Cardiology
Leiden University Medical Center
Leiden, The Netherlands
S. Michelle Bierig, MPH, RDCS, RDMS, FASE, Manager,
Core Echocardiography Laboratory
St. John’s Mercy Heart and Vascular Hospital
St. Louis, MissouriGabe B. Bleeker, MD, PhD, Department of Cardiology
Leiden University Medical Center
Leiden, The Netherlands
William B. Borden, MD, Assistant Professor of Medicine
Cardiovascular Disease
Weill Cornell Medical College
New York, New York
Darryl J. Burstow, MBBS, FRACP, Senior Staff
Cardiologist
Associate Professor of Medicine
Department of Cardiology
The Prince Charles Hospital
Brisbane, Queensland, Australia
Scipione Carerj, MD, Professor of Cardiology
Department of Medicine and Pharmacology
University of Messina
Messina, Italy
Hari P. Chaliki, MD, FASE, FACC, Assistant Professor of
Medicine
Division of Cardiovascular Diseases
Mayo Clinic
Scottsdale, Arizona
Kwan-Leung Chan, MD, FACC, FRCPC, Professor of
Medicine
Division of Cardiology
University of Ottawa Heart Institute
Ottawa, Ontario, Canada
Sonal Chandra, MD, Advanced Imaging Fellow
Section of Cardiology
University of Chicago
Chicago, Illinois
Krishnaswamy Chandrasekaran, MD, FASE, Professor of
Medicine
Mayo Clinic College of MedicineConsultant, Division of Cardiovascular Diseases
Mayo Clinic
Scottsdale, Arizona
Nithima Chaowalit, MD, Assistant Professor
Division of Cardiology, Department of Medicine
Siriraj Hospital
Mahidol University
Bangkok, Thailand
Farooq A. Chaudhry, MD, FASE, FACC, FAHA, FACP,
Associate Professor of Medicine
Columbia University College of Physicians and Surgeons
Associate Chief of Cardiology
Director of Echocardiography
St. Luke’s Roosevelt Hospital Center
New York, New York
Namsik Chung, MD, PhD, FASE, FAHA, Dean
Yonsei University College of Medicine
Professor of Cardiology
Yonsei University College of Medicine
Seoul, Korea
Patrick D. Coon, RDCS, FASE, Program Director,
Echocardiography
Division of Cardiology, Department of Pediatrics
The Cardiac Center at The Children’s Hospital of
Philadelphia
Philadelphia, Pennsylvania
Ronan J. Curtin, MD, MSc, Consultant Cardiologist
Department of Cardiology
Cork University Hospital
Cork, Ireland
Jeanne M. DeCara, MD, FASE, Associate Professor of
Medicine
University of Chicago Medical Center
Chicago, IllinoisGeneviève Derumeaux, MD, PhD, FESC, Professor of
Physiology
Explorations Fonctionnelles Cardiovasculaires
Lyon University
Lyon, France
Veronica Lea J. Dimaano, MD, Senior Research Fellow
Division of Cardiology
Johns Hopkins University, School of Medicine
Baltimore, Maryland
Jean G. Dumesnil, MD, FACC, FRCPC, Professor of
Medicine
Laval University
Cardiologist, Quebec Heart and Lung Institute,
Laval University
Quebec City, Quebec, Canada
Christian Ebner, MD, Senior Cardiologist
Cardiology, Angiology, Intensive Care
Elisabethinen Hospital Linz
Linz, Austria
Holger Eggebrecht, MD, West-German Heart Center
University Duisburg-Essen
Essen, Germany
Raimund Erbel, MD, FACC, FAHA, FESC, Professor of
Medicine/Cardiology
European Cardiologist
Department of Cardiology
West-German Heart Center
University Duisburg-Essen
Essen, Germany
Rebecca B. Fountain, RN, BSN, Section of Internal
Medicine and Cardiovascular Diseases
Mayo Clinic
Rochester, Minnesota
Andreas Franke, MD, FESC, Medical Clinic IRWTH University Hospital
Aachen, Germany
William K. Freeman, MD, FACC, Associate Professor of
Medicine
Division of Cardiovascular Diseases
Mayo Clinic
Rochester, Minnesota
Mario J. Garcia, MD, FACC, FACP, Chief, Division of
Cardiology
Montefiore Medical Center
Albert Einstein College of Medicine
Bronx, New York
Eulogio García-Fernández, MD, Cardiology Department
Hospital General Universitario “Gregorio Marañón”
Madrid, Spain
Miguel Angel García-Fernandez, MD, PhD, Cardiology
Department
Hospital General Universitario “Gregorio Marañón”
Madrid, Spain
José Antonio García-Robles, MD, Cardiology
Department
Hospital General Universitario “Gregorio Marañón”
Madrid, Spain
Steven A. Goldstein, MD, FACC, Director, Noninvasive
Cardiology Lab
Washington Hospital Center
Washington, District of Columbia
José Luis Zamorano Gomez, MD, PhD, FESC, Professor of
Medicine
Universidad Complutense de Madrid
Director, Cardiovascular Institute
University Clinic San Carlos
Madrid, SpainJosé Juan Gómez de Diego, MD, Cardiology Staff
Laboratorio de Imagen Cardíaca
Hospital Universitario La Paz
Madrid, Spain
Jose Luis Gutierrez-Bernal, MD, Hospital Español
Mexico City, Mexico
Jong-Won Ha, MD, PhD, FESC, Cardiology Division
Professor of Medicine
Yonsei University College of Medicine
Seoul, South Korea
David R. Holmes, Jr., MD, FACC, Consultant,
Cardiovascular Diseases
Professor of Medicine
Mayo Clinic
Rochester, Minnesota
Kenneth Horton, RCS, RCIS, FASE, Echo/Vascular
Research Coordinator
Intermountain Healthcare
Salt Lake City, Utah
Judy W. Hung, MD, FASE, Associate Director,
Echocardiography
Assistant Professor of Medicine
Harvard Medical School
Cardiology Division, Department of Medicine
Massachusetts General Hospital
Boston, Massachusetts
Hiroshi Ito, MD, PhD, Department of Cardiovascular
Medicine
Okayama University
Okayama, Japan
James G. Jollis, MD, FACC, Professor of Medicine and
Radiology
Duke University
Durham, North CarolinaChristine Attenhofer Jost, MD, FESC, Professor of
Cardiology
Cardiovascular Center Zurich
Zurich, Switzerland
Gudrun Kabicher, MD, Senior Cardiologist
Cardiology, Angiology, Intensive Care
Elisabethinen Hospital Linz
Linz, Austria
Sanjiv Kaul, MD, FASE, FACC, Professor and Division
Head, Cardiovascular Medicine
Oregon Health & Sciences University
Portland, Oregon
Bijoy K. Khandheria, MD, FASE, FACC, FACP, FESC,
Director, Echocardiography Services
Aurora Health Care, Aurora Medical Group
Aurora/St. Luke Medical Center, Aurora/Sinai Medical
Center
Milwaukee, Wisconsin
James N. Kirkpatrick, MD, FASE, FACC, Assistant
Professor of Medicine
Division of Cardiovascular Medicine
University of Pennsylvania
Philadelphia, Pennsylvania
Allan L. Klein, MD, FASE, FACC, FAHA, FRCP(C), Director
of Cardiovascular Imaging Research
Director of the Center for the Diagnosis and Treatment
of Pericardial Diseases
Cardiovascular Medicine
Cleveland Clinic
Cleveland, Ohio
Smadar Kort, MD, FASE, FACC, Associate Professor of
Medicine
Director, Cardiovascular Imaging
Division of Cardiology
Stony Brook University Medical CenterStony Brook, New York
Itzhak Kronzon, MD, FASE, FACC, FAHA, FESC, FACP,
Professor of Medicine
Director, Non Invasive Cardiology
New York University Medical Center
New York, New York
Karla M. Kurrelmeyer, MD, FASE, Assistant Professor of
Medicine
Weill Cornell Medical College
Department of Cardiology
Methodist DeBakey Heart & Vascular Center
Houston, Texas
Roberto M. Lang, MD, FASE, FACC, FAHA, FESC, FRCP,
Professor of Medicine
President, American Society of Echocardiography
Director, Noninvasive Cardiac Imaging Laboratories
University of Chicago Medical Center
Chicago, Illinois
Pui Lee, MBChB, Advanced Fellow in Echocardiography
Echocardiography Laboratory
Mayo Clinic
Rochester, Minnesota
Vera Lennie, MD, FESC, Cardiologist
Department of Cardiac Imaging
Hospital Carlos III
Madrid, Spain
Steven J. Lester, MD, FASE, FACC, FRCPC, Consultant,
Department of Medicine, Division of Cardiology
Associate Professor of Medicine, College of Medicine
Director of Echocardiography
Mayo Clinic
Scottsdale, Arizona
Dominic Y. Leung, MBBS, PhD, FACC, FRCP(Edin),
FRACP, FHKCP, FCSANZ, Professor of Cardiology,Department of Cardiology
Liverpool Hospital, University of New South Wales
Sydney, New South Wales, Australia
Jonathan R. Lindner, MD, FASE, Professor and Associate
Chief for Education
Cardiovascular Division
Oregon Health & Science University
Portland, Oregon
Joseph A. Lodato, MD, Section of Cardiology
Department of Medicine
University of Chicago Medical Center
Chicago, Illinois
Boris S. Lowe, BHB, MB ChB, FRACP, Consultant
Cardiologist
Green Lane Cardiovascular Service
Auckland City Hospital
Auckland, New Zealand
Joan L. Lusk, RN, RDCS, ACS, FASE, Registered Adult and
Pediatric Cardiac Sonographer
Adult Congenital Heart Disease Clinic Advanced
Clinical/Research Sonographer
Mayo Clinic Cardiac Ultrasound Imaging and
Hemodynamic Laboratory
Mayo Clinic
Scottsdale, Arizona
Joseph F. Malouf, MD, Professor of Medicine
Mayo Clinic College of Medicine
Department of Internal Medicine
Mayo Clinic
Rochester, Minnesota
Randolph P. Martin, MD, FASE, FACC, FESC, Medical
Director, Cardiovascular Imaging
Piedmont Hospital
Chief, Structural & Valvular Heart Disease
Piedmont Heart InstituteProfessor of Medicine, Emeritus
Emory University School of Medicine
Atlanta, Georgia
Thomas H. Marwick, MBBS, PhD, Professor of Medicine
Institution University of Queensland
Brisbane, Queensland, Australia
Gerald Maurer, MD, FACC, FESC, Professor of Medicine
Director, Division of Cardiology
Chair, Department of Medicine II
Medical University of Vienna
Vienna, Austria
Patrick M. McCarthy, MD, FACC, Chief of Cardiac
Surgery Division, Director of the Bluhm Cardiovascular
Institute, and Heller-Sacks Professor of Surgery
Division of Cardiac Surgery
Northwestern University/Northwestern Memorial
Hospital
Chicago, Illinois
Ivàn Melgarejo, MD, Cardiologist, Echocardiographer
Department of Noninvasive Cardiology
Fundaciòn A. Shaio
Professor of Cardiology
Universidad del Rosario
Bogotà, Colombia
Hector I. Michelena, MD, FACC, Assistant Professor of
Medicine
Mayo Clinic College of Medicine
Consultant, Division of Cardiovascular Diseases
Mayo Clinic
Rochester, Minnesota
Victor Mor-Avi, PhD, FASE, Professor
Section of Cardiology, Department of Medicine
Director of Cardiac Imaging Research
University of Chicago
Chicago, IllinoisSherif F. Nagueh, MD, FASE, Professor of Medicine
Weill Cornell Medical College
Associate Director of Echocardiography Laboratory
Methodist DeBakey Heart and Vascular Center
Houston, Texas
Hans Joachim Nesser, MD, FASE, FACC, FESC, Professor
of Medicine
Head, Department of Cardiology, Angiology, Intensive
Care
Hospital Vice Director
Cardiology, Angiology, Intensive Care
Elisabethinen Hospital Linz
Linz, Austria
Johannes Niel, MD, Senior Cardiologist
Cardiology, Angiology, Intensive Care
Elisabethinen Hospital Linz
Linz, Austria
Steve R. Ommen, MD, Consultant
Vice-Chair for Education
Director, Hypertrophic Cardiomyopathy Clinic
Division of Cardiovascular Diseases
Professor of Medicine
Mayo Clinic
Rochester, Minnesota
Alan S. Pearlman, MD, FASE, FACC, FAHA, Professor of
Medicine
Division of Cardiology
University of Washington School of Medicine
Seattle, Washington
Patricia A. Pellikka, MD, FASE, FACC, FAHA, FACP,
Professor of Medicine
Mayo Clinic College of Medicine
Co-Director, Echocardiography Laboratory
Division of Cardiovascular Diseases and Internal
Medicine
Mayo ClinicRochester, Minnesota
Esther Pérez-David, MD, PhD, Cardiology Department
Hospital General Universitario “Gregorio Marañón”
Madrid, Spain
Philippe Pibarot, DVM, PhD, FACC, FAHA, Professor of
Medicine
Department of Medicine
Laval University
Québec City, Quebec, Canada
Michael H. Picard, MD, FASE, FACC, FAHA, Director,
Echocardiography
Massachusetts General Hospital
Associate Professor
Harvard Medical School
Boston, Massachusetts
Fausto J. Pinto, MD, PhD, FASE, FACC, FESC, FSCAI,
Professor of Cardiology/Medicine
Department of Cardiology
Lisbon University Medical School
Lisbon, Portugal
Heidi Pollard, RDCS, Cardiac Sonographer
Department of Cardiology
University of Chicago Medical Centers
Chicago, Illinois
Tamar S. Polonsky, MD, Post Doctoral Fellow
Cardiovascular Epidemiology and Prevention
Northwestern University
Chicago, Illinois
Thomas R. Porter, MD, FASE, Professor of Cardiology
Courtesy Professor of Radiology and Pediatric
Cardiology
Department of Internal Medicine–Division of Cardiology
University of Nebraska Medical Center
Omaha, NebraskaBrian D. Powell, MD, Assistant Professor of Medicine
Cardiovascular Division
Mayo Clinic
Rochester, Minnesota
Jose E. Riarte, MD, Staff, Cardiovascular Ultrasound
Service
Cardiac Imaging Department
Instituto Cardiovascular de Buenos Aires
Ciudad de Buenos Aires, Argentina
Vera H. Rigolin, MD, FASE, FACC, FAHA, Associate
Professor of Medicine
Northwestern University Feinberg School of Medicine
Medical Director, Echocardiography Laboratory
Northwestern Memorial Hospital
Chicago, Illinois
Ricardo E. Ronderos, MD, PhD, Associate Professor of
Cardiology
Director, Instituto de Cardiologia La Plata
Chief, Cardiovascular Imaging Department
Instituto Cardiovascular de Buenos Aires
Universidad Nacional de La Plata
La Plata, Buenos Aires, Argentina
Muhamed Saric, MD, PhD, FASE, FACC, Associate
Professor of Medicine
Noninvasive Cardiology
New York University
New York, New York
Partho P. Sengupta, MD, DM, Assistant Professor of
Medicine
Mayo Clinic College of Medicine
Cardiovascular Division
Mayo Clinic
Scottsdale, Arizona
Dipak P. Shah, MD, Cardiology Fellow
Section of CardiologyUniversity of Chicago
Chicago, Illinois
Stanton K. Shernan, MD, FASE, FAHA, Associate
Professor of Anesthesia
Director of Cardiac Anesthesia Department of
Anesthesiology, Perioperative and Pain Medicine
Brigham and Women’s Hospital
Harvard Medical School
Boston, Massachusetts
Kirk T. Spencer, MD, FASE, Associate Professor of
Medicine
University of Chicago
Chicago, Illinois
Monvadi B. Srichai, MD, Assistant Professor
Department of Radiology and Medicine, Cardiology
Division
New York University School of Medicine
New York, New York
Kathleen Stergiopoulos, MD, PhD, FASE, FACC, Assistant
Professor of Medicine
Director, Inpatient Cardiology Consultation
Stony Brook University School of Medicine
SUNY Health Sciences Center
Stony Brook, New York
G. Monet Strachan, RDCS, FASE, Supervisor,
Echocardiography Lab
University of California San Diego Medical Center
San Diego, California
Lissa Sugeng, MD, MPH, Assistant Professor of Clinical
Medicine
Non-Invasive Cardiovascular Imaging Lab
University of Chicago Medical Center
Chicago, Illinois
Masaaki Takeuchi, MD, PhD, FASE, Associate ProfessorSecond Department of Internal Medicine
University of Occupational and Environmental Health
School of Medicine
Kitakyushu, Japan
Hélène Thibault, MD, PhD, Docteur of Cardiology
Echocardiography Laboratory
Hôpital Louis Pradel
Lyon, France
Wolfgang Tkalec, MD, Senior Cardiologist
Cardiology, Angiology, Intensive Care
Elisabethinen Hospital Linz
Linz, Austria
Paul A. Tunick, MD, Professor, Department of Medicine
Noninvasive Cardiology Laboratory
New York University Medical Center
New York, New York
Matt M. Umland, RDCS, FASE, RT(R), (CT), (QM),
Echocardiography Quality Coordinator
Advanced Hemodynamic and Cardiovascular Laboratory
Aurora Medical Group
Advanced Cardiovascular Services
Milwaukee, Wisconsin
Mani A. Vannan, MBBS, FACC, Professor of Clinical
Internal Medicine
Joseph M. Ryan Chair in Cardiovascular Medicine
Director, Cardiovascular Imaging
The Ohio State University
Columbus, Ohio
Philippe Vignon, MD, PhD, Professor of Critical Care
Medicine
Medical-Surgical ICU and Clinical Investigation Center
Teaching Hospital of Limoges
Limoges, France
Hector R. Villarraga, MD, FASE, FACC, AssistantProfessor of Medicine
Mayo Clinic College of Medicine
Division of Cardiovascular Diseases and Internal
Medicine
Mayo Clinic
Rochester, Minnesota
R. Parker Ward, MD, FASE, FACC, Associate Professor of
Medicine
Non-Invasive Imaging Laboratories
Section of Cardiology
University of Chicago Medical Center
Chicago, Illinois
Nozomi Watanabe, MD, PhD, FACC, Department of
Cardiology
Kawasaki Medical School
Kurashiki, Japan
Kevin Wei, MD, Associate Professor of Medicine
Cardiovascular Division
Oregon Health & Science University
Portland, Oregon
Neil J. Weissman, MD, FASE, Professor of Medicine,
Georgetown University
President, MedStar Health Research Institute at
Washington Hospital Center
Washington, District of Columbia
Siegmund Winter, MD, Senior Cardiologist
Cardiology, Angiology, Intensive Care
Elisabethinen Hospital Linz
Linz, Austria
Malissa J. Wood, MD, FASE, FACC, Co-director MGH
Heart Center Corrigan Women’s Heart Health Program
Assistant Professor of Medicine
Harvard Medical School
Departments of Medicine/Cardiology
Massachusetts General HospitalBoston, Massachusetts
Feng Xie, MD, Associate Professor of Medicine
Division of Cardiology
University of Nebraska Medical Center
Omaha, Nebraska
Hyun Suk Yang, MD, PhD, Division of Cardiovascular
Diseases
Mayo Clinic
Scottsdale, Arizona
Danita M. Yoerger Sanborn, MD, FASE, MMSc, Assistant
Physician, Instructor in Medicine
Cardiology Division
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts
Qiong Zhao, MD, PhD, FASE, Assistant Professor of
Medicine
Cardiology Division, Department of Medicine
Northwestern University, Feinberg School of Medicine
Chicago, Illinois
Concetta Zito, MD, Cardiology Assistant
Unit of Intensive and Invasive Heart Care
Department of Medicine and Pharmacology
University of Messina
Messina, Italy
William A. Zoghbi, MD, FASE, FACC, FAHA, William L.
Winters Endowed Chair in CV Imaging
Professor of Medicine
Weill-Cornell Medical College
Director, Cardiovascular Imaging Institute
The Methodist DeBakey Heart & Vascular Center
Houston, TexasTable of Contents
Front Matter
Copyright
Preface
Foreword
Contributors
Section I: Native Valvular Heart Disease: Aortic Stenosis/Aortic
Regurgitation
Chapter 1: Morphologic Variants of the Aortic Valve
Chapter 2: Aortic Stenosis Quantitation
Chapter 3: Aortic Stenosis: Subaortic Membrane
Chapter 4: Aortic Stenosis With Low Gradient and Poor Left Ventricular
Dysfunction
Chapter 5: Asymptomatic Severe Aortic Stenosis
Chapter 6: Challenges in Aortic Stenosis
Chapter 7: Technical Issues: Aortic Stenosis
Chapter 8: Quantitation of Aortic Regurgitation
Section II: Native Valvular Heart Disease: Mitral Stenosis/Mitral
Regurgitation
Chapter 9: Mitral Stenosis
Chapter 10: Exercise Echocardiography in Mitral Stenosis
Chapter 11: Mitral Valve
Chapter 12: Mitral Stenosis: Complex Disease, Situations That Mimic
Mitral Stenosis, and Technical Pearls
Chapter 13: Morphologic Basis of Valvular Nonischemic Mitral
Regurgitation
Chapter 14: Quantification of Nonischemic Mitral RegurgitationChapter 15: Suitability for Nonischemic Mitral Regurgitation Repair
Chapter 16: Exercise Hemodynamics in Nonischemic Mitral
Regurgitation
Chapter 17: Nonischemic Mitral Regurgitation in Infective Endocarditis
Chapter 18: Nonischemic Mitral Regurgitation and Left Ventricular
Dysfunction
Chapter 19: Ischemic Mitral Regurgitation
Chapter 20: Evaluation of Tricuspid Regurgitation by Two-Dimensional
and Doppler Echocardiography: Implications for Management
Section III: Prosthetic Heart Valve Disease
Chapter 21: Valve Prosthesis-Patient Mismatch
Chapter 22: Valve Prosthesis and Pressure Recovery
Chapter 23: Aortic Prosthetic Valve Obstruction
Chapter 24: Mitral Prosthetic Valve Obstruction
Chapter 25: Prosthetic Mitral Regurgitation
Chapter 26: Prosthetic Aortic Regurgitation
Chapter 27: Technical Echo-Doppler Pearls in Prosthetic Heart Valves
Section IV: Interventional/Intraoperative Echocardiography
Chapter 28: Role of Transesophageal Echocardiography and
Intracardiac Echocardiography in Atrial Fibrillation Ablation
Chapter 29: Left Atrial Appendage Closure: Alternative Treatment to
Prevent Thromboembolism
Chapter 30: Intraoperative Transesophageal Echocardiographic
Evaluation of Ischemic Mitral Regurgitation
Chapter 31: Mitral Valve Repair for Myxomatous Disease of the Mitral
Valve
Chapter 32: Echocardiography in Left Ventricular Infarct Exclusion
Surgery
Chapter 33: Patent Foramen Ovale
Section V: Transesophageal Echocardiography
Chapter 34: Precardioversion Transesophageal Echocardiography in
Atrial FibrillationChapter 35: Cardiac Source of Embolus
Chapter 36: Perivalvular Complications in Infective Endocarditis
Chapter 37: Aortic Dissection
Chapter 38: Aortic Intramural Hematoma
Chapter 39: Aortic Atherosclerosis and Embolic Events
Chapter 40: Featured Expert Commentary and Review: Central Role of
Transesophageal Echocardiography in Clinical Cardiology
Section VI: Coronary Artery Disease
Chapter 41: Stress Echocardiography in Chest Pain Syndromes
Chapter 42: Exercise Echocardiography in Left Ventricular Hypertrophy
(and Other Pitfalls)
Chapter 43: Abnormal Exercise Echocardiography in Coronary Artery
Disease
Chapter 44: Abnormal Dobutamine Stress Echocardiography for
Ischemia (Preoperative Risk Assessment)
Chapter 45: Myocardial Viability
Chapter 46: Use of Tissue Doppler During Dobutamine Stress
Echocardiography
Chapter 47: Diastolic Stress Test for the Evaluation of Exertional
Dyspnea
Chapter 48: Featured Expert Commentary and Review: Prognostic Value
of Stress Echocardiography
Chapter 49: Featured Expert Commentary and Review: Functional
Imaging in the Era of Computed Tomographic Coronary Angiography
Chapter 50: Vasodilator Stress With Myocardial Contrast
Echocardiography: Abnormal Test Indicating Acute Ischemia
Chapter 51: Diagnosis of Coronary Artery Disease by Dobutamine Stress
Real-Time Myocardial Contrast Perfusion Imaging
Chapter 52: Myocardial Contrast Echocardiography After Myocardial
Infarction
Chapter 53: Technical Pearls in Myocardial Contrast Echocardiography
Chapter 54: Featured Expert Commentary and Review: Myocardial
Contrast Echocardiography for Chest Pain Syndromes in the EmergencyDepartment
Section VII: Mechanical Complications of Myocardial Infarction
Chapter 55: Mechanical Complications of Myocardial Infarction
Section VIII: Pericardial Disease and Intracardiac Masses
Chapter 56: Pericardial Tamponade
Chapter 57: Constrictive Pericarditis
Chapter 58: Restrictive Cardiomyopathy
Chapter 59: Rare Pericardial Disorders
Chapter 60: Atrial Masses
Chapter 61: Aortic Valve Masses
Chapter 62: Artifacts Masquerading as Intracardiac Masses
Chapter 63: Use of Contrast to Distinguish Intracardiac Masses From
Thrombi
Chapter 64: Featured Expert Commentary and Review: Pericardial
Disease and Intracardiac Masses
Section IX: Myocardial Diseases
Chapter 65: Hypertrophic Cardiomyopathy
Chapter 66: Technical Issues in Assessing Left Ventricular Outflow Tract
Gradient
Chapter 67: Treatment of Hypertrophic Obstructive Cardiomyopathy
With Left Ventricular Outflow Tract Obstruction
Chapter 68: Apical Hypertrophic Cardiomyopathy
Chapter 69: Dilated Cardiomyopathy
Chapter 70: Takotsubo Cardiomyopathy
Chapter 71: Heart Failure in Idiopathic Hypereosinophilic Syndrome
Chapter 72: Use of Guidelines to Evaluate Chamber Quantitation
Chapter 73: Right Ventricle: Carcinoid Heart Disease
Chapter 74: Right Ventricular Dysplasia
Chapter 75: Primary Pulmonary Hypertension
Chapter 76: Pulmonary Embolism
Chapter 77: Pulmonary StenosisChapter 78: Fenfluramine Valve Disease
Chapter 79: Featured Expert Commentary and Review: Morphologic
and Functional Evaluation of the Right Heart: Progress and Challenges
Section X: Heart Failure Filling Pressures/Diastology
Chapter 80: Evaluation of Diastolic Function
Chapter 81: Mechanics of Heart Failure With Normal Left Ventricular
Systolic Function
Chapter 82: Technical Issues in Diastolic Function Evaluation
Section XI: Cardiac Resynchronization Therapy
Chapter 83: Cardiac Resynchronization Therapy: Is it for Everyone?
Chapter 84: Mitral Regurgitation and Cardiac Resynchronization
Therapy
Chapter 85: Technical Issues in Evaluating Dyssynchrony
Chapter 86: Featured Expert Commentary and Review: Assessment of
Left Ventricular Dyssynchrony in Cardiac Resynchronization Therapy
Section XII: New Technology
Chapter 87: Contrast for Resting Echocardiograms
Chapter 88: Contrast for Stress Echocardiography
Chapter 89: Three-Dimensional Transthoracic and Transesophageal
Echocardiography
Chapter 90: Myocardial Tissue Imaging
Chapter 91: Tissue Doppler Imaging: Quantitation of Myocardial
Mechanics
Chapter 92: Assessment of Left Ventricular Twist, Rotation, and Torsion
Chapter 93: Hand-Carried Echocardiography Systems
Section XIII: Cases From Around the World
Chapter 94: Familial Isolated Noncompaction Left Ventricle
Chapter 95: Takotsubo-like Left Ventricular Dysfunction
Chapter 96: Chagas Cardiomyopathy
Chapter 97: Cardiovascular Behçet’s Disease
Chapter 98: Use of Three-Dimensional Echocardiography in Stress
Testing: Principles and First StudiesChapter 99: Cardiac Involvement in Hypereosinophilic Syndrome
Chapter 100: Traumatic Disruption of the Aorta
Chapter 101: Left Ventricular Free Wall Rupture After Acute Myocardial
Infarction and Thrombolysis
Chapter 102: Transthoracic Coronary Artery Imaging
Chapter 103: A Hole in the Heart
Chapter 104: Transesophageal Echocardiography: In-Procedure
Guidance and Follow-up of Percutaneous Closure of Prosthetic
Paravalvular Leaks
Section XIV: Congenital Heart Disease
Chapter 105: Congenital Heart Disease in Adults
Chapter 106: Echocardiographic Evaluation of Atrial Septal Defects
Chapter 107: Ventricular Septal Defects and Eisenmenger Syndrome
Chapter 108: Patent Ductus Arteriosus
Chapter 109: Anatomic Features of Corrected Transposition of the Great
Arteries
Chapter 110: Coarctation of the Aorta
Chapter 111: Ebstein’s Anomaly
IndexSection I
Native Valvular Heart
Disease: Aortic
Stenosis/Aortic Regurgitation
Chapter 1
Morphologic Variants of the Aortic Valve
Steven A. Goldstein, MD
Valvular aortic stenosis (AS), a chronic progressive disease, usually develops over decades. The
majority of cases of AS are acquired and result from degenerative (calci c) changes in an
anatomically normal trilea et aortic valve that becomes gradually dysfunctional. Congenitally
abnormal valves may be stenotic at birth but usually become dysfunctional during adolescence
or early adulthood. A congenitally bicuspid aortic valve is now the most common cause of
valvular AS in patients younger than 65 years. Rheumatic AS is now much less common than in
prior decades and is almost always accompanied by mitral valve disease. Table 1.1 lists the
most common causes of valvular AS. These are illustrated in Figs. 1.1 to 1.4.
Table 1.1 Etiology of Aortic Stenosis
Congenital (unicuspid, bicuspid)
Degenerative (sclerosis of previously normal valve)
Rheumatic
Fig. 1.1 Diagram showing the three major causes of valvular aortic stenosis. Degenerative:
commissures not fused; calcium deposits in cusps. Bicuspid: two cusps and a raphe in the fused
cusps. Rheumatic: fused commissures with central round or oval opening.

