Principles of Echocardiography E-Book
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Principles of Echocardiography E-Book

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759 pages
English

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Description

Principles of Echocardiography and Intracardiac Echocardiography has everything you need to successfully obtain and interpret cardiac echo images. Stuart J. Hutchison—a premier cardiac diagnostic specialist—explains the dos and don’ts of echocardiography so that you get the best images and avoid artifacts. Get only the coverage you need with clinically-oriented, practical information presented in a consistent format that makes finding everything quick and easy. High-quality images, tables of useful values and settings, and access to the full text and more online at expertconsult.com make this the one echo handbook that has it all.

  • Features access to the full text, an image library, and moving images online at expertconsult.com where you can browse, download, and learn from additional content.
  • Focuses on clinically-oriented and practical information so that you get only the coverage that you need.
  • Presents material in a consistent format that makes it easy for you find information.
  • Explains how to obtain the best image quality and avoid artifacts through instructions on how to and how not to perform echocardiography.
  • Provides excellent visual guidance through high-quality images—many in color—that reinforce the quality of information in the text.
  • Includes numerous tables with useful values and settings to help you master probe settings and measurements.

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Publié par
Date de parution 21 avril 2012
Nombre de lectures 0
EAN13 9781437703535
Langue English
Poids de l'ouvrage 10 Mo

Informations légales : prix de location à la page 0,0253€. Cette information est donnée uniquement à titre indicatif conformément à la législation en vigueur.

Exrait

Principles of Echocardiography and Intracardiac Echocardiography

Stuart J. Hutchison, MD, FRCPC, FACC, FAHA
Clinical Professor of Medicine, University of Calgary
Departments of Cardiac Sciences, Medicine, and Radiology, Director of Echocardiography, Foothills Medical Center, Calgary, Alberta, Canada
Saunders
Table of Contents
Instructions for online access
Cover image
Title page
Copyright
Dedication
Contributors
Preface
Chapter 1: The Aortic Valve
Chapter 2: Aortic Stenosis
Chapter 3: Aortic Insufficiency
Chapter 4: The Mitral Valve
Chapter 5: Mitral Stenosis
Chapter 6: Mitral Insufficiency
Chapter 7: Tricuspid and Pulmonic Valve Disease
Chapter 8: Prosthetic Valves
Chapter 9: Infective Endocarditis
Chapter 10: Echocardiographic Assessment of the Left Ventricle
Chapter 11: Coronary Artery Disease: Ischemia, Infarction, and Complications
Chapter 12: Coronary Artery Disease: Stress Echocardiography
Chapter 13: Cardiomyopathies
Chapter 14: Diastolic Dysfunction and Echocardiographic Hemodynamics
Chapter 15: Contrast Echocardiography
Chapter 16: Proximal Isovelocity Surface Area and Flow Convergence Methods
Chapter 17: Echocardiography and Its Role in Cardiac Resynchronization Therapy
Chapter 18: Stress, Strain, Speckle, and Tissue Doppler Imaging: Practical Applications
Chapter 19: Principles of Transesophageal Echocardiography
Chapter 20: Role of Transesophageal Echocardiography in Mitral Valve Repair
Chapter 21: Intracardiac Echocardiography
Chapter 22: Pericardial Diseases
Chapter 23: Right Heart Diseases
Chapter 24: Cardiac Masses
Chapter 25: Cardiac Trauma
Chapter 26: Echocardiographic Guidance of Procedures
Index
Copyright

1600 John F. Kennedy Blvd.
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PRINCIPLES OF ECHOCARDIOGRAPHY AND INTRACARDIAC ECHOCARDIOGRAPHY ISBN: 978-1-4377-0403-7
Copyright © 2012 by Saunders, an imprint of Elsevier Inc.
All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher. 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).

Notice
Knowledge and best practice in this field 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 identified, 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 authors, contributors, or editors, assume any 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
Hutchison, Stuart J.
 Principles of echocardiography and intracardiac echocardiography / Stuart J. Hutchison. — 1st ed.
  p. ; cm. — (Principles of cardiovascular imaging)
 Includes bibliographical references and index.
 ISBN 978-1-4377-0403-7 (pbk. : alk. paper) 1. Echocardiography. I. Title.
II. Series: Principles of cardiovascular imaging.
 [DNLM: 1. Echocardiography—methods. 2. Heart Diseases—ultrasonography. WG 141.5.E2]
 RC683.5.U5H88 2012
 616.1′207543—dc23 2011023886
Content Strategist: Dolores Meloni
Content Coordinators: Julia Bartz and Bradley McIlwain
Publishing Services Manager: Pat Joiner-Myers
Project Manager: Marlene Weeks
Design Direction: Steven Stave
Printed in China.
Last digit is the print number: 9 8 7 6 5 4 3 2 1
Dedication
To my Cindy, Noel Keith, and Liam James—your gifts of love, time, and belief can only ever be repaid in kind.
To our patients, the center of medicine, and the best teachers.
Contributors

Michael M. Brook, MD
UCSF Medical Center, University of California at San Francisco, San Francisco, California

Dal Disler, RVT
University of Calgary
Alberta Children’s Hospital, Calgary, Alberta, Canada

Stuart J. Hutchison, MD
Clinical Professor of Medicine, University of Calgary
Departments of Cardiac Sciences, Medicine, and Radiology, Director of Echocardiography, Foothills Medical Center, Calgary, Alberta, Canada

Deborah Isaac, MD
Clinical Professor of Medicine, University of Calgary
Director, Cardiac Transplant Clinics, Foothills Medical Center, Calgary, Alberta, Canada

Mark Johnson, MD
University of British Columbia
St. Paul’s Hospital, Vancouver, British Columbia, Canada

Howard Leong-Poi, MD
Associate Professor of MedicineUniversity of Toronto
Head, Division of Cardiology, St. Michael’s Hospital, Toronto, Ontario, Canada

Phillip Moore, MD
Professor of Clinical Pediatrics, Department of Cardiology
Director, Pediatric Cardiac Catheterization Laboratory, UCSF Medical Center, University of California at San Francisco, San Francisco, California

Robert Moss, MD
University of British Columbia
St. Paul’s Hospital, Vancouver, British Columbia, Canada

Brad Munt, MD
University of British Columbia
Cardiologist, Department of Echocardiography, Heart Failure/Heart Transplant Service, St. Paul’s Hospital, Vancouver, British Columbia, Canada

Ahmad S. Omran, MD
Head, Non-Invasive Laboratory, King Abdulaziz Medical City, Riyadh, Saudi Arabia

Grant L. Peters, MD
Clinical Assistant Professor, Department of Cardiac Sciences, Alberta Health ServicesCalgary, Alberta, Canada

Nazmi Said, BSc, RCTA, RDCS
Echocardiography Clinical Instructor, Education Coordinator, Foothills Medical Center, Calgary, Alberta, Canada