Fig. 1.2 A to C, Degenerative aortic stenosis in the elderly. A, Transesophageal
echocardiographic cross-sectional view of an elderly patient with degenerative aortic stenosis
illustrating relative absence of commissured fusion. The resulting ori ce is composed of three
“slits” between each pair of cusps. B, Same view illustrates planimetry of the aortic valve area. C,
Pathologic specimen from a di0erent patient illustrates similar rigid lea ets caused by brosis
and calcium deposition (seen from aortic side of the valve).


Fig. 1.3 Stenotic and calci ed bicuspid aortic valve. Note the median raphe (arrow) in the
larger, conjoined cusp.
Fig. 1.4 A and B, Typical rheumatic aortic stenosis with commissural fusion resulting in a
central triangular (as shown here) or oval or circular ori ce. Typical rheumatic aortic stenosis
with commissured fusion resulting in a central triangular ori ce as shown in the transesophageal
echocardiogram (A) and a pathologic specimen (B).
Bicuspid Aortic Valve
Congenital aortic malformation re ects a phenotypic continuum of unicuspid valve (severe
form), bicuspid valve (moderate form), tricuspid valve (normal, but may be abnormal), and the
rare quadricuspid forms. Bicuspid aortic valves (BAVs) are the result of abnormal cusp formation
during the complex developmental process. In most cases, adjacent cusps fail to separate,
resulting in one larger conjoined cusp and a smaller one. Therefore BAV (or bicommissural aortic
valve) has partial or complete fusion of two of the aortic valve lea ets, with or without a central
raphe, resulting in partial or complete absence of a functional commissure between the fused
1leaflets.
The accepted prevalence of BAV in the general population is 1% to 2%, which makes it the
most common congenital heart defect. Information on the prevalence of BAV comes primarily
1-7from pathology centers. The most reliable estimate of BAV prevalence is often considered the
31.37% reported by Larson and Edwards. These authors have special expertise in aortic valve

disease and found BAVS in 21,417 consecutive autopsies. An echocardiographic survey of
8primary schoolchildren demonstrated a BAV in 0.5% of boys and 0.2% of girls. A more recent
study detected 0.8% BAVs in nearly 21,000 men in Italy who underwent echocardiographic
9screening for the military. Table 1.2 summarizes data on the prevalence of bicuspid valves.
10-12BAV is seen predominantly in males with a 2-4 : 1 male/female ratio. Although a BAV may
occur in isolation, it may be associated with many forms of congenital heart disease.
Table 1.2 Prevalence of Bicuspid Aortic Valves
Other less common congenital abnormalities of the aortic valve include the unicuspid valve
and the quadricuspid valve. The unicuspid valve is dome shaped and has a central stenotic
ori ce. These valves generally become stenotic during adolescence or early adulthood and are
seldom seen in older adults. Quadricuspid valves are rare and may be either regurgitant or
13-17stenotic. With advances in echocardiography, more cases of quadricuspid aortic valves
(QAVs) are being diagnosed antemortem. The preoperative diagnosis of QAV is important
14because it can be associated with abnormally located coronary ostia. Echocardiographic
diagnosis can be established by either transthoracic or transesophageal echocardiography (Fig.
1.5). On the short-axis view of the aortic valve in diastole, the commissural lines formed by the
adjacent cusps result in an X con guration rather than the Y of the normal tricuspid aortic valve
(Tables 1.3 to 1.5).Fig. 1.5 Quadricuspid aortic valve. Transesophageal echocardiographic short-axis view (37
degrees) illustrates failure of lea et coaptation in diastole (arrow) with a square-shaped central
opening and typical X-shaped configuration of the four commissures.
Table 1.3 Prevalence of Quadricuspid Aortic Valves
Table 1.4 Function of Quadricuspid Aortic Valves
Valve Function No. (%)
Aortic regurgitation 115 (75)
Aortic stenosis + aortic regurgitation 13 (8)
Aortic stenosis 1 (1)
Normal 25 (16)
From Tutarel O: The quadricuspid aortic valve: a comprehensive review. J Heart Valve Dis
2004;13:534537.
Table 1.5 Quadricuspid Aortic Valves: Morphologic Types
Anatomic Variation: Cusps No.
4 equal 51
3 equal, 1 smaller 43
2 equal larger, 2 equal smaller 10
1 large, 2 intermediate, 1 small 7
3 equal, 1 larger 4
2 equal, 2 unequal smaller 4
4 unequal 5
From Hurwitz LE, Roberts WC: Quadricuspid semilunar valve. Am J Cardiol 1973;31:623-626.
Natural History of Bicuspid Valves
Although BAVs in some patients may go undetected or present no clinical consequences over a






lifetime, complications that usually require treatment, including surgery, develop in most
patients. The most important clinical consequences of BAV are valve stenosis, valve
regurgitation, infective endocarditis, and aortic complications such as dilation, dissection, and
rupture (Table 1.6).
Table 1.6 Complications of Bicuspid Aortic Valves
Valve Complications Aortic Complications
Stenosis Dilation
Regurgitation Aneurysm
Infection Dissection, rupture
Isolated AS is the most frequent complication of BAV, occurring in approximately 85% of all
10BAV cases. BAV accounts for the majority of patients aged 15 to 65 years with signi cant AS.
The progression of the congenitally deformed valve to AS presumably re ects its propensity for
premature brosis, sti0ening, and calcium deposition in these structurally abnormal valves. The
speci c anatomy may in uence the propensity for obstruction. Stenosis may be more rapid if the
2 18aortic cusps are asymmetric or in the anteroposterior position. Novaro and colleagues suggest
that stenosis was more frequent in females and in patients with fusion of the right and
noncoronary cusps. In addition, patients with abnormal lipid pro les and those who smoke may
12be at increased risk of development of signi cant stenosis. In fact, some recent evidence
18,19indicates that statins may slow the progression of AS. However, more evidence is needed
before evidence-based therapy can be recommended.
10Aortic regurgitation, present in approximately 15% of patients with BAV, is usually due to
dilation of the sinotubular junction of the aortic root, preventing cusp coaptation. It may also be
caused by cusp prolapse, brotic retraction of lea et(s), or by damage to the valve from
infective endocarditis. Aortic regurgitation tends to occur in younger patients than in those with
AS.
Why stenosis develops in some patients with a BAV and regurgitation develops in others is
21unknown. As mentioned, in rare cases no hemodynamic consequences develop. Roberts et al.
reported three congenital BAVs in nonagenarians undergoing surgery for AS. Why some patients
with a congenital BAV do not experience symptoms until they are in their 90s and others have
symptoms in early life is also unclear.
Infective Endocarditis
Patients with BAVs are particularly susceptible to infective endocarditis. Although the exact
incidence of endocarditis remains controversial, the population risk, even in the presence of a
22functionally normal valve, may be as high as 3% over time. In a series of 50 patients with
23native valve endocarditis, 12% had a BAV. In a similar study, BAV accounted for 70% of all
24native valve endocarditis cases and was the single most important predisposing factor.
In many cases of BAV, endocarditis is the rst indication of structural valve disease, which
emphasizes the importance of either clinical or echocardiographic screening for the diagnosis of
BAV. Unexplained systolic ejection murmurs, diastolic decrescendo murmurs, and/or aortic


ejection sounds (clicks) should prompt echocardiographic evaluation. Bacterial endocarditis
prevention is vital for patients with BAV and is highly recommended by the American Heart
25Association/American College of Cardiology (AHA/ACC) Guidelines.
Aortic Complications
BAV is associated with several additional abnormalities, including displaced coronary ostia, left
coronary artery dominance, and a shortened left main coronary artery; coarctation of the aorta;
aortic interruption; Williams syndrome; and most important, aortic dilation, aneurysm, and
dissection. Given these collective ndings, BAV may the result of a developmental disorder
involving the entire aortic root and arch. Although the pathogenesis is not well understood, these
26associated aortic malformations suggest a genetic defect.
Although they are less well-understood, these aortic complications of BAV disease can cause
signi cant morbidity and mortality. BAV may also be associated with progressive dilation,
aneurysm formation, and dissection (Tables 1.7 and 1.8). These vascular complications may
9,11occur independent of valvular dysfunction and can manifest in patients without signi cant
9stenosis or regurgitation. According to Nistri and colleagues, 50% or more of young patients
with normally functioning BAV have echocardiographic evidence of aortic dilation.
Table 1.7 Frequency of Aortic Dissection in Persons With a Bicuspid Aortic Valve
Table 1.8 Frequency of Bicuspid Aortic Valve in Aortic Dissection
Author Year No. BAV/ Dissection (%)
Gore and Seiwert38 1952 11/85 (13)
Edwards et al.39 1978 11/119 (9)
Larson and Edwards3 1984 18/161 (11)
Roberts and Roberts37 1991 14/186 (7.5)
Totals 54/551 (9.8)
The diameter of the ascending aorta measured at the level of the sinuses of Valsalva appears to
1-3be the best predictor of the occurrence of aortic complications. However, no consensus exists
regarding the threshold value of the diameter of the ascending aorta that should not be
exceeded. Nevertheless, there is a general trend toward aggressive treatment of ascending aortic
dilation in patients with BAV using criteria similar to those for patients with Marfan26-34syndrome. However, evidence supporting this approach does not exist and the optimal
diameter at which replacement of the ascending aorta should be performed in patients with BAV
is not known. The recent ACC/AHA guidelines for the management of patients with valvular
heart disease recommend surgery to prevent dissection or rupture when the diameter of the
ascending aorta exceeds 50 mm (a lower threshold value should be considered for patients of
27small stature) or if the rate of increase in diameter is ≥5 mm per year. These indications are
based largely on criteria from echocardiographic studies.
Coarctation
BAV may occur in isolation or with other forms of congenital heart disease. The association of
3,35-45BAV with coarctation is well documented. An autopsy study found coexisting coarctation
1of the aorta in 6% of cases of BAV, and an echocardiographic study found coarctation in 10%
43of patients with BAV. On the other hand, as many as 30% to 55% of patients with coarctation
42,45have a BAV. Therefore, when a BAV is detected on an echocardiogram, coarctation of the
aorta should always be sought.
Echocardiographic Findings
The importance of diagnosing BAV should be evident from the previous discussions; BAV is
common, requires endocarditis prophylaxis, can develop into stenosis or regurgitation, and is
associated with aortic complications. Echocardiography remains the most practical and widely
available method for detecting BAV. An outline of the role of echocardiography for detecting
and evaluating BAVs is listed in Table 1.9.
Table 1.9 Bicuspid Aortic Valve: Role of Echocardiography
Evaluation for aortic stenosis/regurgitation
Careful measurements of aortic root
Search for coarctation
Consider screening first-degree family members
M-mode echocardiography of a BAV may demonstrate an eccentric diastolic closure line.
However, an eccentric closure line also may be seen in patients with a normal tricuspid aortic
valve; and a normal, central closure line is often present in patients with a BAV. Therefore
twodimensional echocardiography is required for reliable detection of a BAV. The most reliable and
useful views are the parasternal long-axis and short-axis views.
The long-axis view typically shows systolic doming (Figs. 1.6 to 1.8) resulting from the
limited valve opening; normally the lea ets are parallel to the aortic walls (Fig. 1.9). In diastole,
one of the lea ets (the larger, conjoined cusp) may prolapse. The parasternal long-axis (PLAX)
view with color Doppler is also useful to evaluate for aortic regurgitation (diastolic aortic
regurgitant jet) and AS (turbulence in the aortic root and ascending aorta in systole). Lastly, the
PLAX view is also important for sizing the sinus of Valsalva, sinotubular junction, and ascending
aorta.

Fig. 1.6 A to C, Bicuspid aortic valve. A, Short-axis view shows “ sh mouth” or football-shaped
opening. B, Long-axis view shows systolic doming. C, Color Doppler shows eccentric aortic
regurgitant jet.
Fig. 1.7 Bicuspid aortic valve. Systolic doming with small, stenotic opening at the apex of the
dome (arrow).
Fig. 1.8 A and B, Bicuspid aortic valve. Transesophageal echocardiography demonstrates
several features of BAV: “ sh mouth” opening in systole (white arrow) and median raphe (yellow
arrow) (A) and systolic doming of the lea ets (red arrow) and dilated ascending aorta
(doubleheaded arrow) (B). AO, Aorta; LVOT, left ventricular outflow tract.


Fig. 1.9 Normal tricuspid valve opens normally. Note that the aortic lea ets are parallel to the
aortic walls.
The parasternal short-axis (SAX) view is useful in examining the number and position of the
commissures, the opening pattern, the presence of a raphe, and the lea et mobility. The normal
(trilea et) aortic valve appears like a Y in diastole with the commissures at the 10 o’clock, 2
o’clock, and 6 o’clock positions. When the commissures deviate from these clock-face positions,
BAV should be suspected with subsequent careful evaluation. In systole, the BAV opens with a
“ sh mouth” or football shape appearance (Figs. 1.10 and 1.11). There is typically a raphe
(region where the cusps failed to separate), which is usually distinct and extends from the free
margin to the base. Calci cation generally occurs rst along this raphe, ultimately hindering the
46motion of the conjoined cusp.
Fig. 1.10 Transesophageal echocardiographic short-axis view illustrates typical football-shaped
opening and median raphe at the 5 o’clock position.
Fig. 1.11 Variations in bicuspid valves. Relative positions of raphe and conjoined cusp.
(Adapted from Sabet HY, Edwards WD, Tazelaar HD, et al. Congenitally bicuspid aortic valves: a
surgical pathology study of 542 cases (1991 through 1996) and a literature review of 2,715 additional
cases. Mayo Clin Proc 1999;74:14-26.)
False-positive diagnosis of BAV may occur if all three lea ets are not imaged in systole or if
their closure lines are not imaged in diastole. If images are suboptimal or heavily
fibrotic/sclerotic, then transesophageal echocardiography may be helpful for accurate evaluation
of the aortic valve anatomy and con rmation of a BAV. Diastolic images in the parasternal SAX
view can also be misleading if the raphe is mistaken for a third commissural closure line.
Aortic root measurements should be made in the PLAX view at four levels: the annulus, sinuses
of Valsalva, sinotubular junction, and proximal ascending aorta (Fig. 1.12). The aortic arch and
descending thoracic aorta should be imaged from the suprasternal notch view, looking for
coarctation.
Fig. 1.12 Aortic dimensions: measurement locations. 1, Annulus; 2, midpoint of sinuses of
Valsalva; 3, sinotubular junction; 4, ascending aorta at level of its largest diameter. LV, Left
ventricle; Ao, aorta; LA, left atrium.
Surveillance
Because of the risk of progressive aortic valve disease (stenosis and/or regurgitation) and
ascending aortic disease, serial echocardiographic monitoring is warranted in patients with BAV
even when no symptomatic are reported. The 2006 ACC/AHA guidelines recommend monitoring
of adolescents and young adults, older patients with AS, and patients with a BAV and dilation of
27the aortic root or ascending aorta. If the aortic root is poorly visualized on echocardiography,
cardiac computed tomography or magnetic resonance imaging are excellent substitutes.
Indications for Echocardiography for Incidental Murmurs
The 2006 ACC/AHA guidelines on the management of patients with valvular heart disease
recommend the use of echocardiography in patients with symptomatic and asymptomatic
27murmurs and ejection sounds (Table 1.10 and Fig. 1.13). A diagram (Fig. 1.14) and actual
phonocardiogram (Fig. 1.15) illustrate typical physical findings in patients with BAV.
Table 1.10 Evaluation of Heart Murmurs: Role of Echocardiography
Differentiate pathologic vs. physiologic causeDefine the etiology
Determine severity of the lesion
Determine the hemodynamics
Detect secondary or coexisting lesions
Evaluate chamber sizes and function
Establish reference point for future
Adapted from Bonow RO, Carabello BA, Chatterjee K, et al: ACC/AHA 2006 guidelines for the
management of patients with valvular heart disease: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol
2006;48:e1-e148.
Fig. 1.13 Strategy for evaluating heart murmurs. ECG, Electrocardiogram; CXR, chest x-ray.
(Adapted from Bonow RO, Carabello BA, Chatterjee K, et al: ACC/AHA 2006 Guidelines for the
management of patients with valvular heart disease: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol
2006;48:e1-e148.)
Fig. 1.14 Valvular aortic stenosis auscultatory features.
Fig. 1.15 Aortic ejection sound in a patient with a bicuspid aortic valve. S , rst heart sound;1
ES, ejection sound (red arrows) ; A2, aortic closure; P2, pulmonic closure; CAR, carotid pulse;
PA , pulmonic area, medium frequency; SB , left sternal border, medium frequency.MF MF
References
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2. Ward C. Clinical significance of the bicuspid aortic valve. Heart. 2000;83:81-85.
3. Larson EW, Edwards WD. Risk factors for aortic dissection: a necropsy study of 161 cases. Am J
Cardiol. 1984;53:849-855.
4. Wauchope GM. The clinical importance of variations in the number of cusps forming the aortic
and pulmonary valves. Quart J Med. 1928;21:383-399.
5. Gross L. So-called congenital bicuspid aortic valve. Arch Pathol. 1937;23:350-362.
6. Datta BN, Bhusnurmah B, Khatri HN, et al. Anatomically isolated aortic valve disease.
Morphologic study of 100 cases at autopsy. Jpn Heart J. 1988;29:661-670.
7. Pauperio HM, Azevedo AC, Ferreira C. The aortic valve with two leaflets. A study in 2000
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8. Basso C, Boschello M, Perrone C, et al. An echocardiographic survey of primary school children
for bicuspid aortic valve. Am J Cardiol. 2004;93:661-663.
9. Nistri S, Basso C, Marzari C, et al. Frequency of bicuspid aortic valve in young male conscripts by
echocardiogram. Am J Cardiol. 2005;96:718-721.
10. Sabet HY, Edwards WD, Tazelaar HD, et al. Congenitally bicuspid aortic valves: a surgical
pathology study of 542 cases (1991 through 1996) and a literature review of 2,715 additional
cases. Mayo Clin Proc. 1999;74:14-26.
11. Keane MG, Wiegers SE, Plappert T, et al. Bicuspid aortic valves are associated with aortic
dilatation out of proportion to coexistent valvular lesions. Circulation. 2000;102:1135-1139.
12. Chan KL, Ghani M, Woodend K, et al. Case-controlled study to assess risk factors for aortic
stenosis in congenitally bicuspid aortic valve. Am J Cardiol. 2001;88:690-693.
13. Feldman BJ, Khandheria BK, Warnes CA, et al. Incidence, description and functional assessment
of isolated quadricuspid valves. Am J Cardiol. 1990;65:937-938.
14. Timperly J, Milner R, Marshall AJ, Gilbert TJ. Quadricuspid aortic valves. Clin Cardiol.
2002;25:548-552.
15. Hurwitz LE, Roberts WC. Quadricuspid semilunar valve. Am J Cardiol. 1973;31:623-626.
16. Moore GW, Hutchins GM, Brito JC, et al. Congenital malformations of the semilunar valves.
Hum Pathol. 1980;11:367-372.
17. Simonds JP. Congenital malformations of the aortic and pulmonary valves. Am J Med Sci.
1923;166:584-595.
18. Novaro GM, Tiong IY, Pearce GL, et al. Features and predictors of ascending aortic dilatation in
association with a congenital bicuspid aortic valve. Am J Cardiol. 2003;92:99-101.
19. Olson LJ, Subramanian MB, Edwards WD. Surgical pathology of pure aortic insufficiency: a
study of 725 cases. Mayo Clin Proc. 1984;59:835-841.
20. Tutarel O. The quadricuspid aortic valve: a comprehensive review. J Heart Valve Dis.
2004;13:534-537.
21. Roberts WC, Ko JM, Matter GJ. Isolated aortic valve replacement without coronary bypass for
aortic valve stenosis involving a congenitally bicuspid aortic valve in a nonagenarian. Am J
Geriatr Cardiol. 2006;15:389-391.
22. Rosenhek R, Rader F, Loho N, et al. Statins but not angiotensin-converting enzyme inhibitors
delay progression of aortic stenosis. Circulation. 2004;110:1291-1295.
23. Bellamy MF, Pellikka PA, Klarich KW, et al. Association of cholesterol levels,
hydroxymethylglutaryl coenzyme A reductase inhibitor treatment, and progression of aorticstenosis in the community. J Am Coll Cardiol. 2002;40:1723-1730.
24. Mills P, Leech G, Davies M, et al. The natural history of a non-stenotic bicuspid valve. Br Heart
J. 1978;40:951-957.
25. Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 Guidelines for the management of
patients with valvular heart disease: a report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2006;48:e1-e148.
26. Lamas CC, Eykyn SJ. Bicuspid aortic valve—a silent danger: analysis of 50 cases of infective
endocarditis. Clin Infect Dis. 2000;30:336-341.
27. Dyson C, Barnes RA, Harrison GA. Infective endocarditis: an epidemiological review of 128
episodes. J Infect. 1999;38:87-93.
28. Fedak PW, Verma S, David TE, et al. Clinical and pathophysiological implications of a bicuspid
aortic valve. Circulation. 2002;106:900-904.
29. Gott VL, Greene PS, Alejo DE, et al. Replacement of the aortic root in patients with Marfan’s
syndrome. N Engl J Med. 1999;341:1473-1474.
30. Leggett ME, Unger TA, O’Sullivan CK, et al. Aortic root complications in Marfan’s syndrome:
identification of a lower risk group. Heart. 1996;75:389-395.
31. Devereux RB, Roman MJ. Aortic disease in Marfan’s syndrome. N Engl J Med.
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32. Ergin MA, Spielvoge D, Apaydin A, et al. Surgical treatment of the dilated ascending aorta:
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33. Svensson LG, Kim KH, Lytle BW, et al. Relationship of aortic cross-sectional area to height ratio
and the risk of aortic dissection in patients with bicuspid aortic valves. J Thorac Cardiovasc Surg.
2003;26:892-893.
34. Borger MA, Preston M, Ivanov J, et al. Should the ascending aorta be replaced more frequently
in patients with bicuspid aortic valve disease? J Thorac Cardiovasc Surg. 2004;128:677-683.
35. Isselbacher EM. Thoracic and abdominal aortic aneurysms. Circulation. 2005;111:816-828.
36. Fenoglio JJ, McAllister HA, DeCastro CM, et al. Congenital bicuspid aortic valve after age 20.
Am J Cardiol. 1977;39:164-169.
37. Roberts CS, Roberts WC. Dissection of the aorta associated with congenital malformation of the
aortic valve. J Am Coll Cardiol. 1991;17:712-716.
38. Gore I, Seiwert VJ. Dissecting aneurysm of the aorta, pathologic aspects: an analysis of
eightyfive fatal cases. Arch Pathol. 1952;53:121-141.
39. Edwards WD, Leaf DS, Edwards JE. Dissecting aortic aneurysm associated with congenital
bicuspid aortic valve. Circulation. 1978;57:1022-1025.
40. Liberthson RR, Pennington DG, Jacobs ML, et al. Coarctation of the aorta: review of 234
patients and clarification of management problem. Am J Cardiol. 1979;43:835-840.
41. Folger GMJr, Stein PD. Bicuspid aortic valve morphology when associated with coarctation of
the aorta. Cathet Cardiovasc Diagn. 1984;10:17-25.
42. Nihoyannopoulos P, Karas S, Sapsford RN, et al. Accuracy of two-dimensional echocardiography
in the diagnosis of aortic arch obstruction. J Am Coll Cardiol. 1987;10:1072-1077.
43. Huntington K, Hunter AG, Chan KL. A prospective study to assess the frequency of familial
clustering of congenital bicuspid aortic valve. J Am Coll Cardiol. 1997;30:1809-1812.
44. Warnes CA. Bicuspid aortic valve and coarctation: two villains part of a diffuse problem. Heart.
2003;89:965-966.45. Fernandes SM, Sanders SP, Khairy P, et al. Morphology of bicuspid aortic valve in children and
adolescents. J Am Coll Cardiol. 2004;44:1648-1651.
46. Waller BF, Carter JB, Williams HJJr, et al. Bicuspid aortic valve. Comparison of congenital and
acquired types. Circulation. 1973;48:1140-1150.+
+
Chapter 2
Aortic Stenosis Quantitation
Steven A. Goldstein, MD
Aortic stenosis is the most common valvular heart disease requiring valve
replacement. The indications for valve replacement depend on symptoms and
hemodynamic variables, such as aortic valve area (AVA) and transaortic gradients.
Therefore accurate hemodynamic evaluation of the aortic valve is important for
clinical decision-making. Transthoracic echocardiography (TTE) is used most
frequently in clinical practice to quantify the severity of aortic valve stenosis
because it is noninvasive, widely available, and generally reliable. With careful
attention to technique, an experienced echocardiography laboratory can accurately
measure transaortic pressure gradients and AVA in nearly all patients. The
accuracy of both Doppler-determined pressure gradients (using the Bernoulli
equation) and the calculation of AVA (using the continuity equation) is well
established and provides sufficient information in most instances.
However, these methods are limited in some patients with poor acoustic windows
1,2and by several technical issues. Some of the technical limitations and pitfalls are
listed in Table 2.1. A major source of error can result from imprecision in the
measurement of the cross-sectional area of the left ventricular out ow tract
(LVOT). Generally measured in the parasternal long-axis view, the LVOT diameter
can be di/ cult to measure in patients for whom limitations are imposed by poor
acoustic window(s) or those with heavy calcium deposits in the aortic annulus,
especially when the calcium extends onto the anterior mitral lea et. In the latter
1case, reverberations can obscure the true dimension. Moreover, the LVOT is
assumed to be circular, although this is not always the case. Furthermore, the LVOT
diameter can be di/ cult to measure in patients with subaortic obstruction. Another
important source of error is failure to display and measure the highest velocity
signals in either the LVOT or the transvalvular velocity. If the echo beam is not
parallel to the velocity jet, peak transvalve velocity is underestimated, and thus the
calculated peak and mean gradients also are underestimated. On occasion, when
the nonimaging transducer (Pedo4 transducer) is used, a mitral regurgitant jet or a
tricuspid regurgitant jet can be mistaken for the transvalvular aortic jet. This can
be recognized since generally both the mitral regurgitant and tricuspid regurgitant
jets are longer in duration and begin during isovolumic relaxation.
Table 2.1 Technical Limitations and Pitfalls of Quantitating Valvular Aortic Stenosisby Transthoracic Echo-Doppler
1. Intercept angle between AS jet and Doppler beam
2. Outflow tract diameter
• Heavily calcified aortic annulus
• Upper septal bulge (“sigmoid septum”)
3. Coexisting subaortic obstruction
4. Flow signal origin (AS vs. MR or TR)
5. Beat-to-beat variability (atrial fibrillation, PVCs)
AS, Aortic stenosis; MR, mitral regurgitation; PVCs, premature ventricular
contractions; TR, tricuspid regurgitation.
Indications for Transesophageal Echocardiography Planimetry
When the reliability of TTE in estimating the degree of aortic stenosis is questioned,
a second noninvasive modality may be necessary. Transesophageal
echocardiography (TEE), by providing superior image resolution, enables direct
3-11aortic valve planimetry in the majority of patients. The anatomic area
measured with multiplane TEE correlates well with calculation of AVA using the
4-811Gorlin formula at catheterization and with the continuity equation. In
another study, good correlation was also obtained when the planimetered valve
area was compared with direct intraoperative measurement of the anatomic area
12by the surgeon. The indications for use of TEE to assess the severity of aortic
stenosis are listed in Table 2.2.
Table 2.2 Indications for Using TEE to Assess Severity of Aortic Stenosis
1. Suboptimal transthoracic echo-Doppler study
a. Heavy aortic valve calcification, especially when extending onto base of
anterior mitral leaflet
b. Poor-quality LVOT velocity (V ) or transvalvular velocity (V )1 2
c. Coexisting subaortic obstruction
d. “Sigmoid” septum
2. Conflict between invasive and noninvasive date+
3. Patients undergoing CABG with coexisting aortic stenosis
CABG, Coronary artery bypass grafting; LVOT, left ventricular outflow tract.
Method for Optimal Transesophageal Echocardiography
Planimetry
Optimal positioning for planimetry of the aortic valve Brst requires visualization of
the aortic valve and ascending aorta in the long-axis view (usually between 100
and 150 degrees). Then the lea et tips should be positioned in the center of the
two-dimensional sector (to take advantage of axial resolution). With the TEE probe
held stable, the ultrasound beam should be electronically steered to obtain the
short-axis view of the aortic valve (generally 90 degrees less than the long-axis
view). The true short-axis of the aortic valve is between 30 and 60 degrees in most
cases; but in individual patients may be found anywhere between 0 and 90
degrees. Minimal probe manipulations are then made to ensure that the smallest
oriBce of the aortic valve (at its tips) is identiBed. In the optimal view for
planimetry, the aortic wall has a circular shape and all aortic cusps are visualized
simultaneously. Special care should be taken to optimize gain settings. The gain
should be reduced to the lowest value that permits complete delineation of the
cusps. Maximal opening of the aortic valve generally occurs in early systole. The
smallest oriBce during maximum opening of the aortic valve in systole should be
measured using a magniBed image in the zoom mode. The area can then be
measured by tracing the contours of the inner cusps with a digitizing caliper. It is
advisable to measure and average several consecutive beats. On occasion, color
Doppler can be useful in helping to identify the stenotic opening. It is important
that the minimal oriBce size be measured. This detail is particularly important in
congenital bicuspid aortic valves, in which case the smallest oriBce is at the apex of
a domed valve. Planimetry at a more basal level appears larger and can be
misleading. The feasibility of planimetry of the AVA by TEE is listed in Table 2.3.
Table 2.3 Feasibility of Planimetry of AVA by TEE
Author Year Feasibility (%)
Hofmann et al.3 1987 20/24 (83)
Stoddard et al.4 1991 64/67 (95)
Hoffmann et al.5 1993 38/41 (93)
Tribouilly et al.6 1994 51/55 (94)
Stoddard et al.9 1996 81/86 (94)+
+
+
+
Cormier et al.8 1996 41/45 (91)
Bernard et al.11 1997 48/52 (92)
Chandrasekaran et al.12 1991 85/95 (89)
Tardif et al.7 1995 32/32 (100)
Although the results obtained with TEE two-dimensional echocardiography
planimetry are encouraging, potential sources of error exist with this method.
Measuring the smallest AVA accurately requires the imaging plane to be located at
the tips of the valve lea ets. The longitudinal motion of the aortic root during the
cardiac cycle can make this di/ cult. ConBrmation that the image plane is
positioned at the smallest anatomic area is subjective and requires careful
manipulation of the TEE probe. Heavy calciBcation of the aortic valve also presents
problems. Acoustic shadowing behind the calciBcation often projects into the AVA,
resulting in gaps in the outline of the oriBce. In addition, prominent reverberations
may lead to underestimation of the AVA.
Gradients by Transesophageal Echocardiography
Measurement of gradients and valve area by the continuity equation by means of
TEE requires proper alignment of the continuous wave Doppler beam to obtain
peak aortic valve velocity. Although this measurement is di/ cult and technically
13,14 13demanding by TEE, it can be performed in many patients. Stoddard et al.
have demonstrated that a signiBcant learning curve exists, but this technique
14appears feasible in the majority of patients.
Continuous wave Doppler of the transaortic valve ow and pulsed wave Doppler
of the LVOT flow can be performed from at least two views:
1. Deep transgastric apical four-chamber view
2. Transgastric long-axis view
Ideally, the continuous wave cursor should be parallel to the aortic stenotic jet;
color ow Doppler can be used to assist this alignment. The diameter of the LVOT
can be measured from an esophageal long-axis view. The zoom mode can be used
to maximize the LVOT. The diameter of the LVOT should be measured immediately
beneath the insertion of the aortic valve lea ets in the LVOT during early systole
using the “inner edge–to–inner edge” technique.
The feasibility of this method is listed in Table 2.4. The feasibility, accuracy,
and reproducibility of measurements of the AVA are being evaluated by
three15-19 20-22dimensional echocardiography and magnetic resonance imaging.
Comparative studies among these different diagnostic methods are needed.Table 2.4 Feasibility of Determining AVA by TEE Using Continuity Equation
Author Year Feasibility (%)
Stoddard et al.14 1996 62/86 (72)
First 43 patients 24/43 (56)
Last 43 patients 38/43 (88)
Blumberg et al.14 1998 25/28 (89)
Reporting and Classification of Severity
The ACC/AHA Practice Guidelines, revised in 2006, recommend grading the
severity of aortic stenosis based on a variety of hemodynamic and natural history
data, using deBnitions of aortic jet velocity, mean pressure gradient, and AVA
23(Table 2.5). In applying these deBnitions, the examiner should recognize the
potential for imprecision in the measurements for both catheterization and
echoDoppler techniques. Therefore particular attention should be paid to the technical
quality of these studies in individual patients. In addition, transvalvular pressure
gradients depend on and vary with stroke volume. Decisions about intervention are
based predominantly on symptom status, and because symptom onset does not
correspond to a single hemodynamic value in all patients, no absolute breakpoints
define severity.
Table 2.5 Classification of the Severity of Aortic Stenosis in Adults
References
1. Zoghbi WA, Farmer KL, Soto JG, et al. Accurate noninvasive quantification of
stenotic valve area by Doppler echocardiography. Circulation. 1986;73:452-459.
2. Zhou YQ, Faerestrand S, Matre K. Velocity distributions in the left ventricularoutflow tract in patients with valvular aortic stenosis. Effect on the measurement
of aortic valve area by using the continuity equation. Eur Heart J.
1995;16:383393.
3. Hofmann T, Kasper W, Meinertz T, et al. Determination of aortic valve orifice area
in aortic valve stenosis by two-dimensional transesophageal echocardiography.
Am J Cardiol. 1987;59:330-335.
4. Stoddad MF, Arce J, Liddell NE, et al. Two-dimensional echocardiographic
determination of aortic valve area in adults with aortic stenosis. Am Heart J.
1991;122:1415-1422.
5. Hoffmann R, Flachskampf FA, Hanrath P. Planimetry of orifice area in aortic
stenosis using multiplane transesophageal echocardiography. J Am Coll Cardiol.
1993;22:529-534.
6. Tribouilloy C, Shen WF, Peltier M, et al. Quantitation of aortic valve area in aortic
stenosis with multiplane transesophageal echocardiography: comparison with
monoplane transesophageal approach. Am Heart J. 1994;128:526-532.
7. Tardif JC, Miller DS, Pandian NG, et al. Effects of variations in flow on aortic valve
area in aortic stenosis bases on in vivo planimetry of aortic valve area by
transesophageal echocardiography. Am J Cardiol. 1995;76:193-198.
8. Cormier B, Iung B, Porte JM, et al. Value of multiplane transesophageal
echocardiography in determining aortic valve area in aortic stenosis. Am J Cardiol.
1996;77:882-885.
9. Stoddard MF, Hammons RT, Longaker RA. Doppler transesophageal
echocardiographic determination of aortic valve area in adults with aortic
stenosis. Am Heart J. 1996;132:337-342.
10. Kim KS, Maxted W, Nanda NC, et al. Comparison of multiplane and biplane
transesophageal echocardiography in the assessment of aortic stenosis. Am J
Cardiol. 1997;79:436-441.
11. Bernard Y, Meneveau N, Vuillemenot A, et al. Is planimetry of aortic valve area
using multiplane transesophageal echocardiography a reliable method for
assessing severity of aortic stenosis? Heart. 1997;78:68-73.
12. Chandrasekaran K, Foley R, Weintraub A, et al. Evidence that transesophageal
echocardiography can reliably and directly measure the aortic valve area in
patients with aortic stenosis—a new application that is independent of LV
function and does not require Doppler data. J Am Coll Cardiol. 1991;17(Suppl
A):20A.
13. Stoddard MF, Prince CR, Ammash N, et al. Pulsed Doppler transesophageal
echocardiographic determination of cardiac output in human beings: comparison
with thermodilution technique. Am Heart J. 1993;126:956-962.
14. Blumberg FC, Pfeifer M, Holmer SR, et al. Quantification of aortic stenosis in
mechanically ventilated patients using multiplane transesophageal Dopplerechocardiography. Chest. 1998;114:94-97.
15. Nanda NC, Roychoudhry D, Chung S, et al. Quantitative assessment of normal and
stenotic aortic valve using transesophageal three-dimensional echocardiography.
Echocardiography. 1994;11:617-625.
16. Menzel T, Mohr-Kahaly S, Kolsch B, et al. Quantitative assessment of aortic
stenosis by three-dimensional echocardiography. J Am Soc Echocardiogr.
1997;10:215-223.
17. Kasprzak JD, Nosir YFM, dall’Agata A, et al. Quantification of the aortic valve
area in three-dimensional echocardiographic datasets: analysis of orifice
overestimation resulting from suboptimal cut plane selection. Am Heart J.
1998;135:995-1003.
18. Ge S, Warner JGJr, Abraham TP, et al. Three-dimensional surface area of the
aortic valve orifice by three-dimensional echocardiography: clinical validation of
a novel index for assessment of aortic stenosis. Am Heart J. 1998;136:1042-1050.
19. Handke M, Shafer DM, Heinrichs G, et al. Quantitative assessment of aortic
stenosis by three-dimensional anyplane and three-dimensional volume-rendered
echocardiography. Echocardiography. 2002;19:45-53.
20. Friedrich MG, Schulz-Menger J, Poetsch T, et al. Quantification of valvular aortic
stenosis by magnetic resonance imaging. Am Heart J. 2002;144:329-334.
21. John AS, Dill T, Brandt RR, et al. Magnetic resonance to assess the aortic valve
area in aortic stenosis: how does it compare to current diagnostic standards? J Am
Coll Cardiol. 2003;42:519-526.
22. Kupfahl C, Honold M, Meinhardt G, et al. Evaluation of aortic stenosis by
cardiovascular magnetic resonance imaging: comparison with established routine
clinical techniques. Heart. 2004;90:893-901.
23. Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 Guidelines for the
management of patients with valvular heart disease: a report of the American
College of Cardiology/American Heart Association Task Force on Practice
Guidelines. J Am Coll Cardiol. 2006;48:e1-e148.Chapter 3
Aortic Stenosis
Subaortic Membrane
Vera Lennie, MD, José Luis Zamorano Gomez, MD