Glen Sumner, MD
Assistant Professor of Medicine, University of Calgary
Foothills Medical Center
Libin Cardiovascular Institute of Alberta, Calgary, Alberta, Canada
Preface
For more than two decades, I have aspired to learn the optimal role and contribution of transthoracic and transesophageal echocardiography toward the management of patients with cardiac and aortic disease. Initially, I approached echocardiography as a lot of younger attendings did, as being the “answer” to all questions. At that time, the use of echocardiography had grown rapidly; CT had little to offer for the assessment of cardiac disease; and cardiac MRI was an exotic diagnostic modality of great complexity but that had little availability and minimal involvement in acute cases.
At a later juncture, I endeavored to learn cardiac CT and cardiac MRI because they promised more insofar as cardiac and aortic imaging were concerned. CT has grown spectacularly over the past decade, and cardiac MRI has gained clinically powerful and well-validated pulse sequences. As I came to know the three methods with a more balanced approach, investment of time, and level of awareness, I discovered that I wanted to understand none of them as singular diagnostic entities. Rather, I wanted to understand their individual strengths and weaknesses and how they may together afford the best possible means to satisfy the diagnostic needs of all of our cases, especially the most complicated ones. The greater challenge appears to be establishing the boundaries of the contributions of the different modalities, a matter that continues to evolve as the frontiers of each modality progress.
Whilst learning cardiac CT and cardiac MRI I gained, by way of relative comparison, a better understanding of, and a definitely renewed appreciation of, what role echocardiography, my first diagnostic modality of interest, affords patients with cardiovascular disease. When on-call after hours, when the sense of medicine is immediate and real—because the clinical stakes of decisions and their consequences are real—echocardiography is a wonderful diagnostic test to reach for as a means to contribute to the best of our abilities toward patient care.

With Acknowledgment and Sincere Appreciation
Sandeep Aggarwal, MD; Junja Ako, MD; Nanette Alvarez, MD; Monica Attwood; Doris Basic, MD; Jason M. Berstein, MD; Daniel Bonneau, MD; John H. Burgess, MD; Patrick Champagne, MD; Kanu Chatterjeee, MBBS; Anson Cheung, MD; Robert J. Chisholm, MD; Tony M. Chou, MD; Michael S. Connelly, MD; Prakash C. Deedwania, MD; Patrick Disney, MD; Lee E. Errett, MD; Neil P. Fam, MD; Quentin Forrest, PhD, MD; David J. Gilmour; Marko S. Hansen, MD; Bryan Har, MD; Michael C. Hartlieb, MD; John Janevski, MD; Sanjeet J. Jolly, MD; Majo Joseph, MBBS; Michael Kanakos, MD; Han Ho Kim, MD; David A. Latter, MD; Yves LeClerc, MD; Howard Leong-Poi, MD; Mat Lotfi, MD; Naeem Merchant, MD; Brad I. Munt, MD; Stuart F. Nicholson, MD; Christopher B. Overguaard, MD; William W. Parmley, MD; Grant L. Peters, MD; Mark D. Peterson, MD, PhD; Geoffrey S. Puley, MD; Shahabuddin H. Rahimtoola, MD; Nazmi Said, BSc, RCTA, RDCS; Gary C. Salicidis, MD; Nelson B. Schiller, MD; James A. Stewart, MD; Kishnankutty Sudhir, MD, PhD; Glen L. Summer, MD; Lisa Tolton; Inga Tomas; Julio F. Tubau, MD; Atul Verma, MD; Ram Vijayaraghavan, MD; John G. Webb, MD; Joel M. Wolkowicz, MD; Richard W. Wright; and Sayeh Zielke, MBA, MD

Stuart J. Hutchison
1 The Aortic Valve
The aortic valve opens and closes through an average of 105,000 cardiac cycles daily, or about 3.5 billion times in a lifetime. Given the systemic arterial pressures it is subjected to through all phases of the cardiac cycle, it is remarkable that most aortic valves function adequately through life.

Normal Aortic Valve Anatomy
The aortic valve is a complex, three-dimensional (3D) structure. In diastole, its three cusps (pockets) swell (fill) like three apposing parachutes to achieve a competent seal. In systole, the three pockets are pushed aside so that they do not impede ventricular ejection.
Because the valve is a 3D structure, it may appear in a variety of ways on tomographic imaging modalities, including echocardiography.
Normally, the dimensions of the aortic annulus and of the sinotubular junction are nearly identical.
From below the valve, the fibrous aortic annulus provides optimal support for the base of the leaflets as well as optimal apposition of the base of the leaflets at the site of their attachment to the aortic wall. From above the valve, the sinotubular junction maintains optimal support (suspension) of the top of the leaflets, transmitted along their commissures to the body of the leaflets. The sinotubular junction also imparts optimal apposition of the upper part of the leaflets, acting essentially as a “supra-annular” support for the valve.
The sinotubular junction, the ring-like union of the top of the aortic root sinuses with the ongoing tubular portion of the ascending aorta, is critically important for correct suspension of the aortic valve leaflets. Dilation of the sinotubular junction exerts radial traction on (tethers) the superior part of the aortic cusps, reducing the length of coaptation surface of the aortic valve leaflets and moving the coaptation point higher into the aorta. Excessive dilation of the sinotubular junction compromises coaptation and renders the valve apparatus insufficient, typically through a central regurgitant orifice. Thus, aortic annular dilation comprises aortic cusp coaptation as mitral annular dilation comprises mitral leaflet coaptation, and sinotubular dilation comprises aortic leaflet coaptation as left ventricular (LV) dilation comprises mitral leaflet coaptation. Dissection and intramural hematoma of the aortic wall into the sinotubular junction or beneath it results in loss of suspension of the adjacent aortic cusp(s), with development of aortic valve prolapse, and insufficiency.
The sinuses allow for (1) sufficient systolic excursion of the aortic valve leaflets and (2) a low-pressure zone that facilitates inflow into the coronary ostia by creating flow vortices.
The aortic valve is 1.5 to 2.0 cm tall (about 80% of the height of the sinus), with a circumference of 7 to 9 cm. The normal valve is tricuspid with three equal-size cusps. There are one anterior and two posterior (left and right) cusps. The usual nomenclature alludes to the origins of the coronary arteries; hence, the cusps/sinuses of Valsalva are named right (for right coronary; the anterior cusp/sinus), left (for left coronary; the left posterior cusp/sinus), and the noncoronary (right posterior cusp/sinus). The cusps are normally of equal size. They consist of endocardial folds with thin fibrous sheets with small central nodules at their centers. There is a ventricular surface and an arterial surface. The fibrous center is thicker along the free edges, and particularly along the insertion of the cusp to the wall, allowing maximal flexibility of the body of the cusp. The ventricular surface has three components: (1) a free edge; (2) a thicker closing surface 1 to 2 mm beneath the free edge (i.e., coaptation occurs not along the free edge but underneath it); and (3) the nodule of Arantius (or Morgangi) along the center of the free edge, which may optimize coaptation at the very center of the curving free edge because otherwise the free edge could not achieve a sharp triangular center. The nodule is seldom apparent by imaging other than transesophageal echocardiography (TEE) or cardiac computed tomography (CT). The arterial surface of the cusp forms a pocket—the sinuses of Valslva.
The valve annulus is not planar; it consists of three semicircular arcs (open-upwards) that drape from the level of the sinotubular junction down to the base of the body of the cusp. The annulus inserts in its upper part into the sinus wall of the aorta, and at its base inserts into different structures: the right coronary cusp into the muscular septum, the left coronary cusp into the aortomitral fibrosa (“curtain”) that is contiguous with the anterior mitral leaflet (involvement by endocarditis of the aortomitral fibrosa portends major clinical risks), and the noncoronary cusp into the interventricular and atrioventricular portions of the membranous septum (hence annulus abscess and rupture can fistulize into the right atrium via the atrioventricular portion of the septum—a Gerbode defect), as well as the mitral annulus.
Normally there are three cusps; hence, normally there are three commissures—the lines of diastolic apposition and systolic separation of the cusps. The normal commissures have the following relationships: (1) the right–left commissure abuts the same commissure of the more anteriorly pulmonic valve; (2) the right–noncoronary commissure lies beneath the membranous septum near the His bundle (hence aortic ring abscesses and surgical trauma from aortic valve replacement surgery may result in heart block); and (3) the left–noncoronary commissure abuts the middle part of the anterior mitral leaflet. Normally the noncoronary cusp abuts the interatrial septum via the posterior trigone of fibrous skeleton.