Subvalvular (subaortic) stenosis (SAS) is the second most common form of aortic
stenosis. It is considered an acquired lesion with genetic predisposition because it is
rarely found in the embryologic or neonatal period (Table 3.1). Up to 50% of all
cases are associated with other congenital abnormalities (ventricular septal defect,
aortic coarctation, atrioventricular septal defect, patent ductus arteriosus, bicuspid
1aortic valve). SAS can develop after acquired heart diseases in rare instances.
Table 3.1 Subaortic Stenosis: Summary
Acquired lesion With strong genetic predisposition
ECHOCARDIOGRAPHIC FINDINGS
Morphology (classification)
Congenital defects (50%)
LVOT obstruction: severity
Aortic regurgitation
DIFFERENT NATURAL HISTORY DEPENDING ON AGE
Children: rapid hemodynamic deterioration
Adults: slow course
INDICATIONS FOR SURGERY: CONTROVERSIAL
Children: LVOT obstruction >30 mm Hg
Adults: LVOT obstruction >40 mm Hg
High incidence of recurrencesSurgery does not prevent the appearance of AR
Morphologic Variants of Subaortic Membrane
An extensive range of lesions has been described to cause SAS. The classi8cation
has always been controversial. Kelly’s morphologic classi8cation in type I (thin
2membrane) and type II (8bromuscular stenosis) lesions is currently underused.
3Choi and Sullivan presented a classification based on echocardiographic features:
1. Short-segment subaortic obstruction (length less than one third of the aortic
valve diameter) includes previous membranous, diaphragmatic, discrete, fixed,
fibrous, or fibromuscular stenosis. Short-segment obstruction can be complete
(annular) or incomplete (semilunar) (Fig. 3.1), as well as fibrous or muscular
(Fig. 3.2).
2. Long-segment subaortic obstruction (length greater than one third of the aortic
valve diameter) is usually tunnel-like and diffuse. It usually coexists with
hypoplasia of the aortic valve annulus (Fig. 3.3).
3. SAS can result from a malalignment of septal structures in the presence of a
ventricular septal defect (VSD) (Fig. 3.4). It can include a posterior malalignment
with obstruction above the VSD, usually associated with aortic arch interruption,
and anterior malalignment with obstruction below the VSD.
4. SAS resulting from atrioventricular valve tissue in the left ventricular outflow
tract (LVOT) (Fig. 3.5) includes accessory mitral valve tissue, anomalous
attachment of mitral valve chordae, tricuspid valve tissue prolapsing through a
VSD, and abnormal left atrioventricular valve in the atrioventricular septal defect
(AVSD).Fig. 3.1 Subaortic membrane (short segment).
Fig. 3.2 Muscular membrane.Fig. 3.3 Tunnel-like subaortic membrane (long segment).
Fig. 3.4 Subaortic stenosis caused by malalignment of septal structures in the
presence of a ventricular septal defect. RA, Right atrium; LA, left atrium; RV, right
ventricle; VSD, ventricular septal defect; LV, left ventricle.?
Fig. 3.5 Subaortic stenosis resulting from atrioventricular valve tissue in the left
ventricular out ow tract. RA, Right atrium; LA, left atrium; RV, right ventricle; LV,
left ventricle.
The clinical features of SAS are determined by the severity of the LVOT
obstruction. Patients with mild gradients normally have no symptoms; the defect is
often diagnosed when proceeding for surgery of another congenital defect. In
patients with symptoms, the most common presentation is limited exercise
4tolerance, but syncope and angina pectoris have also been described.
Diagnosis
On physical examination, a “harsh” systolic ejection murmur—best heard at the
left sternal border—is characteristically found. A thrill can be palpable in the same
position. An early diastolic murmur is also present in cases of aortic regurgitation.
The diagnosis through physical examination remains a challenge because this
feature can also be found in other causes of LVOT obstruction. The
electrocardiographic 8ndings are usually abnormal, with nonspeci8c 8ndings
including left ventricular hypertrophy (LVH), strain patterns, and left atrial
enlargement. Chest radiographic findings are often normal.
The echocardiogram is the cornerstone of diagnosis of SAS. It de8nes the
anatomy and type of defect as well as functioning of the LVOT. Associated cardiac
defects can also be diagnosed with this imaging technique. The objective?
?
?
measurements of systolic Doppler pressure gradient, aortic regurgitation, or mitral
regurgitation are vital to establishing patient treatment and follow-up. If surgery
has already been performed, the echocardiogram should help the physician to
determine the type of intervention (simple resection, myotomy, myectomy, Konno’s
intervention, valve prosthesis, and so on) and rule out the existence of iatrogenic
VSD.
Three-Dimensional Echocardiography of the Subaortic Membrane
Two-dimensional (2-D) transthoracic echocardiography (TTE) and transesophageal
echocardiography (TEE) are the standard techniques for diagnosing SAS. However,
these methods are often limited in their ability to visualize the details of SAS and
5the LVOT. Three-dimensional TEE can accurately diagnose and measure SAS and
6in the future could be a useful tool for guiding transcatheter interventions. The
“aortotomy view” just below the plane of the aortic valve provides an excellent
perspective for assessing the entire SAS and quantifying the LVOT obstruction by
7planimetry.
Cardiac catheterization was the classic technique for diagnosis of SAS before the
development of 2-D echocardiography. Catheterization provides anatomic and
hemodynamic data but lacks good de8nition of small anatomic structures and
assessment of mitral apparatus. The measurement of the peak-to-peak gradient at
catheterization has no good correlation with the maximum instantaneous gradient
8of the echocardiogram, and therefore these should not be compared. The Doppler
mean pressure gradient correlated well with mean pressure gradient measured at
9catheterization, as Bengur et al. studied. The presence of low cardiac output or
arrhythmias could mask the presence of signi8cant gradient across the LVOT.
10Leichter, Sullivan, and Gersony described 35 patients with no signi8cant LVOT
obstruction at initial cardiac catheterization but who later were shown to have
signi8cant SAS. Today catheterization is performed only when multiple levels of
obstruction are suspected.
Pathophysiology and Natural History
The development of a subaortic lesion is genetically in uenced. Nevertheless,
various abnormal ow patterns are believed to take part in the process: septal
ridge, malalignment of the septum, elongated or hypoplastic LVOT, apical
4muscular band, an abnormality between the LVOT axis and aortic axis, and so on.
All such phenomena have the potential to harm the endothelium of the LVOT,
where 8brosis would take place as a result of the chronic contact with the ow. As
a result, a 8brous or muscular structure would display in the LVOT, causing the
clinical and hemodynamic compromise.?
Progression of SAS occurs, but the rate is variable and the factors in uencing it
are unknown. SAS usually causes LVOT obstruction of various degrees. If it
manifests during early childhood, it is normally accompanied with a rapid
hemodynamic worsening of symptoms and more severe gradient of LVOT
obstruction. In adults, it can have a slow course (over several decades). Therefore
SAS in patients with initially mild stenosis is likely to progress less rapidly than in
those who initially have a higher gradient. Patients with an increasing gradient
need early surgery, but surgery in mild cases may be delayed if close follow-up can
11be ensured.
Aortic regurgitation (AR) is present in half of patients with SAS but is usually
mild. The mechanism is thought to be damage to the aortic valve resulting from the
repetitive trauma of the subvalvular jet or direct extension of subvalvular tissue
4 12into the aortic valve. AR is also associated with bicuspid aortic valve. The
existing literature shows correlation between the severity of stenosis and the
12severity of AR in both children and in adults. However, Oliver et al. found no
relationship between AR and age. Surgical repair in children does not prevent the
development of AR in adults. It appears that signi8cant AR is more likely to be
found in patients who have undergone surgical intervention than those who have
not had surgery. In some annular forms, extension to the anterior mitral leaflet may
exist, causing various degrees of fibrosis and deficits in coaptation. This extension is
believed to be related to longer distances from the membrane to the valves.
A high rate of restenosis after surgery also has been reported. The simple
resection of the ridge renders it more likely to develop restenosis (the ventricular
geometry has not been modi8ed and the hemodynamics of the forces continue to
act the same way). In some cases, SAS appears after VSD repair; the risk of
endocarditis is especially high among these patients.
Impact of Echocardiographic Findings on Therapeutic Strategies
The decision whether to perform corrective surgery should be based on the
presence of LVH, left ventricular ejection fraction, severity of LVOT obstruction,
AR, and patient age. The optimal surgical timing remains highly controversial. In
patients with severe obstruction (gradient >40 mm Hg), surgery is the
recommended option. An infant or child with a gradient of 30 mm Hg or more also
should have removal of the subvalvular obstruction. If the gradient is less but the
presence of LVH is important, surgery should also be considered. Children with
mild gradients should have close follow-up to monitor progression. The same
guideline is applicable for adults with stable gradients (
SAS often recurs after surgical resection and early surgery does not prevent it.
Reoperation rates vary from 4% to 35%. The higher the preoperative gradient, the13higher the recurrence rate. Various studies have shown no clinical bene8t for
14early surgery in patients with mild gradients.
References
1. Cilliers AM, Gewillig M. Rheology of discrete subaortic stenosis. Heart.
2002;88:335336.
2. Kelly DT, Wulfsberg E, Rowe RD. Discrete subaortic stenosis. Circulation.
1972;46:309-322.
3. Choi JY, Sullivan ID. Fixed subaortic stenosis: anatomical spectrum and nature of
progression. Br Heart J. 1991;65:280-286.
4. Darcin OT, Yagdi T, Atay Y, et al. Discrete subaortic stenosis. Tex Heart Inst J.
2003;30:286-292.
5. Miyamoto K, Nakatani S, Kanzaki H, et al. Detection of discrete subaortic stenosis
by 3-dimensional transesophageal echocardiography. Echocardiography.
2005;22:783-784.
6. Ge S, Warner JG, Fowler KM, et al. Morphology and dynamic change of discrete
subaortic stenosis can be imaged and quantified with three-dimensional
transesophageal echocardiography. J Am Soc Echocardiogr. 1997;10:713-716.
7. Agrawal GG, Nanda NN, Htay T, et al. Live three-dimensional transthoracic
echocardiographic identification of discrete subaortic membranous stenosis.
Echocardiography. 2003;20:617-619.
8. Currie PJ, Hagler DJ, Seward JB, et al. Instantaneous pressure gradient: a
simultaneous Doppler and dual catheter correlative study. J Am Coll Cardiol.
1986;7:800-806.
9. Bengur AR, Snider AR, Serwer GA, et al. Usefulness of the Doppler mean gradient in
evaluation of children with aortic stenosis and comparison to gradient at
catheterisation. Am J Cardiol. 1989;64:756-761.
10. Leichter DA, Sullivan I, Gersony WM. “Acquired” discrete subvalvular aortic
stenosis: natural history and hemodynamics. J Am Coll Cardiol.
1989;14:15391544.
11. Gersony WM. Natural History of discrete subvalvular aortic stenosis: management
implications. J Am Coll Cardiol. 2001;38:843-845.
12. Oliver JM, González A, Gallego P, et al. Discrete subaortic stenosis in adults:
increased prevalence and show rate of progression of the obstruction and aortic
regurgitation. J Am Coll Cardiol. 2001;38:835-842.
13. Brauner R, Laks H, Drinkwater DC, et al. Benefits of early surgical repair in fixed
subaortic stenosis. J Am Coll Cardiol. 1997;30:1835-1842.
14. Kitchiner D. Subaortic stenosis: still more questions than answers. Heart.
1999;82:647-648.Chapter 4
Aortic Stenosis With Low Gradient and Poor Left
Ventricular Dysfunction
Alan S. Pearlman, MD, FASE
The majority of patients with valvular aortic stenosis (AS) have preserved systolic
left ventricular (LV) function. Occasionally, however, a patient with AS has
substantial depression of LV function, a low ejection fraction (EF), and a low
transvalvular pressure gradient (PG).
1More than 25 years ago, Carabello et al. demonstrated that while surgical aortic
valve replacement (AVR) was likely to bene- t patients with AS, depressed LVEF,
and a mean systolic PG greater than 30 mm Hg, the results were poor and the risk
of AVR was high in patients with AS who had depressed LVEF and a PG less than or
2equal to 30 mm Hg. Subsequently, Cannon et al. described a small group of
patients with apparently severe AS who were referred for AVR; in these patients,
valve inspection during surgery demonstrated only mild AS. These patients were
deemed to have “pseudo-AS,” with reduced systolic opening of the valve lea6ets
caused by low forward stroke volume. In this setting, the calculated aortic valve
ori- ce area (AVA) was small not because of severe AS, but because of depressed LV
function.
Because AVR surgery is clearly indicated in patients with severe AS who have
3symptoms of angina, syncope, or heart failure and in those with depressed LVEF,
it is important to identify those patients with LV dysfunction caused by severe AS
and to distinguish them from patients with primary LV dysfunction and mildly
thickened aortic lea6ets, in whom a reduced AVA and low PG are due to—and not
the cause of—depressed LV function.
Pathophysiology
Valvular AS resulting from calci- cation of a bicuspid or trilea6et valve is
characterized by reduced mobility of the aortic valve lea6ets, with decreased
systolic opening and increased resistance to LV ejection. Typically, LV hypertrophy
(LVH) develops over time and results in increased systolic LV pressure, generally
maintaining LV wall stress, forward stroke volume, and LVEF at the expense of
increased LV mass. LVH may also cause diastolic dysfunction. In severe AS, mean
2 3transvalvular gradients typically are greater than 40 mm Hg, and AVAs are . Insome patients, however, chronic increases in LV work because the the resistance of
the stenotic aortic valve leads to reduced LVEF; this phenomenon has been termed
4afterload mismatch. In such patients, forward stroke volume declines, as do
transvalvular gradients. Because transvalvular PGs vary directly with forward
volumetric 6ow, and inversely with AVA, mean gradients are typically less than
30 mm Hg in patients with severe AS and depressed LV function caused by
afterload mismatch.
Patients with primary LV contractile dysfunction (due to coronary artery disease
or a nonischemic cardiomyopathy) also will have depressed LVEF and reduced
forward stroke volume. In such patients, if the aortic valve lea6ets become
thickened and mildly to moderately stenotic, the valve opening is markedly
reduced as a result of LV dysfunction, and not as its cause. Note that valve lea6et
opening (even in normal valves) is caused by transvalvular 6ow—the valve lea6ets
open widely enough and stay open long enough to allow the volume of 6ow to pass
through. Thus a patient with intrinsic LV dysfunction, a low EF, and abnormal
(though not severely stenotic) aortic lea6ets also may have an AVA less than
21.0 cm and a mean gradient less than 30 mm Hg. Distinguishing the patient with
severe AS causing LV dysfunction from the patient with LV dysfunction and
coexisting mild to moderate AS is an important diagnostic challenge. Data from a
patient that illustrate this dilemma are shown in Fig. 4.1.
Fig. 4.1 Transthoracic echocardiographic and Doppler data obtained at rest from
an 85-year-old man with progressive dyspnea and evidence of AS on physicalexamination. Real-time imaging demonstrated aortic valve calci- cation and
reduced lea6et opening during systole, as well as impaired LV systolic function
(ejection fraction, 23%). By using the continuity equation and the measures of LV
out6ow tract diameter (upper left) and velocity-time integrals (VTI) in the LV
outflow tract (lower left) and across the stenotic valve (lower right), aortic valve area
was calculated as 0.44 cm2. The mean transvalvular gradient was 23 mm Hg. These
data show apparent severe AS, despite being of low gradient, in a patient with
depressed LV function.
Diagnosis
Although it is possible to evaluate AS severity by left heart catheterization, this
approach is used infrequently in most contemporary practices. Instead, Doppler
ultrasonography is used to measure peak instantaneous and mean transvalvular PG
5and to determine AVA using the continuity equation. When transthoracic
echocardiography cannot assess AS severity (usually because of poor image
quality), transesophageal echocardiography can be used to visualize and measure
6AVA by planimetry. In a patient with LV dysfunction, low EF, and calci- ed aortic
valve lea6ets with a small calculated AVA, resting hemodynamics do not
distinguish severe AS with afterload mismatch from pseudo-AS with LV
dysfunction.
In this case, evaluation of aortic valve hemodynamics using Doppler techniques
during dobutamine infusion is quite valuable. The feasibility, safety, and potential
7applicability of this approach were - rst described by DeFilippi et al. in 1995.
Using incremental doses of intravenous dobutamine (from 5 to 20 mcg/kg/min)
and monitoring heart rate, blood pressure, heart rhythm, and LV wall motion
carefully, these investigators demonstrated improvement in EF in some, but not all,
of their patients. Doppler echocardiography demonstrated increases in PG and AVA
in patients with, but not in those without, “contractile reserve” (CR). Figs. 4.2 and
4.3 show an example of changing Doppler hemodynamics in a patient with
lowgradient AS in whom dobutamine infusion demonstrated contractile reserve. In a
subsequent report, 8 dobutamine infusion was used in the cardiac catheterization
laboratory in patients with low-gradient AS, and some of these patients underwent
subsequent AVR. Those with CR had much lower perioperative mortality than
those without CR (7% vs. 33%).Fig. 4.2 Transthoracic echocardiographic and Doppler data obtained from the
same patient in Figure 4.1 during dobutamine infusion. Real-time imaging
demonstrated an improvement in contractile function with ejection fraction
measured at 36%. Doppler velocity-time integrals (VTI) in the LV out6ow tract
(lower left) have more than doubled, indicating an improvement in stroke volume.
By using the continuity equation, aortic valve area was calculated as 0.7 cm2, and
the mean transvalvular gradient was 41 mm Hg.
Fig. 4.3 Comparison of hemodynamic data obtained from the same patient in
Figures 4.1 and 4.2 obtained at rest (left column) and during dobutamine infusion(right column). During adrenergic stress, contractile reserve is evident, with an
increase in the left ventricular ejection fraction and velocity-time integrals
measured in the left ventricular outflow tract (this is a surrogate for stroke volume).
With increased transvalvular volume 6ow, the peak and mean pressure gradients
(ΔP) increase. Aortic valve area (AVA) also increases but remains in the critical
range. These - ndings demonstrate severe aortic stenosis with depressed left
ventricular function at rest, and a low gradient as a consequence, as well as
contractile reserve with dobutamine infusion. VTI , Flow-velocity integral ofLVOT
the left ventricular outflow tract; LVEF, left ventricular ejection fraction.
Treatment
AVR is clearly indicated in patients with severe AS causing symptoms of angina,
syncope, or heart failure and in those with AS and afterload mismatch and
3depressed LV function. The role of AVR in patients with low-gradient AS has been
1more controversial. Carabello et al. reported high perioperative mortality and
poor outcomes in a small group of patients with low-gradient AS who underwent
AVR in the 1970s. Other investigators also reported high perioperative mortalities
8-10in patients with low-gradient AS, although results were better in those patients
8in whom CR was demonstrated.
The importance of CR, the role of dobutamine stress hemodynamics, and the
outcome after AVR has been evaluated by a recent French multicenter study.
11Monin and colleagues evaluated 136 patients with low-gradient AS and used
dobutamine stress hemodynamics to determine the presence or absence of CR
(de- ned as >20% increase in stroke volume). Perioperative mortality (within 30
days of AVR) was 5% in patients with CR and 33% in those without CR. These
investigators also demonstrated that Kaplan-Meier survival curves were
signi- cantly better in patients with CR who underwent AVR compared with those
with CR but treated medically. Survival was worse in patients without CR than in
those with CR; again, patients without CR who nevertheless underwent AVR
demonstrated better survival than those treated medically; prognosis was extremely
poor in the latter group.
The same group of French investigators has published the results of
intermediate12term follow-up after AVR in patients with low-gradient AS. In 80 such patients,
perioperative deaths were noted in 6% of those with CR and in 33% of those
without CR on preoperative evaluation using dobutamine stress Doppler
hemodynamics. Survivor follow-up averaged 26 months, and improvement was the
norm. New York Heart Association heart failure symptoms improved by at least one
class in 94% of patients, and average EF increased from 29% preoperatively to
47% after AVR. Although operative risk was high in patients with low-gradient ASundergoing AVR, survivors did well. Survival at 2 years was 90% in those with
preoperative CR and 92% in those without preoperative CR. When AVR survivors
with CR were compared with those without CR, no signi- cant diKerences were
noted in the percentage of patients in whom functional class improved, or in the
frequency and degree of improvement in EF. On multivariate analysis, patients
with low preoperative PG and those with multivessel coronary artery disease were
less likely to demonstrate an improved EF during follow-up. Key study - ndings are
summarized in Table 4.1.
Summary of Key Points From a French Multicenter Study12Table 4.1
With Contractile
Variable No Contractile Reserve
Reserve
Δ Stroke volume with >20% increase <_2025_>
dobutamine infusion 5 →
20 mcg/kg/min
Perioperative mortality rate 5% 32%
(AVR)
Improved NYHA class post- 96% 90%
AVR
Change in LVEF post-AVR 28% → 47% 31% → 48%
AVR indicated Yes; reasonable Probably; high risk but good
risk and good outcome, dismal results
outcome without AVR
AVR, Aortic valve replacement; NYHA, New York Heart Association; LVEF, left
ventricular ejection fraction.
From Quere J-P, Monin J-L, Levy F, et al. Influence of preoperative left ventricular
contractile reserve on postoperative ejection fraction in low-gradient aortic stenosis.
Circulation 2006;113:1738-1744.
These results indicate that dobutamine stress hemodynamics are helpful in
determining operative risk in patients with low-gradient AS and con- rm that
perioperative death is much less likely in those with CR. However, most survivors of
AVR demonstrate clinical improvement. Since prognosis is “abysmal” in patients
with low-gradient AS who do not show CR on dobutamine stress hemodynamic
13testing, it seems reasonable to consider such patients for AVR.
References1. Carabello BA, Green LH, Grossman W, et al. Hemodynamic determinants of
prognosis of aortic valve replacement in critical aortic stenosis and advanced
congestive heart failure. Circulation. 1980;62:42-48.
2. Cannon JD, Zile MR, Crawford FAJr, et al. Aortic valve resistance as an adjunct to
the Gorlin formula in assessing the severity of aortic stenosis in symptomatic
patients. J Am Coll Cardiol. 1992;20:1517-1523.
3. Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the
management of patients with valvular heart disease: a report of the American
College of Cardiology/American Heart Association Task Force on Practice
Guidelines. Circulation. 2006;114:e84-e231.
4. Ross JJr. Afterload mismatch and preload reserve: a conceptual framework for the
analysis of ventricular function. Prog Cardiovasc Dis. 1976;18:255-264.
5. Otto CM, Pearlman AS, Comess KA, et al. Determination of the stenotic aortic valve
area in adults using Doppler echocardiography. J Am Coll Cardiol..
1986;7:509517.
6. Hoffmann R, Flachskampf FA, Hanrath P. Planimetry of orifice area in aortic
stenosis using multiplane transesophageal echocardiography. J Am Coll Cardiol..
1993;22:529-534.
7. DeFilippi CR, Willett DL, Brickner E, et al. Usefulness of dobutamine
echocardiography in distinguishing severe from nonsevere valvular aortic stenosis
in patients with depressed left ventricular function and low transvalvular
gradients. Am J Cardiol. 1995;75:191-194.
8. Nishimura RA, Grantham JA, Connolly HM, et al. Low-output, low-gradient aortic
stenosis in patients with depressed left ventricular systolic function—the clinical
utility of the dobutamine challenge in the catheterization laboratory. Circulation.
2002;106:809-813.
9. Brogan WC, Grayburn PA, Lange RA, et al. Prognosis after valve replacement in
patients with severe aortic stenosis and a low transvalvular pressure gradient. J
Am Coll Cardiol. 1993;21:1657-1660.
10. Connolly HM, Oh JK, Schaff HV, et al. Severe aortic stenosis with low
transvalvular gradient and severe left ventricular dysfunction: result of aortic
valve replacement in 52 patients. Circulation. 2000;101:1940-1946.
11. Monin J-L, Quere J-P, Monchi M, et al. Low-gradient aortic stenosis. Operative
risk stratification and predictors for long-term outcome: a multicenter study using
dobutamine stress hemodynamics. Circulation. 2003;108:319-324.
12. Quere J-P, Monin J-L, Levy F, et al. Influence of preoperative left ventricular
contractile reserve on postoperative ejection fraction in low-gradient aortic
stenosis. Circulation. 2006;113:1738-1744.
13. Lange RA, Hillis LD. Dobutamine stress echocardiography in patients with
lowgradient aortic stenosis. Circulation. 2006;113:1718-1720.


Chapter 5
Asymptomatic Severe Aortic Stenosis
Helmut Baumgartner, MD
Aortic stenosis (AS) has become the most frequent valvular heart disease and the
most frequent cardiovascular disease after hypertension and coronary artery
disease in Europe and North America. In the adult population, it primarily presents
as calci c AS at advanced age. The prevalence in the population older than 65
years has been reported in the range of 2% to 7% and aortic sclerosis, the precursor
1of AS, has been found in 25%.
The characteristic systolic murmur of AS generally rst draws attention and
guides the further diagnostic workup into the right direction. Doppler
echocardiography is the ideal tool to con rm diagnosis and quantify AS by
calculating pressure gradients (Fig. 5.1) and valve area.
Fig. 5.1 Continuous wave Doppler recordings of an asymptomatic patient with
severe aortic stenosis. Note that the recording from a right parasternal approach
(lower panel) yields signi cantly higher velocities (peak velocity, 5.3 m/s; mean
gradient, 75 mm Hg) than that from an apical approach (4.6 m/s, 54 mm Hg).
During the long latent period with increasing out1ow tract obstruction that
results in increasing left ventricular (LV) pressure load, patients remain
asymptomatic and acute complications are rare. However, outcome becomes
dismal as soon as symptoms such as exertional dyspnea, angina or dizziness, and
syncope occur. Average survival after the onset of symptoms has been reported as
2less than 2 to 3 years. In this situation, valve replacement not only results in
2dramatic symptomatic improvement but also in good long-term survival. This
improvement applies even for patients with already reduced LV function, as long as
functional impairment is indeed caused by AS. Thus there is consensus that urgent
3,4surgery must be strongly recommended in symptomatic patients. In contrast, the
2,3management of asymptomatic patients with severe AS remains controversial.