Imaging the Aortic Valve by Echocardiography
On transthoracic echocardiography, a normal tricuspid aortic valve in diastole (in the parasternal short axis view) appears as three commissures and three cusps, all of equal size, producing an inverted Y configuration, popularly (and longingly) referred to as the “Mercedes-Benz sign.” By TEE, the appearance is rotated 30 degrees counterclockwise. The systolic appearance of a normal tricuspid aortic valve is of a rounded triangle whose three sides are the three free edges of the aortic valve.
Some congenitally tricuspid aortic valves are composed of cusps of unequal size, with or without degrees of commissural fusion. Not all tricuspid aortic valves are structurally normal, and not all will function normally through life.
The appearance of the valve in systole should be scrutinized to determine whether the valve is tri- or bicuspid (the most common congenital malformation of the aortic valve encountered in adulthood). The systolic appearance of a bicuspid valve is not triangular, but, rather, ellipsoid. An ellipsoid appearance of the aortic valve in systole is, as assessed by somewhat dated transthoracic studies, 96% specific and of 93% diagnostic accuracy 1 for the bicuspid aortic valve anomaly. The long axis of the ellipse may lie in several possible orientations, of which left-upper to right-lower is the most common. In adults, the orientation has little or no clinical relevance.
If only one or two cusps are present, the cusp(s) are predisposed to restriction of their free edge. This restriction results in the systolic doming motion of bicuspid (and unicuspid) valves.
The diastolic appearance of the aortic valve is of little utility in identifying whether the valve has two or three commissures and cusps, because a raphae of the aortic valve may be indistinguishable in diastole from a commissure. A raphae essentially is a commissure, but one that did not divide. The term raphae derives from the Latin word meaning “seam suture, to sew” and refers to any seamlike line or line of union between two similar parts of the body, or, in this case, of the aortic valve.
In children, the right–noncoronary fusion subtype of bicuspid aortic valve appears more prone to valvular dysfunction and provides a shorter time to intervention. 2 This subtype is the predominant morphology associated with coarctation of the aorta. 3

Anatomic Variants/Malformations of the Aortic Valve

Unicuspid aortic valves are very rare: <1% incidence. They are apparent by their prominent systolic doming motion, and eccentric, teardrop-shaped systolic orifice. Congenitally unicuspid aortic valves are intrinsically stenotic from birth, usually severely, and are symptomatic within the first and second decades of life.
Quadricuspid aortic valves are exceedingly rare, with an incidence of 0.01%. They may be composed of three normal and one smaller cusp or four equal-sized cusps. The systolic orifice appears triangular if the fourth cusp is small. The diastolic appearance looks like a four-leafed clover if the cusps are of equal size. 4 Congenitally quadricuspid aortic valves and pulmonary valves may be predisposed to developing insufficiency, although this association is debated. 5, 6
Bicuspid aortic valves are an important and relatively common congenital cardiac anomaly, with an incidence of 1.37% incidence based on a Mayo Clinic series, 2 and an 0.5% incidence on review of two large databases. 7 There is a strong male gender preponderance, with a male-to-female ratio of 3 or 4 to 1. 8 Bicuspid aortic valves may be heritable. In a series of 309 probands and relatives, 74 bicuspid aortic valves were found, for a prevalence of 24% and heritability of 89%. 9 It is important to recognize bicuspid aortic valves for three reasons:
1. Up to one third will become sufficiently dysfunctional to require replacement. Most bicuspid valves that develop functional disturbance will become stenotic or have mixed aortic stenosis and aortic insufficiency. 10 A congenitally bicuspid aortic valve is the most common underlying cause of aortic stenosis in adults younger than 65 years of age. Development of pure aortic insufficiency is uncommon; if present, it usually is due to infection or cusp prolapse.
2. Bicuspid aortic valves appear to be prone to infection.
3. Associated congenital cardiovascular anomalies and malformations, discussed in the next section, may be life-threatening.
Structural associations or complications of bicuspid aortic valves include aortic associations and shunts.

Aortic associations
• Ascending aortic dilatation/aneurysm independent of the degree of aortic stenosis or aortic insufficiency. 11 Over half of younger patients with bicuspid aortic valves have been shown to have one measurement of aortic diameter greater than the 95th age-adjusted percentile, usually of the ascending aorta. 12 Dilation of the ascending aorta may be of aneurysmal severity in the presence of an entirely functional bicuspid aortic valve.
• Coarctation of the aorta. 13 Most cases of coarctation are associated with bicuspid valves.
• Dissection of the aorta. In younger adult patients with acute aortic dissection, bicuspid valves are associated nearly ten times more frequently than is Marfan syndrome.
Shunts
• Intracardiac shunts (e.g., ventricular septal defect)
• Extra-cardiac shunts (e.g., patent ductus arteriosus)
“Berry aneurysms” of the cerebral vasculature
Ineffective endocarditis
Other defects