Because of the widespread use of Doppler echocardiography it is estimated that
about 50% of patients who come to medical attention with severe AS still have no
symptoms. Thus cardiologists are increasingly faced with the di9 cult decision
whether to perform surgery in asymptomatic patients with severe AS. Several
criteria including ndings of echocardiography and exercise testing have been
proposed for risk strati cation. Potential arguments for surgery in asymptomatic AS
must be reviewed before discussing the value of the risk stratification criteria.
Potential Arguments for Surgery in Asymptomatic Aortic Stenosis
Risk of Sudden Cardiac Death
Sudden death is probably the major concern when asymptomatic patients with
severe AS are monitored conservatively. However, this risk appears to be low. In
addition to several studies that included patients with nonsevere AS and no sudden
deaths, two prospective studies report the outcome of sizable cohorts of patients
5with exclusively severe AS (peak aortic jet velocity ≥4.0 m/s): Pellikka et al.
observed two sudden deaths among 113 patients during a mean follow-up of 20
months. Both patients, however, had experienced symptoms at least 3 months
before death. We have reported one sudden death that was not preceded by any
6symptoms among 104 patients with 27 months of average follow-up. In a recent
retrospective study of 622 patients with a mean follow-up of 5.4 ± 4.0 years,
7Pellikka et al. reported the rate of sudden death as 1% per year. However, in
almost half of these sudden deaths, information on patients’ status was missing for
the last year before death. Furthermore, a small but still signi cant risk of sudden
death (0.3% to 0.4%) has been reported even after surgery, at least for congenital
8AS. Thus prevention of sudden death is not a strong argument for surgery in
asymptomatic patients.
Unfortunately, patients do not always promptly report their symptoms. In
addition, in some countries patients must wait several months for surgery.
However, mortality has been reported as already quite signi cant within the
9months following symptom onset. In a Scandinavian study, for example, 7 of 99
patients with severe AS who were scheduled for surgery died during an average
waiting period of 6 months.
Risk of Irreversible Myocardial Damage
In contrast to valvular regurgitation, patients with asymptomatic severe AS in
whom impaired systolic LV function has already developed are rare. It has been
speculated, however, that myocardial brosis and severe LV hypertrophy that may
not be reversible after delayed surgery could preclude an optimal postoperative
3long-term outcome. To date, no data exist to con rm this hypothesis, and the






excellent outcome after valve replacement in patients with isolated AS with normal
systolic LV function raises doubts that the risk of developing irreversible
hypertrophy and myocardial brosis during the asymptomatic phase may bolster
the argument for surgery in asymptomatic patients. Further studies are required to
clarify this question.
Surgical Considerations
Patients with severe symptoms have a signi cantly higher operative mortality than
those with no or only mild symptoms. According to the Society of Thoracic
Surgeons U.S. cardiac surgery database 1997, patients in New York Heart
Association (NYHA) classes I or II had an operative mortality of less than 2%
compared with 3.7% and 7.0% for patients in NYHA classes III and IV,
10respectively. In addition, urgent or emergent valve replacement carries a
10signi cantly higher risk than elective surgery. Nevertheless, operative risk—even
if small—must always be weighed against the potential bene t(s). Although
operative mortality can ideally range from 1% to 3%, it may be as high as 10% in
older patients and even markedly higher in the presence of signi cant additional
11comorbidity. Even more important, not only must operative risk be considered
but also prosthetic valve–related long-term morbidity and mortality.
Thromboembolism, bleeding, endocarditis, valve thrombosis, paravalvular
regurgitation, and valve failure occur at the rate of at least 2% to 3% per year, and
death directly related to the prosthesis has been reported at a rate of up to 1% per
3year.
Duration of the Asymptomatic Phase
Some studies reported a rapid disease progression and thus poor outcome with up
12to 80% of the patients requiring valve replacement within 2 years. Such
observations have also questioned the bene t of delaying surgery in
stillasymptomatic patients. However, other investigators have reported better overall
outcomes with individual outcome varying widely. For example, survival without
surgery or with eventual valve replacement indicated by the development of
symptoms was 56% ± 5% at 2 years in our series of asymptomatic patients with
6severe AS. These discrepant results may be explained by the fact that in some
studies patients underwent surgery without having preoperative symptoms
developed while these interventions were, nevertheless, counted as events. Thus the
event-free survival reported in the literature should be viewed with caution.
Predictors of Outcome and Risk Stratification in Asymptomatic
Severe Aortic Stenosis
Because it appears unlikely from current data that the potential bene t of valve













replacement can outweigh the risk of surgery and the long-term risk of
prosthesisrelated complications in all asymptomatic patients, surgery is not generally
3,4recommended in patients with AS before symptom onset. In particular, the fact
that patients frequently do not present immediately when symptoms develop and
that some may need to wait some time for surgery while symptoms are present
represents signi cant risk. The ideal approach would be to refer patients for
surgery just before symptom onset. Echocardiography and exercise testing have
been of value with this regard.
Rest Echocardiography
Among the rest echocardiographic parameters, peak aortic jet velocity, aortic valve
area, the rate of hemodynamic progression, and left ventricuclar hypertrophy and
4ejection fraction have been identi ed as independent predictors of outcome.
However, these ndings were obtained retrospectively and do not allow any
speci c recommendations on prospective selection of high-risk patients who may
3,4benefit from early elective surgery.
Aortic valve calci cation has become a powerful independent predictor of
6outcome. Event-free survival at 4 years was 75% ± 9% in patients with no or
only mild calci cation versus 20% ± 5% in those with moderately or severely
calci ed valves (Fig. 5.2). The worse outcome in patients with more severe
calci cation appeared to be paralleled by a more rapid hemodynamic progression.
However, even in the presence of calci cation the rate of hemodynamic
2,6progression varies widely. In fact, the hemodynamic progression as determined
by serial echocardiographic examination appears to yield important prognostic
information beyond the degree of calci cation. The combination of a markedly
calci ed valve with a rapid increase in velocity of 0.3 m/s or greater from one visit
to the next one scheduled within 1 year has identi ed a high-risk group of patients.
Approximately 80% of patients so identi ed required surgery or died within 2
6years. This criterion has been included in the European recommendations as a IIa
4indication for valve replacement, whereas the American College of
Cardiology/American Heart Association (ACC/AHA) guidelines list “high likelihood
of rapid progession” among other features by marked valve calci cation as a IIb
indication.






Fig. 5.2 Short-axis views of patients with severe aortic stenosis and various
degrees of valve calci cation. Left upper panel: No calci cation; right upper panel:
mild calci cation; left lower panel: moderate calci cation; right lower panel: severe
calcification.
Exercise Testing
An abnormal response to exercise has been found to predict outcome. Amato and
14colleagues performed exercise testing in 66 asymptomatic patients with an aortic
2valve area who had follow-up for 15 ± 12 months. Criteria for a positive test
result were occurrence of symptoms, new ST-segment depression, systolic blood
pressure increase less than 20 mm Hg, or complex ventricular arrhythmias. At 24
months, event-free survival (with events de ned as development of symptoms in
daily life or death) was 85% in 22 patients with negative test results but only 19%
(including 4 sudden deaths!) in patients with a positive test result. Although these
results seem impressive, they leave many unanswered questions. The majority of
patients with a positive test result ful lled the criterion of symptom development.
In particular, three of the patients who died had symptoms during the test.
Although the study allowed the conclusion that patients with a negative exercise
test result appear to have a good outcome and may not require surgery, whereas
those limited by typical symptoms should undergo valve replacement, the positive
predictive value of an abnormal blood pressure response and/or ST-segment
depression without occurrence of symptoms remained unclear.
15More recently, Das and colleagues clari ed some of the unanswered questions.
2In 125 patients with asymptomatic AS (eLective valve area 0.9 ± 0.2cm ), they
assessed the accuracy of exercise testing in predicting symptom onset within 12
months. Similar to previous reports, in approximately one third of the patients







symptoms developed on exercise. Abnormal blood pressure response, more strictly
de ned as no increase in systolic blood pressure at peak exercise compared to
baseline, was found in 23% and ST-segment depression greater than 2 mm in 26%
of patients. No deaths occurred during follow-up, but spontaneous symptoms
developed in 29% of their patients. The absence of limiting symptoms had a high
negative predictive accuracy of 87%. An abnormal blood pressure response or
STsegment depression, however, provided no statistically signi cant bene t above
limiting symptoms with respect to predictive accuracy. In the absence of limiting
symptoms, only two patients with abnormal blood pressure response, two with
STsegment depression, and one with both conditions had symptoms develop during
follow-up. Negative predictive values were 78% and 77% and positive predictive
values 48% and 45%, respectively. These ndings suggest that abnormal blood
pressure response and ST-segment depression are rather nonspeci c ndings and
are not helpful in identifying asymptomatic patients who may bene t from elective
valve replacement. Even limiting symptoms on exercise testing had a positive
predictive accuracy of only 57% in the present study when including all patients
and all symptoms. When considering only physically active patients younger than
70 years, positive predictive accuracy rose to 79%. Apparently, it also matters
which symptoms occur on exercise testing: In the entire study group, 83% of
patients with dizziness developed spontaneous symptoms compared with only 50%
of patients with chest tightness and 54% of patients with breathlessness. The most
likely explanation for these ndings is that breathlessness on exercise may be
di9 cult to interpret in patients with only low physical activity and particularly in
older patients (>70 years). In this group, it is di9 cult to decide whether
breathlessness on exercise is indeed a symptom of AS.
Thus exercise testing is primarily helpful in physically active patients younger
than 70 years. A normal exercise test result indicates a very low likelihood of
symptom development within 12 months and watchful waiting is safe. Conversely,
clear symptom development on exercise testing indicates in physically active
patients younger than 70 years a very high likelihood of symptom development
within 12 months and valve replacement should be recommended. However,
abnormal blood pressure response and/or ST-segment depression without
symptoms on exercise have a low positive predictive value and may not justify
elective surgery.
Incremental Value of Exercise Hemodynamics Assessed by
Doppler Echocardiography
Exercise hemodynamics have also been reported as predictors of outcome.
13Lancellotti et al. found the change in mean gradient with exercise to be an
independent predictor of event-free survival in asymptomatic AS. Patients with an
increase in mean gradient or 18 mm Hg or more had a markedly worse outcome

than those with less than 18 mm Hg. In their series, a positive conventional exercise
test was again a signi cant predictor of outcome but they were able to demonstrate
that exercise echo was of incremental value. However, the number of patients was
small, and the majority had valve replacement while the precise indication for
surgery was not clearly stated. Thus further studies are required to de ne the
actual role of adding hemodynamics as assessed by echo to basic exercise testing.
Echocardiographic predictors of outcome in AS are summarized in Table 5.1.
Table 5.1 Echocardiographic Predictors of Outcome in Aortic Stenosis
Rest transvalvular velocity/gradient
Rest aortic valve area
Extent of valve calcification
Hemodynamic progression rate
Increase of gradient with exercise
Left ventricular hypertrophy
Left ventricular ejection fraction
Degree of concomitant functional mitral regurgitation*
Pulmonary artery pressure*
* No data for asymptomatic aortic stenosis.
Other Predictors of Outcome in Asymptomatic Severe Aortic
Stenosis
Plasma levels of cardiac neurohormones increase with the hemodynamic severity of
AS and with increasing symptoms. More importantly, plasma levels of
16neurohormones may predict symptom-free survival in AS. In a recent study
published by our group, patients with brain natriuretic peptide (BNP) levels
<_130c2a0_pg l="" or="">N-terminal BNP levels <_80c2a0_pmol were=""
unlikely="" to="" develop="" symptoms="" within="" 9="" months=""
_28_symptom-free="" survival="" _e288bc_9025_29_2c_="" whereas="" those=""
with="" higher="" levels="" frequently="" required="" surgery="" this=""
period=""><_5025_29_. thus="" serial="" measurements="" of=""
neurohormones="" during="" follow-up="" may="" also="" help="" identify=""
the="" optimal="" time="" for="" _surgery2c_="" but="" further="" studies=""
are="" required="" to="" define="" solid="" cutoff="">
Current recommendations of the American College of Cardiology and the
American Heart Association and those of the European Society of Cardiology,
which slightly diLer, are summarized in Table 5.2. Echocardiography plays an
important role for management decision making by providing systolic LV function,
hemodynamic progression and extent of valve calci cation, extent of LV
hypertrophy, and actual severity of AS (mean gradient and aortic valve area).
Table 5.2 Recommendations for Isolated Aortic Valve Replacement in Asymptomatic
Aortic Stenosis*
3 4Class ACC/AHA Guidelines ESC Guidelines
I Patients with reduced systolic LV Patients with reduced systolic LV
function (LVEF function (LVEF
I Patients in whom symptoms develop
during exercise testing
IIa Patients with moderate to severe
valve calcification, a peak jet velocity
>4 m/s, and a rate of peak velocity
progression ≥0.3 m/s/yr
IIa Patients with a decrease in blood
pressure below baseline during
exercise testing
IIb Patients with abnormal response Patients who develop complex
to exercise (symptoms, ventricular arrhythmias during
hypotension) exercise testing
IIb Patients with high likelihood of
rapid progression (age, CAD,
calcification)
IIb Patients with severe LV hypertrophy
(≥15 mm) unless due to hypertension
IIb Patients with extremely severe
AS (valve area 2, mean gradient
>60 mm Hg) and expected
operative mortality ≤1%












ACC, American College of Cardiology; AHA, American Heart Association; AS, aortic
stenosis; CAD, coronary artery disease; EF, ejection fraction; ESC, European Society
of Cardiology; LV, left ventricular.
* No indication for bypass surgery, other valve surgery, or aortic surgery.
Does Medical Treatment Prevent Progression of Aortic Setenosis?
Calci c AS is a chronic progressive disease that starts with thickening and
calcification of valve cusps without hemodynamic significance (i.e., aortic sclerosis)
and eventually ends in heavily calci ed stiL cusps causing severe valve stenosis.
The progression from aortic sclerosis that can already easily be detected by
echocardiography or computed tomography to hemodynamically severe AS takes
many years. Thus, clinicians face the rather unique situation in valvular heart
disease that the disorder can be diagnosed at an early stage, thereby oLering the
chance of interfering with its further progression to a clinically relevant valve
problem. Although calci c aortic valve disease was until recently considered a
degenerative and unmodi able process basically induced by long-lasting
mechanical stress, histopathologic studies have made it clear that it is an active
17process that shares several similarities with atherosclerosis. In1ammation, lipid
in ltration, dystrophic calci cation, ossi cation, platelet deposition, and
endothelial dysfunction have been observed in both diseases and
hypercholesterolemia, elevated lipoprotein(a), smoking, hypertension, and diabetes
17have been reported as common risk factors for both disorders. Thus, modification
of atherosclerotic risk factors may slow progression of aortic valve calci cation. In
addition, the renin-angiotensin system that plays a role in atherosclerosis may also
17,18be important in the pathogenesis of calci c AS. Thus drugs that interfere with
this system may delay disease progression. However, the agents that have gained
most interest in recent years with regard to AS progression prevention are de nitely
statins.
Indeed, several retrospective studies have consistently demonstrated that statin
19-21therapy is associated with markedly lower hemodynamic progression of AS.
The question of whether this eLect is dependent on cholesterol lowering (or not),
20however, remains controversial. Although Novaro et al. have reported an
association between AS progression and cholesterol levels, Bellamy and
19 21colleagues and the author’s group in Vienna could not nd such an association
supporting the hypothesis that the eLects of statins may rather be caused by their
pleiotropic and antiin1ammatory properties than by cholesterol lowering. The
bene cial eLects of statin therapy do not appear to be restricted to the early stage
21of disease. Since a rapid increase of the peak aortic jet velocity among patients
with severe AS and moderately to severely calci ed valves has been shown to