Echocardiographic Recognition of Bicuspid Aortic Valves
Two-dimensional (2D) imaging is the most reliable means to identify bicuspid aortic valves by echocardiography. Parasternal long-axis views offer suggestions (e.g., systolic doming; possible downward displacement of a raphe into the LVOT, or “reverse doming”; possible prolapse of a cusp 15 ; thickening of leaflets), but actual recognition is achieved through short-axis views that demonstrate the systolic ellipsoid shape (“football” or “fish mouth” shape depending on your recreational interests). Using the criterion of systolic shape, 2D echocardiography is 78% sensitive and 96% specific for the diagnosis of bicuspid aortic valve using the sign of systolic orifice, 2 according to somewhat dated studies. The inability to clearly image the aortic valve appearance is regularly encountered. 16 It is likely that improved imaging has improved the level of recognition.
M-mode signs are now out of date. Valve thickening and very eccentric closure (>1.5:1) formerly were recognized as signs of a bicuspid valve, but neither was of particular sensitivity or specificity. However, obvious eccentric closure by 2D or M-mode imaging should prompt consideration of a bicuspid valve.
The true bicuspid aortic valve has one (long) commissure, two cusps, and two sinuses of Valsalva. A “functionally” bicuspid valve has a raphae, an incompletely developed commissure that is still fused over part of its length. The residual fusion tends to be thickened. In diastole it may not be distinguishable from a normal commissure. Occasionally, an acquired disease process—especially rheumatic valve disease, but occasionally endocarditis—may result in fusion of a previously functioning commissure, rendering the valve functionally bicuspid.

The Vicissitudes of Aging: Age-Related Changes of the Aortic Valve and Root 17
The aortic valve seldom retains pristine architecture in older adults. Typically, lesser degrees of thickening and a more echogenic appearance develop as the valve scleroses. Most of this thickening is wear-and-tear injury and response, and occurs most prominently at the line of closure. 17
Bright, thin Lambl’s excrescences (fibrous whiskers) on the free edge and the closure line, 18 which invariably are directed upward into the aorta and do not have mobility, may develop at advanced age. They have no functional consequence or clinical relevance, but may be a source of confusion with respect to endocarditis. Lambl’s excrescences differ in appearance from vegetations in that they are on the aortic side of the leaflets, whereas vegetations are most commonly on the underside. Lambl’s excrescences have little motion independent from the valve, whereas longer vegetations usually have independent motion.
As a result of gradually rising systolic blood pressure through adult life, the diameters of the aortic root and ascending aorta tend to increase. Elongation of the aorta occurs concurrent with age- and hypertension-related diameter increase of the aorta. This elongation often results in a rightward tilt of the root of the aorta with downward protrusion, angling the interventricular septum into a sigmoid shape. Unfolding of the aorta from its normally tight “candy-cane” curvature displaces the aortic root downward into the superior aspects of the atria.
Atheromatous disease may extend into the root and onto the aortic valve, thickening both and often making the appearance more echogenic.
Age-related sclerosis and atherosclerosis of the aorta and aortic valve are extremely common by the time patients reach their late 70s and 80s. These processes stiffen the aorta, reducing its compliance, and result in a wide pulse pressure and systolic hypertension. The systolic hypertension imparted by a stiffened sclerotic aorta, often associated with a sclerotic aortic valve, is commonly associated with concentric LV hypertrophy.

Summary

The anatomy of the aortic valve involves support from below and above, from the annulus and the sinotubular junction, respectively, and the three cusps. Coaptation occurs along a surface beneath the free edge rather than at the edge. A small nodule commonly occurs along the center of the free edge. The mitral-aortic fibrosa joins the aortic annulus to the mitral annulus.
Congenital variants include uni-, bi-, and quadricuspid malformations, all of which can be recognized by echocardiography using specific views and criteria, as may be the associated functional disturbances and complications.
Bicuspid aortic valves are the most common congenital malformation. These are significant for their tendency to degenerate into stenosis (usually), their heritablility, the association with dilation of the ascending aorta, and other extracardiac and intracardiac lesions. Bicuspid aortic valves may occur with two sinuses and one commissure or three sinuses and three cusps, with the commissure between two incompletely divided, leaving a “raphae.”
Age-related changes to the aortic valve are inevitable and are seen most prominently in cases with hypertension and atherosclerosis, both of which thicken the valve and result in sclerosis.

BOX 1-1 Bicuspid Aortic Valve with Dilated Ascending Aorta: ACC/AHA 2006 Recommendations

Class I

1. Patients with known bicuspid aortic valves should undergo an initial transthoracic echocardiogram to assess the diameters of the aortic root and ascending aorta. (Level of evidence: B)
2. Cardiac MRI or cardiac CT scanning is indicated in patients with bicuspid aortic valves when morphology of the aortic root or ascending aorta cannot be assessed accurately by echocardiography. (Level of evidence: C)
3. Patients with bicuspid aortic valves and dilation of the aortic root or ascending aorta (diameter >4.0 cm) should undergo serial evaluation of aortic root/ascending aorta size and morphology by echocardiography, cardiac MRI, or CT on a yearly basis. (Level of evidence: C)
4. Surgery to repair the aortic root or replace the ascending aorta is indicated in patients with bicuspid aortic valves if the diameter of the aortic root or ascending aorta is greater than 5.0 cm or if the rate of increase in diameter is 0.5 cm per year or more. (Level of evidence: C)
5. In patients with bicuspid valves undergoing AVR because of severe aortic stenosis or aortic regurgitation, repair of the aortic root or replacement of the ascending aorta is indicated if the diameter of the aortic root or ascending aorta is greater than 4.5 cm. (Level of evidence: C)
From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. Circulation. 2006;114(5):e84–e231.

BOX 1-2 Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Aortic Valve Morphology *

Transthoracic Echocardiography

ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 19

For Murmur or Click with TTE

Initial evaluation when there is a reasonable suspicion of valvular or structural heart disease
Appropriateness criteria: A; median score: 9
Initial evaluation when there are no other symptoms or signs of valvular or structural heart disease
Appropriateness criteria: I; median score: 2
Re-evaluation in a patient without valvular disease on prior echocardiogram and no change in clinical status or cardiac examination
Appropriateness criteria: I; median score: 1
Re-evaluation of known valvular heart disease with a change in clinical status or cardiac examination or to guide therapy
Appropriateness criteria: A; median score: 9

Adult Congenital Heart Disease

No specific mention of bicuspid aortic valves
Initial evaluation of known or suspected adult congenital heart disease
Appropriateness criteria: A; median score: 9

ACC/AHA/ASE 2003 Guideline Update for the Clinical Application of Echocardiography

No specific mention of bicuspid aortic valves

Recommendations for Echocardiography in the Evaluation of Patients with a Heart Murmur

Class I
• A patient with a murmur and cardiorespiratory symptoms
• An asymptomatic patient with a murmur in whom clinical features indicate at least a moderate probability that the murmur is reflective of structural heart disease
Class IIa
• A murmur in an asymptomatic patient in whom there is a low probability of heart disease, but in whom the diagnosis of heart disease cannot be reasonably excluded by the standard cardiovascular clinical evaluation
Class III
• In an asymptomatic adult, a heart murmur that has been identified by an experienced observer as functional or innocent

Recommendations for Echocardiography in the Adult Patient with Congenital Heart Disease

Class I
• Patients with clinically suspected congenital heart disease, as evidenced by signs and symptoms such as a murmur, cyanosis, or unexplained arterial desaturation, and an abnormal ECG or radiograph suggesting congenital heart disease
• Patients with known congenital heart disease on follow-up when there is a change in clinical findings
• Patients with known congenital heart disease for whom there is uncertainty as to the original diagnosis or when the precise nature of the structural abnormalities or hemodynamics is unclear
Class IIb
• A follow-up Doppler echocardiographic study, annually or once every 2 years, in patients with known hemodynamically significant congenital heart disease without evident change in clinical condition
Class III
• Multiple repeat Doppler echocardiography in patients with repaired patent ductus arteriosus, atrial septal defect, ventricular septal defect, coarctation of the aorta, or bicuspid aortic valve without change in clinical condition

ACC/AHA 1997 Guideline Update for the Clinical Application of Echocardiography 20

No specific mention of evaluation of bicuspid aortic valve malformations

ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 21

With respect specifically to the evaluation of bicuspid aortic valve malformations

• Patients with known bicuspid aortic valves should undergo an initial TTE echocardiogram to assess the diameters of the aortic root and ascending aorta. (Class I; level of evidence: B)
Indications for echocardiography in the evaluation of heart murmurs
• A murmur in an asymptomatic patient if the clinical features indicate at least a moderate probability that the murmur is reflective of structural heart disease. (Class I)

Transesophageal Echocardiography

ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2011 Appropriateness Use Criteria for Echocardiography 19

TEE as Initial or Supplemental Test—General Uses

Use of TEE when there is a high likelihood of a nondiagnostic TTE due to patient characteristics or inadequate visualization of relevant structures
Appropriateness criteria: A; median score: 8
Routine use of TEE when a diagnostic TTE is reasonably anticipated to resolve all diagnostic and management concerns
Appropriateness criteria: I; median score: 1

Cardiac Computed Tomography

ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 22

Characterization of native cardiac valves
Suspected clinically significant valvular dysfunction
Inadequate images from other noninvasive methods
Appropriateness criteria: A; median score: 8

ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 23

With respect specifically to the evaluation of bicuspid aortic valve malformations
• Cardiac MRI or cardiac CT is indicated in patients with bicuspid aortic valves when morphology of the aortic root or ascending aorta cannot be assessed accurately by echocardiography. (Class I; level of evidence: C)
Cardiac MRI or cardiac CT is reasonable in patients with bicuspid aortic valves when aortic root dilation is detected by echocardiography to further quantify severity of dilatation and involvement of the ascending aorta. (Class IIa; level of evidence: B)

Cardiac Magnetic Resonance Imaging

ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Magnetic Resonance Imaging 23

Characterization of native and prosthetic cardiac valves—including planimetry of stenotic disease and quantification of regurgitant disease
Patients with technically limited images from echocardiography or TEE
Appropriateness criteria: A; median score: 8

SCMR Consensus Panel Report: Indication for Cardiac Magnetic Resonance Imaging 24

For bicuspid aortic valves (Class II)

ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 21

With respect specifically to the evaluation of bicuspid aortic valve malformations


• Cardiac MRI or cardiac CT is indicated in patients with bicuspid aortic valves when morphology of the aortic root or ascending aorta cannot be assessed accurately by echocardiography. (Class I; level of evidence: C)
Cardiac MRI or cardiac CT is reasonable in patients with bicuspid aortic valves when aortic root dilatation is detected by echocardiography to further quantify severity of dilatation and involvement of the ascending aorta. (Class IIa; level of evidence: B)

Nuclear

ACCF / ASNC/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging 25

No specific mention of bicuspid aortic valves

Other

ACC/AHA 2008 Guidelines on Valvular Disease: Focused Update on Endocarditis 26

Management of Congenital Valvular Heart Disease in Adolescents and Young Adults

Antibiotic prophylaxis is no longer indicated in the adolescent and young adult with native heart valve disease for prevention of infective endocarditis.

ACC/AHA 2008 Guideline Update on Valvular Heart Disease: Focused Update on Infective Endocarditis 26

In select circumstances, the committee also understands that some clinicians and some patients may still feel more comfortable continuing with prophylaxis for infective endocarditis, particularly for those with bicuspid aortic valve or coarctation of the aorta, severe mitral valve prolapse, or hypertrophic obstructive cardiomyopathy. In those settings, the clinician should determine that the risks associated with antibiotics are low before continuing a prophylaxis regimen.
Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain.
TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

* See Chapter 2 for appropriateness of cardiac imaging modalities for the assessment of aortic stenosis and Chapter 3 for the appropriateness of cardiac imaging modalities for the assessment of aortic insufficiency.
TABLE 1-1 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Aortic Valve Morphology and Related Disturbances and Associations MODALITY PROS CONS/CAVEATS Transthoracic Echocardiography

• 2D short-axis imaging in systole, if the images are clear, can detect most bicuspid aortic valves by their elliptical orifice (78% sensitive, 96% specific).
• Doppler echocardiography can assess functional disturbance of the aortic valve.
• Can depict bicuspid aortic valve associated aortopathy and coarctation

• Inability to sufficiently image the aortic valve occurs (15–20% of adult cases) Transesophageal Echocardiography

• 2D short-axis imaging (30°–50°) in systole can reliably depict most bicuspid (>95%) aortic valves by their ellipitical orifice.
• Doppler echocardiography can assess functional disturbance of the aortic valve.
• Can well depict bicuspid aortic valve–associated aortopathy, coarction, and dissection

• Patient discomfort/semi-invasive Cardiac CT

• ECG-gated contrast-enhanced cardiac CT can yield excellent images of the valve morphology, but the images must include systolic phase.
• An excellent means to depict associated aortopathy, coarction, and dissection

• Radiation
• Motion sensitive imaging
• Calcium is over-represented, and may “bloom.”
• Cannot provide functional assessment Cardiac MRI

• SSFP sequences are able to depict the aortic valve morphology well (>95%).
• SSFP sequences and MR aortography can well depict associated aortopathy, coarctation, and dissection.
• Phase contrast sequences can quantify bicuspid aortic valve–associated aortic insufficiency.

• Motion sensitive imaging
• Calcium appears as signal voids. Chest Radiography Can demonstrate heart failure and some findings of bicuspid aortic–valve associated aortopathy. — Cardiac Catheterization

• Cardiac catheterization with left ventriculography can reveal doming of the aortic valve leaflets consistent with bicuspid morphology.
• Calcification is readily appreciated by fluoroscopy.
• Contrast aortography is a standard and excellent means to identity
• Associations of bicuspid aortic valves such as aneurysms and especially coarctation
• Complications such as aortic valve stenosis, aortic insufficiency, and aortic dissection

• Not a standard test to assess aortic valve morphology
2D, two dimensional; ECG, electrocardiographic; SSFP, steady-state free precession.