6indicate a poor outcome, slowing disease progression in these patients may still
bene cially alter their outcome with respect to the development of symptoms and
the necessity of surgery. Thus retrospective data suggested that statin therapy may
be indicated in any patient with AS, regardless of AS severity and cholesterol levels.
Surprisingly, the rst prospective randomized trial on statin therapy in AS did
22not show any signi cant eLect on the progression of AS. However, this study
may not have included enough patients (N = 155) and the follow-up may have
been too short (26 months on average). However, a large recent randomized trial
has con rmed that statin treatment, in patients for whom have no otherwise
currently recommended indication for such therapy, has no eLect on the
24progression and event rate in aortic stenosis.
The fact that angiotensin-converting enzyme (ACE) and angiotensin II can be
found in sclerotic but not in normal aortic valves suggests a potential role of the
17,18renin-angiotensin system in the pathogenesis of calci c AS. ACE is also found
in atherosclerotic lesions, and angiotensin II is assumed to contribute to the
atherosclerotic process via its proin1ammatory eLects. Clinical trials have
demonstrated clinical bene t of treatment with agents that block renin-angiotensin
system components in patients who either have had or are at high risk for
atherosclerosis, suggesting similar effects in calcific AS. Indeed, ACE inhibitors have
indeed been shown to slow the calcium accumulation in aortic valves in a
23retrospective study using electron beam computed tomography. To date, only
one study has evaluated the eLects of ACE inhibitors on the hemodynamic
21progression of AS. This retrospective analysis, however, could not nd any
diLerence in progression rates between patients with and without ACE inhibitor
treatment. Nevertheless, initiation of ACE inhibitor therapy at an earlier stage of
disease and longer treatment still may have positive eLects on disease progression.
Further studies may therefore be required.
In conclusion, there is no solid evidence that AS progression can be prevented
with any medical therapy and it is too early for treatment recommendations.
References
1. Stewart BF, Siscovick D, Lind BK, et al. Clinical factors associated with calcific
aortic valve disease. Cardiovascular Health Study. J Am Coll Cardiol.
1997;29:630634.
2. Rosenhek R, Maurer G, Baumgartner H. Should early elective surgery be performed
in patients with severe but asymptomatic aortic stenosis. Eur Heart J.
2002;23:1417-1421.
3. Bonow RO, Carabello DA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the
management of patients with valvular heart disease: a report of the AmericanCollege of Cardiology/American Heart Association task force on practice
guidelines. J Am Coll Cardiol. 2006:e1-e48.
4. Vahanian A, Baumgartner H, Bax J, et al. Guidelines on the management of
valvular heart disease: The Task Force on the Management of Valvular Heart
Disease of the European Society of Cardiology. Eur Heart J. 2007;28:230-268.
5. Pellikka PA, Nishimura RA, Bailey KR, Tajik AJ. The natural history of adults with
asymptomatic, hemodynamically significant aortic stenosis. J Am Coll Cardiol.
1990;15:1012-1017.
6. Rosenhek R, Binder T, Porenta G, et al. Predictors of outcome in severe,
asymptomatic aortic stenosis. N Engl J Med. 2000;343:611-617.
7. Pellikka PA, Sarano ME, Nishimura RA, et al. Outcome of 622 adults with
asymptomatic, hemodynamically significant aortic stenosis during prolonged
follow-up. Circulation. 2005;111:3290-3295.
8. Keane JF, Driscoll DJ, Gersony WM, et al. Second natural history study of
congenital heart defects. Results of treatment of patients with aortic valvar
stenosis. Circulation. 1993;87(suppl):I16-I27.
9. Lund O, Nielsen TT, Emmertsen K, et al. Mortality and worsening of prognostic
profile during waiting time for valve replacement in aortic stenosis. Thorac
Cardiovasc Surg. 1996;44:289-295.
10. STS national database: STS U.S. cardiac surgery database: 1997 Aortic valve
replacement patients: preoperative risk variables. Chicago: Society of Thoracic
Surgeons, 2000. available at http://www.ctsnet.org/doc/3031
11. Otto CM. Timing of aortic valve surgery. Heart. 2000;84:211-218.
12. Otto CM, Burwash IG, Legget ME, et al. Prospective study of asymptomatic
valvular aortic stenosis. Clinical, echocardiographic, and exercise predictors of
outcome. Circulation. 1997;95:2262-2270.
13. Lancellotti P, Lebois F, Simon M, et al. Prognostic importance of quantitative
exercise Doppler echocardiography in asymptomatic valvular aortic stenosis.
Circulation. 2005;112(Suppl):1377-1382.
14. Amato MC, Moffa PJ, Werner KE, et al. Treatment decision in asymptomatic aortic
valve stenosis: role of exercise testing. Heart. 2001;86(4):381-386.
15. Das P, Rimington H, Chambers J. Exercise testing to stratify risk in aortic stenosis.
Eur Heart J. 2005;26:1309-1313.
16. Bergler-Klein J, Klaar U, Herger M, et al. Natriuretic peptides predict
symptomfree survival and postoperative outcome in severe aortic stenosis. Circulation.
2004;109:2302-2308.
17. Mohler ER. Mechanisms of aortic valve calcification. Am J Cardiol.
2004;94:13961402.
18. O’Brien KD, Shavelle DM, Caulfield MT, et al. Association of angiotensin-converting enzyme with low-density lipoprotein in aortic valvular lesions and in
human plasma. Circulation. 2002;106:2224-2230.
19. Bellamy MF, Pellikka PA, Klarich KW, et al. Association of cholesterol levels,
hydroxymethylglutaryl coenzyme-A reductase inhibitor treatment, and progression
of aortic stenosis in the community. J Am Coll Cardiol. 2002;40:1723-1730.
20. Novaro GM, Tiong IY, Pearce GL, et al. Effect of hydroxymethylglutaryl coenzyme
A reductase inhibitors on the progression of calcific aortic stenosis. Circulation.
2001;104:2205-2209.
21. Rosenhek R, Rader F, Loho N, et al: Statins but not ACE inhibitors delay
progression of aortic stenosis. 110:1291-1295, 2004
22. Cowell SJ, Newby DE, Prescott RJ, et al. Scottish Aortic Stenosis and Lipid
Lowering Trial, Impact on Regression (SALTIRE) investigators. A randomized trial
of intensive lipid-lowering therapy in calcific aortic stenosis. N Engl J Med.
2005;352:2389-2397.
23. O’Brien KD, Probstfield J, Caulfield MT, et al. Angiotensin-converting enzyme
inhibitors and change in aortic valve calcium. Arch Intern Med. 2005;165:858-862.
24. Rossebø AB, Pedersen TR, Boman K, et al. Intensive lipid lowering with
simvastatin and ezetimibe in aortic stenosis. N Engl J Med. 2008;359:1343-1356.Chapter 6
Challenges in Aortic Stenosis
Joseph A. Lodato, MD, Roberto M. Lang, MD, FASE
The natural history of aortic stenosis (AS) is characterized by a prolonged latent
period during which patients have no symptoms. During this phase a gradual
increase in aortic valve obstruction and compensatory hypertrophy of the
myocardium counter the increase in afterload. Morbidity and mortality rates are
low during this latent phase, presumably because of preservation of cardiac output.
Although historically sudden death has been reported in those without symptoms,
several prospective echocardiographic studies indicate that this is a rare event—
1-6probably less than 1%. However, the eventual onset of the classical symptoms of
AS—angina, syncope, or heart failure—is a harbinger of a poor outcome without
surgical replacement. Once these cardinal symptoms are manifest, the average
1,7-9survival is 2 to 3 years and the risk of sudden death is high.
Hemodynamic progression of AS has been well studied by both cardiac
catheterization and echocardiography. Results of invasive and noninvasive testing
are concordant. The mean rate of progression is an increase in the jet velocity by
0.3 m/s per year, an increase in mean pressure gradient of 7 mm Hg per year, and
2 6,10-14a decrease in valve area of 0.1 cm per year. However, there is considerable
heterogeneity in the rate of progression across patients. For example, evidence
suggests that calci4c degenerative disease progresses more rapidly than congenital
6-15or rheumatic AS. Because progression in an individual patient is unpredictable,
frequent and regular follow-up is important in patients with asymptomatic AS.
Clinical progression from asymptomatic to symptomatic disease is common in
3those with severe AS (jet velocity ≥4 m/s) and is as high as 79% at 3 years.
However, often the challenge in patients with AS is identifying those with
symptoms, even after careful history taking. This is an important distinction as the
morbidity and mortality without valve replacement markedly di: ers between the
two groups. Diminished exercise tolerance may be the initial or only symptom
related to AS progression. Because AS is typically a disease of the elderly, reduced
exercise tolerance is blamed on aging and other factors. Exercise testing can help in
16-21risk strati4cation of patients previously labeled asymptomatic. It may also
identify patients with an abnormal hemodynamic response to exercise (failure to
augment systolic blood pressure >20 mm Hg, or hypotension), which is a poor
17,22prognostic 4nding in severe AS. It is important to remember that there is noindication for exercise testing in symptomatic patients, and the results of testing are
not adequate to diagnose signi4cant coronary artery disease. An additional bene4t
of exercise testing in asymptomatic patients is that it may help de4ne exercise
limitations in those with moderate or severe AS.
Echocardiography has emerged as the primary diagnostic tool for the evaluation
of AS because of the ease of operation and relative safety pro4le compared with
heart catheterization. Echocardiography not only provides information on the
structure and function of the aortic valve, but it also characterizes the response of
the left ventricle to increased afterload and can identify other associated valvular
pathology. Recommendations for serial echocardiographic evaluation of patients
with asymptomatic AS are every year for severe AS, every 1 to 2 years for moderate
23AS, and every 3 to 5 years for mild AS.
Performing echocardiography to evaluate AS severity mandates careful attention
to technical details. Underestimation of AS is common if the study is not performed
and interpreted correctly. For the ultrasonographer, the Doppler intercept angle
with the AS jet should be less than 15 degrees. Multiple transducer locations and
optimal patient positioning is recommended to yield the highest jet velocity.
Suggested patient positions and transducer locations are left lateral decubitus with
the transducer at the apex; right lateral decubitus with right parasternal transducer
location; and suprasternal transducer position with the neck extended. For the
interpreter, it is important to correctly identify the origin of the high-velocity jet.
The Doppler signal of mitral or tricuspid regurgitation, as well as a ventricular
septal defect, and other vascular lesions can mimic the signal of AS. Additionally,
accurate measurement of the left ventricular outAow tract diameter is crucial to
obtaining reliable estimates of the aortic valve area from the continuity equation.
Since this value is squared, it can introduce considerable error in calculation. As
always, with any hemodynamic study, heart rate variability from premature beats
24or atrial fibrillation must be taken into account.
The case depicted in Figs. 6.1 and 6.2 illustrates some key points in the
evaluation of an “asymptomatic” patient with AS. Aortic stenosis is a progressive
disease that necessitates frequent and regular follow-up for the detection of
symptoms. Exercise testing can be used for risk strati4cation of patients when the
clinical history is equivocal. Echocardiography, when correctly performed, is the
optimal method of assessing severity and hemodynamic progression of disease.Fig. 6.1 Doppler pro4le of a 67-year-old woman who was evaluated for a heart
murmur. Her echocardiogram demonstrated mild to moderate concentric left
ventricular hypertrophy and normal left ventricular systolic function. She insisted
that she had no symptoms. Using the continuity equation, her aortic valve area
(AVA) is consistent with severe aortic stenosis. TVI , Velocity-time integral ofLVOT
the left ventricular outAow tract; TVI , velocity-time integral of the aortic valve;AV
D, diameter.
Fig. 6.2 Review of an echocardiogram performed 2 years previously shows a
marked change in mean gradient and peak velocity, greater than would be
expected for the normal rate of progression. Exercise testing con4rmed thesuspicion that this patient was not truly asymptomatic; she only completed 4
minutes on the Bruce protocol and failed to augment systolic blood pressure more
than 20 mm Hg. PG, Peak gradient; V, velocity; VTI, velocity-time integral.
References
1. Kelly TA, Rothbart RM, Cooper CM, et al. Comparison of outcome of asymptomatic
to symptomatic patients older than 20 years of age with valvular aortic stenosis.
Am J Cardiol. 1988;61:123-130.
2. Kennedy KD, Nishimura RA, Holmes DRJr., et al. Natural history of moderate aortic
stenosis. J Am Coll Cardiol. 1991;17:313-319.
3. Otto CM, Burwash IG, Legget ME, et al. Prospective study of asymptomatic valvular
aortic stenosis: clinical, echocardiographic, and exercise predictors of outcome.
Circulation. 1997;95:2262-2270.
4. Pellikka PA, Nishimura RA, Bailey KR, et al. The natural history of adults with
asymptomatic, hemodynamically significant aortic stenosis. J Am Coll Cardiol.
1990;15:1012-1017.
5. Pellikka PA, Sarano ME, Nishimura RA, et al. Outcome of 622 adults with
asymptomatic, hemodynamically significant aortic stenosis during prolonged
follow-up. Circulation. 2005;111:3290-3295.
6. Rosenhek R, Binder T, Porenta G, et al. Predictors of outcome in severe,
asymptomatic aortic stenosis. N Engl J Med. 2000;343:611-617.
7. Iivanainen AM, Lindroos M, Tilvis R, et al. Natural history of aortic valve stenosis
of varying severity in the elderly. Am J Cardiol. 1996;78:97-101.
8. Schwarz F, Baumann P, Manthey J, et al. The effect of aortic valve replacement on
survival. Circulation. 1982;66:1105-1110.
9. Turina J, Hess O, Sepulcri F, et al. Spontaneous course of aortic valve disease. Eur
Heart J. 1987;8:471-483.
10. Brener SJ, Duffy CI, Thomas JD, et al. Progression of aortic stenosis in 394
patients: relation to changes in myocardial and mitral valve dysfunction. J Am
Coll Cardiol. 1995;25:305-310.
11. Davies SW, Gershlick AH, Balcon R. Progression of valvar aortic stenosis: a
longterm retrospective study. Eur Heart J. 1991;12:10-14.
12. Faggiano P, Ghizzoni G, Sorgato A, et al. Rate of progression of valvular aortic
stenosis in adults. Am J Cardiol. 1992;70:229-233.
13. Otto CM, Pearlman AS, Gardner CL. Hemodynamic progression of aortic stenosis
in adults assessed by Doppler echocardiography. J Am Coll Cardiol.
1989;13:545550.
14. Roger VL, Tajik AJ, Bailey KR, et al. Progression of aortic stenosis in adults: new
appraisal using Doppler echocardiography. Am Heart J. 1990;119:331-338.15. Rosenhek R, Klaar U, Schemper M, et al. Mild and moderate aortic stenosis:
natural history and risk stratification by echocardiography. Eur Heart J.
2004;25:199-205.
16. Alborino D, Hoffmann JL, Fournet PC, et al. Value of exercise testing to evaluate
the indication for surgery in asymptomatic patients with valvular aortic stenosis.
J Heart Valve Dis. 2002;11:204-209.
17. Amato MCM, Moffa PJ, Werner KE, et al. Treatment decision in asymptomatic
aortic valve stenosis: role of exercise testing. Br Heart J. 2001;86:381-386.
18. Atwood JE, Kawanishi S, Myers J, et al. Exercise testing in patients with
aorticstenosis. Chest. 1988;93:1083-1087.
19. Clyne CA, Arrighi JA, Maron BJ, et al. Systemic and left ventricular responses to
exercise stress in asymptomatic patients with valvular aortic stenosis. Am J
Cardiol. 1991;68:1469-1476.
20. Das P, Rimington H, Chambers J. Exercise testing to stratify risk in aortic stenosis.
Eur Heart J. 2005;26:1309-1313.
21. Otto CM, Pearlman AS, Kraft CD, et al. Physiologic changes with maximal exercise
in asymptomatic valvular aortic stenosis assessed by Doppler echocardiography. J
Am Coll Cardiol. 1992;20:1160-1167.
22. Takeda S, Rimington H, Chambers J. Prediction of symptom-onset in aortic
stenosis: a comparison of pressure drop/flow slope and haemodynamic measures
at rest. Int J Cardiol. 2001;81:131-137.
23. Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the
management of patients with valvular heart disease: executive summary: a report
of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines. J Am Coll Cardiol. 2006;48:598-675.
24. Otto CM. Textbook of clinical echocardiography, ed 4. Philadelphia: Elsevier; 2009.+
+


Chapter 7
Technical Issues
Aortic Stenosis
Matt M. Umland, RDCS, FASE
Transthoracic echocardiography provides a comprehensive assessment of aortic
stenosis (AS). This allows for con dent and proper clinical management decisions.
Technical issues can arise in the assessment of the stenotic aortic valve, which
reduces the quantitative accuracy of stenosis, thus a ecting clinical decision
making. These technical pitfalls are listed in Table 7.1.
Table 7.1 Technical Pitfalls in Echocardiographic Evaluation of Aortic Stenosis
Technical Error Consequence
LVOT diameter measured incorrectly Incorrect aortic valve area
Doppler sample volume placement Incorrect aortic valve area
Single window Severity may be underestimated
Nonaligned transducer Severity underestimated
Doppler signal differentiation Incorrect assessment
Stroke volume across the aortic valve must be calculated to determine aortic
1valve area. The formula for calculating aortic valve stroke volume is
2where LVOT is the left ventricular out ow tract, (d) denotes diameter, and TVI
denotes the time-velocity integral.
The diameter should be measured in the parasternal long-axis view during
systole. The distance should be measured from the insertion of the anterior aortic
cusp to where the posterior cusp meets the mitral valve anterior lea et (Fig. 7.1).
Accurate measurement of the LVOT diameter is crucial to the calculation of the
aortic valve area because of squaring of the dimension. Table 7.2 demonstrates
corresponding LVOT stroke volumes calculated from various diameters with aconstant LVOT TVI of 18 cm.
Fig. 7.1 Measurement of LVOT diameter. Parasternal long-axis view: Insertion of
anterior aortic cusp to posterior cusp. Average three cycles (sinus rhythm); average
5 to 8 cycles (atrial fibrillation).
Table 7.2 Corresponding LVOT Stroke Volumes Calculated From Various Diameters
With a Constant LVOT TVI of 18 cm
LVOT Diameter (cm) Stroke Volume* (mL)
2.0 57
2.1 62
2.2 68
2.3 75
2.4 81
TVI, Time-velocity integral.
Stroke volume is calculated as LVOT (d)2 × 0.785 × LVOT TVI.*
Correct measurement of the LVOT velocity/TVI ratio is also an integral part of
the calculation of aortic valve area when the continuity method is used. The
acquisition of the LVOT velocity/TVI ratio should be accomplished in the apical



+
+
+

+

+
+
+
+
+
long-axis view. The pulsed wave sample volume should be placed 3 to 5 mm below
1the aortic valve annulus. If the sample volume is too close to the aortic valve,
1prestenotic acceleration jet velocity may be recorded. An important consideration
during this measurement is to attempt to achieve Doppler cursor placement as
parallel to the ow of blood as possible. Color ow imaging may also be useful in
aligning the continuous wave Doppler beam parallel with the blood flow.
Once the pulsed wave Doppler has been obtained, the next step is to acquire the
continuous wave Doppler through the aortic valve. In achieving this Doppler
pattern, it is imperative to be as parallel to ow as possible. Any deviation from
parallel to ow results in an underestimation of the Doppler jet velocity. For
example, an intercept angle of 30 degrees results in a measured velocity of 4.3 m/s
2when the actual velocity is 5.0 m/s. If the underestimated velocity is used, it will
result in signi cant errors in the pressure gradient and the valve area calculation.
Intercept angles within 15 degrees of parallel result in an error in velocity
2,3measurement of ≤5%.
Multiple imaging windows should be used to align the continuous wave Doppler
to the blood ow. The most common acoustic windows include the apical,
suprasternal notch, right supraclavicular, right parasternal, and subcostal. These
acoustic windows may also be obtained using the nonguided continuous wave
(Pedo ) transducer. This transducer has a smaller footprint, which allows for easier
manipulation around the thoracic cavity. The highest velocity Doppler signal
2obtained is assumed to represent the most parallel intercept angle.
1-6It is important to ensure that the Doppler waveform is correctly identi ed.
Systolic ow velocities by continuous wave Doppler should be analyzed on the
following bases: (1) peak velocity, (2) flow duration or ejection time, (3) location of
the Doppler window, (4) accompanying diastolic flow signals, and (5) Doppler flow
con guration. The di erentiation of Doppler signals may be more bene cial if
two1dimensional and continuous wave Doppler is used. The duration of a mitral
regurgitation jet is longer than that of AS jets. Aortic stenosis jets occur during
ejection time only, whereas the mitral regurgitation occurs during isovolumic
relaxation time, ejection time, and isovolumic contraction time. Mitral
regurgitation jet velocity is always higher than the AS velocity when they both
occur in the same patient. The ow velocity of a dynamic out ow tract obstruction
produces a late-peaking dagger-shaped Doppler pattern. Dynamic out ow
obstructions should increase while attempting provocable maneuvers, such as the
Valsalva maneuver, while the fixed AS obstruction will not change.
1The Doppler pattern of pulmonary stenosis is almost identical to that of AS. The
pulmonary stenosis signal is best obtained from the subcostal or left upper
parasternal window, whereas an AS jet is usually obtained from the apex or right