Figure 1-1 Examples of bicuspid valves, seen in short-axis echocardiography. Upper left (tranesophageal echocardiography [TEE] view): Bicuspid valve with an elliptical orifice and two sinuses. Upper right (TEE view): Bicuspid valve with a triangular orifice, and two sinuses. Middle left (transthoracic echocardiography [TTE] view): Bicuspid valve with an elliptical orifice and two sinuses. Middle right (TTE view): Bicuspid valve with an elliptical orifice and three sinuses/raphae. Lower left (TTE view): Bicuspid valve with an elliptical orifice with two sinuses. Lower right (TTE view): “Functionally bicuspid” (acquired bicuspid) morphology resulting from rheumatic disease fusing the left posterior commissure creating a left posterior raphae. Note also the dilated left atrium from mitral stenosis, this patient’s predominant disease.

Figure 1-2 Neonate with unicuspid aortic valve stenosis. Upper left: Posterior long-axis view shows doming of the aortic valve. Upper right: Posterior short-axis view demonstrates an eccentric orifice. Lower left: A long-axis view depicting doming of the valve. Lower right: Color Doppler flow mapping reveals proximal isovelocity surface area before the doming valve, consistent with flow acceleration before aortic stenosis.

Figure 1-3 Transesophageal echocardiography images of a quadricuspid aortic valve in diastole ( left ) and systole ( right ) .

Figure 1-4 Examples of infective complications of bicuspid valves seen on transesophageal echocardiography. Upper left: Long-axis view reveals doming of a bicuspid valve that is not infected. Upper right: Long-axis view shows vegetation on the anterior leaflet of the aortic valve. Lower left: Short-axis view shows vegetations rendering the free edge of the bicuspid valve shaggy in appearance. Lower right: Short-axis (another patient): shows vegetation at the right aspect of the commissure.

Figure 1-5 Examples of distal aortic associations and complications of bicuspid valves. Upper left: Long-axis transesophageal echocardiography view of the proximal descending aorta shows a “waist-like” narrowing of the aorta, consistent with coarctation. Upper right: Flow convergence and associated jet. Lower left: A very narrow site of coarctation and then a ballooning of the post-coarctation aorta are seen. Lower right: Associated jet emerging from the coarctation.

Figure 1-6 Examples of proximal aortic associations of bicuspid valves. Upper left: Long-axis transesophageal echocardiography (TEE) view shows doming of a bicuspid valve and aneurysmal dilation of the sinuses, a less common level of dilation of the aorta (than the ascending aorta) associated with bicuspid aortic valves. Upper right: Parasternal long-axis TEE view shows an aneurysm of the ascending aorta above the sinuses of Valsalva, which is more commonly associated with bicuspid aortic valves. Lower left: Long-axis TEE view of the ascending aorta shows a linear intimal flap in an aneurysmal ascending aorta. Lower right: Aortographic view in the same patient as bottom left image shows an aneurysm of the aorta above the sinuses of Valsalva, with a medial linear intimal flap with vertical orientation.

Figure 1-7 Lambl’s excrescences on the aortic valve. Fine “whisker-like” excrescences are seen pointing upward and arising from the free edge of the valve.

Figure 1-8 Transthoracic ( top ) and transesophageal ( bottom ) images of the same patient with a bicuspid valve. The left images are diastolic and the right images are systolic. Despite the use of zoom views of the aortic valve, transthoracic echocardiography is in this case incapable of affording clear enough images to determine the morphology of the valve. Transesophageal images reliably determine the aortic valve morphology by using short-axis images between 30 and 70 degrees rotation.

Figure 1-9 Transesophageal images of a tricuspid aortic valve in diastole ( top ) and systole ( bottom ). In both systole and diastole the three aortic sinuses are evident. It is only in systole, however, that the triangular orifice of the aortic valve is apparent, establishing its trileaflet morphology.

Figure 1-10 Age-related changes. The chest radiograph ( left ) is notable for extensive calcific plaques in the aorta seen best at the arch level, where they project largely tangentially. The parasternal long-axis echo image ( upper right) reveals sclerosis of the aortic and mitral valves, some mitral calcification, and sclerosis or atherosclerosis of the aorta. There is concentric left ventricular hypertrophy (LVH) of the left ventricle. The spectral Doppler image of left ventricular inflow ( lower right ) reveals summation of the E and A waves, with A wave dominance consistent with the impaired relaxation pattern of diastolic dysfunction, typical of LVH due to hypertension. Calcification of the aorta diminishes the aorta’s compliance, resulting in systolic hypertension, which then incites LVH, with its diastolic dysfunction.

Figure 1-11 Transthoracic (top ), transesophageal ( middle ), and cardiac steady-state free precession MRI ( bottom) images . Left panels are systole images; right panels are diastole images. The bicuspid nature of the valves is apparent on all three forms of imaging.

Figure 1-12 Ascending aortic dilation and very mild coarctation of the aorta (“aortopathy”) associated with bicuspid aortic valvulopathy. Upper images: Transthoracic views obtained from the supersternal position. Color Doppler flow mapping ( upper left ) reveals flow convergence in the isthmus portion of the descending aorta. Spectral Doppler ( upper right ) demonstrates mild flow acceleration and also spectral broadening, consistent with a mild gradient. Middle images: Long-axis 2D transesophageal echocardiography images with color Doppler flow mapping reveal a near-field fold, or shelf, in the aorta with some flow convergence depicted as a result. Continuous wave Doppler sampling ( middle left ) at the site of flow convergence yields a similar-shaped spectral profile to that obtained by transthoracic echocardiography ( middle right ); due to less than optimal alignment, however, it has undersampled the true velocity. Lower images: Magnetic resonance imaging. Lower left: The contrast-enhanced aortic MR aortogram nicely depicts the shape and course aorta and its branches. Only a mild degree of coarctation is present. The fold in the proximal descending aorta is well depicted. Lower right: Steady-state free precession sequence reveals mild dilation of the ascending aorta and mild coarctation. This view, however, overdepicts the severity of the coarctation, because the plane of imaging is not through the center line of the aorta.

References

1. Brandenburg R.O.Jr., Tajik A.J., Edwards W.D., et al. Accuracy of 2-dimensional echocardiographic diagnosis of congenitally bicuspid aortic valve: echocardiographic-anatomic correlation in 115 patients. Am J Cardiol . 1983;51(9):1469-1473.
2. Fernandes S.M., Khairy P., Sanders S.P., Colan S.D. Bicuspid aortic valve morphology and interventions in the young. J Am Coll Cardiol . 2007;49(22):2211-2214.
3. Fernandes S.M., Sanders S.P., Khairy P., et al. Morphology of bicuspid aortic valve in children and adolescents. J Am Coll Cardiol . 2004;44(8):1648-1651.
4. Herman R.L., Cohen I.S., Glaser K., Newcomb E.W.III. Diagnosis of incompetent quadricuspid aortic valve by two-dimensional echocardiography. Am J Cardiol . 1984;53(7):972.
5. Butany J., Collins M.J., Demellawy D.E., et al. Morphological and clinical findings in 247 surgically excised native aortic valves. Can J Cardiol . 2005;21(9):747-755.
6. Hwang D.M., Feindel C.M., Butany J.W. Quadricuspid semilunar valves: report of two cases. Can J Cardiol . 2003;19(8):938-942.
7. Movahed M.R., Hepner A.D., Ahmadi-Kashani M. Echocardiographic prevalance of bicuspid aortic valve in the population. Heart Lung Circ . 2006;15(5):297-299.
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(5):661-663.
9. Cripe L., Andelfinger G., Martin L.J., et al. Bicuspid aortic valve is heritable. J Am Coll Cardiol . 2004;44(1):138-143.
10. Roberts W.C., Morrow A.G., McIntosh C.L., et al. Congenitally bicuspid aortic valve causing severe, pure aortic regurgitation without superimposed infective endocarditis. Analysis of 13 patients requiring aortic valve replacement. Am J Cardiol . 1981;47(2):206-209.
11. Hahn R.T., Roman M.J., Mogtader A.H., Devereux R.B. Association of aortic dilation with regurgitant, stenotic and functionally normal bicuspid aortic valves. J Am Coll Cardiol . 1992;19(2):283-288.
12. Morgan-Hughes G.J., Roobottom C.A., Owens P.E., Marshall A.J. Dilatation of the aorta in pure, severe, bicuspid aortic valve stenosis. Am Heart J . 2004;147(4):736-740.
13. Lindsay J.Jr. Coarctation of the aorta, bicuspid aortic valve and abnormal ascending aortic wall. Am J Cardiol . 1988;61(1):182-184.
14. Januzzi J.L., Isselbacher E.M., Fattori R., et al. Characterizing the young patient with aortic dissection: results from the International Registry of Aortic Dissection (IRAD). J Am Coll Cardiol . 2004;43(4):665-669.
15. Stewart W.J., King M.E., Gillam L.D., et al. Prevalence of aortic valve prolapse with bicuspid aortic valve and its relation to aortic regurgitation: a cross-sectional echocardiographic study. Am J Cardiol . 1984;54(10):1277-1282.
16. Zema M.J., Caccavano M. Two dimensional echocardiographic assessment of aortic valve morphology: feasibility of bicuspid valve detection. Prospective study of 100 adult patients. Br Heart J . 1982;48(5):428-433.
17. Sahasakul Y., Edwards W.D., Naessens J.M., Tajik A.J. Age-related changes in aortic and mitral valve thickness: implications for two-dimensional echocardiography based on an autopsy study of 200 normal human hearts. Am J Cardiol . 1988;62(7):424-430.
18. Hurle J.M., Garcia-Martinez V., Sanchez-Quintana D. Morphologic characteristics and structure of surface excrescences (Lambl’s excrescences) in the normal aortic valve. Am J Cardiol . 1986;58(13):1223-1227.
19. Douglas P.S., Garcia M.J., Haines D.E., et al. ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 appropriate use criteria for echocardiography. J Am Coll Cardiol . 2011;57(9):1126-1166.
20. Cheitlin M.D., Chair J.S., Alpert J.S., et al. ACC/AHA guidelines for the clinical application of echocardiography: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Clinical Application of Echocardiography). Circulation . 1997;95:1686-1744.
21. Bonow R.O., Blase A.C., 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.
22. Taylor A.J., Cerqueira M., Hodgson J.M., et al. ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 appropriate use criteria for cardiac computed tomography. J Am Coll Cardiol . 2010;56(22):1864-1894.
23. Hendel R.C., Manesh P.R., Kramer C.M., Poon M. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging. J Am Coll Cardiol . 2006;48(7):1475-1497.
24. Pennell D.J., Sechtem U.P., Higgins C.B., et al. Clinical indications for cardiovascular magnetic resonance (CMR): Consensus Panel report. J Cardiovasc Magn Reson . 2004;6(4):727-765.
25. Hendel R.C., Berman D.S., Di Carli M.F., et al. ACCF/ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 appropriate use criteria for cardiac radionuclide imaging. J Am Coll Cardiol . 2009;53(23):2201-2229.
26. Nishimura R.A., Carabello B.A., Faxon D.P., et al. ACC/AHA 2008 guideline update on valvular heart disease: focused update on infective endocarditis: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol . 2008;52:676-685.
2 Aortic Stenosis
Given the prevalence of valvar aortic stenosis (AS), its huge clinical burden, and the impressive salvage rate with surgical valve replacement, and now with percutaneous valve replacement, identification and description of AS is a prime application of echocardiography. It is also one of the most elegant and relevant applications of Doppler physics in the evaluation of cardiac disease.
Although the basic principles of gradient and area determination are simple, the disease of AS and its innumerable permutations are not, and neither are the subtleties of testing that are responsible for many instances of discordance between different modalities. Rigorous attention to scanning details is paramount, as is proficiency with both noninvasive and invasive aortic valve assessment of hemodynamics, and the ability to navigate discordance with catheterization-derived estimates of aortic stenosis.

Goals of Echocardiography in Aortic Stenosis

To determine that aortic stenosis is present
To determine the level(s) of obstruction/stenosis (valvar versus other)
To determine the hemodynamic severity of the aortic stenosis
To assess the regional and overall left ventricular (LV) function carefully
To determine the stroke volume
To assess for bicuspid valve anomaly, its associations, and its complications

Scanning Issues

Required Parameters to Obtain from Scanning

Valve parameters
Morphology (bicuspid?)—use a zoom view, focus in systole
Mean gradient, V 1 , V 2
Severity of associated aortic insufficiency
Left ventricular outflow tract (LVOT) diameter
LV parameters
Stroke volume
Ejection fraction (EF) or “grade” of dysfunction
Wall motion abnormalities
Aortic diameters
Sinotubular junction (STJ) level (more pressure recovery when STJ is <30 mm)
Ascending aorta level (associated dilation)
Other
Exclusion or identification of concurrent subvalvar obstruction
Noting height and weight for body surface area normalization

Scanning Notes

LVOT measurement
To minimize error, a zoom view must be used.
If the image quality confers ambiguity, repeat the measurement on several different zoom views.
LVOT is the single most important measurement: a 2-mm error confers a 20% aortic valve area (AVA) calculation error.
If the LVOT diameter is in doubt, consider:
• Transesophageal echocardiography (TEE)
• Echocardiogram–gated cardiac CT
• Cardiac steady-state free precession sequence MRI, using a long-axis three-chamber view
V 1 measurement
Ensure that V 1 Doppler sampling is correctly aligned—in some cases a more lateral apical sampling site is required to achieve acceptable alignment (within 20 degrees) if the LVOT long axis deviates markedly from that of the LV.
Do not record the V 1 from within the LV cavity, or the recorded velocity and AVA tend to be too low.
Record the subvalvar V 1 before the flow acceleration (easily depicted by the proximal isovelocity surface area [PISA]). Establishing the location of the PISA and sampling V 1 to avoid the PISA is better technique than is arbitrarily placing the sample volume “1 cm beneath the aortic valve,” which may actually be within flow acceleration from the valvar stenosis or from concurrent subvalvar obstruction.
Although ideally the spectral envelope would be measured (planimetered) at the modal frequency (velocity), this is seldom discernable; therefore, planimetry is, for clinical purposes, performed on the outermost aspect of the spectral profile.
AVA calculations traditionally are made from integrals; peak velocities are a surrogate.
If sinus rhythm: measure three spectral profiles.
If in atrial fibrillation: measure five spectral profiles.
V 2 measurement
Ensure that the apical five-chamber and apical three-chamber V 2 Doppler sampling views are correctly aligned (within 20 degrees). In some cases, a more lateral sampling site is needed.
If a concurrent subvalvar stenosis (LVOT velocity [V 1 ] >1.5 m/sec) is likely, record the pre-subvalvar flow velocity, the pre-valvar velocity (V 1 ), and also the V 2 . The modified Bernouilli equation should not be used if V 1 is ≥1.5 m/sec.
AVA calculations traditionally are made from integrals; peak velocities are a surrogate, although a reasonably accurate one.
If sinus rhythm: measure three spectral profiles.
If in atrial fibrillation: measure five spectral profiles.
If in the idea world: measure ten spectral profiles.
Annotate the site of sampling for future reference comparison.
Confounders
Verify whether there is/is not concurrent intracavitary flow acceleration (subaortic valve velocity ≥ 1.5 m/sec), as discussed in the following section.
A narrow aortic root (STJ ≤ 30 mm): a narrow aorta facilitates the “pressure recovery” phenomenon that detects a higher gradient than the recovered gradient measured by catheterization.

Equations

Continuity equation:

 
Velocity ratio (VR) equation:

 
Mean gradient equation:

 
LV stroke work loss (LVSWL) equation:

 
where AVG = average gradient, CSA = cross-sectional area, SBP = systolic blood pressure, and VTI = velocity time integral.

Pathophysiology and Findings of Aortic Stenosis
The fundamental pathophysiology of AS is the excess pressure imposed on the LV, known as pressure overload . Secondarily, or indirectly, a lesser pressure load is imposed on the LA by diastolic failure of the LV. The LV response to pressure overload— concentric hypertrophy— is adaptive; it normalizes the wall stress on myocytes, but it is physiologically expensive. Essentially, the wall thickness increases in proportion to the pressure increase. Laplace’s law states that wall stress (i.e., myocyte stress) is proportional to intracavitary pressure and radius, and inversely proportional to wall thickness. Therefore, if the proportional increase in LV wall thickness is the same as the proportional increase in left ventricular pressure (due to imposition of the transvalvar gradient), then wall stress is normalized, and myocyte preservation is facilitated.
The pattern of hypertrophy in AS is typical of pressure overload, therefore, and should be present in most cases of severe AS. In concentric hypertrophy, myocardial sarcomeres replicate in parallel; therefore the walls thicken and the cavity dimensions do not increase (in fact, they often decrease). Therefore, the pattern is thick walls and no increase in cavitary dimensions, unless complications arise, or the disease is in a terminal state.
In severe AS, where the systolic pressure within the LV doubles, LV mass essentially doubles (increases to 178 g/m 2 vs. normal of 86 g/m 2 ), 1 due to near doubling of the wall thickness to normalize wall stress that otherwise would be nearly doubled ( Fig. 2-1 ).

Figure 2-1 Doubling of wall thickness in severe aortic stenosis.
Given the increase in both myocardial mass and generated systolic pressure, myocardial O 2 demand increases (mVO 2 ∝ LV mass, developed systolic pressure, contractility, and heart rate). In AS, coronary flow (supply) is a problematic issue that compounds the potential problem of increased demand; about half of adult patients with AS have concurrent coronary artery disease (CAD).
Severe AS may remain seemingly static and compensated for years, or may progress. The rate of progression depends on many factors, few of which are well understood. Progression rates between –0.01 cm 2 /year and –0.1 cm 2 /year have been described. Calcification of the aortic valve is somewhat predictive of a faster rate of progression, but it is not known how to quantify calcification toward this purpose. Electron beam CT studies have not shown good correlation of calcification quantification by Agatston score with aortic valve area, especially for moderate and severe AS. 2
Both increasing left ventricular systolic pressure and LV hypertrophy impair LV compliance; left atrial hypertrophy and augmented atrial systolic function occur to maintain left ventricular filling. In severe AS, the left atrium typically is mildly enlarged.
In summary, the pathophysiology of severe AS generates expected findings: increased wall thickness, no increase in left ventricular cavitary size, and left atrial dilation. An increase in cavitary size requires additional explanation, such as concurrent volume overload from aortic insufficiency or mitral regurgitation, impaired systolic function from CAD or cardiomyopathy, or terminal decompensated AS.

Role of Transesophageal Echocardiography in Aortic Stenosis
There is no routine role for TEE in the assessment of AS.
A minor role for TEE is in cross-sectional imaging of the aortic valve, in cases where the severity of the stenosis is unclear, to enable planimetry for valve area—but this assumes that the orifice is planar, which is a considerable assumption.
TEE is a technically demanding and difficult means by which to sample aortic valve gradients. TEE Doppler sampling from the lower esophagus is never acceptably aligned; deep retroflexed transgastric five-chamber sampling is validated to detect the gradient accurately, but is prone to misalignment and under-sampling in unpracticed hands.
TEE probably is the best test available to image subvalvar lesion morphology in detail.
TEE assumes an important useful role intraoperatively to validate the preoperative diagnosis of severe AS; identify or exclude complications, associations, and confounders; and verify successful aortic valve replacement.
TEE is a standard test prior to percutaneous aortic valve replacement (AVR) (see Chapter 26 ) and optimally is used to determine the size of the prosthesis and the morphology of the annuli, valve, and root.

Reporting Issues
Aortic valve gradient is a per-beat (volume) function. The gradient of aortic stenosis occurs through the systolic ejection period. The mean gradient is the most suitable expression of the average pressure load imposed on the LV through this period. The gradient reflects both the severity of the impedance to ejection (imparted by the aortic valve) and the function of the LV. The expression of LV function that is most germane to aortic stenosis is the stroke volume, not the EF or CO.

Gradient Issues
When reporting, the combination of mean gradient and stroke volume must be emphasized. For example: “The mean gradient is 65 mm Hg with a normal stroke volume of 75 mL.” Normal stroke volume index is 45 ± 13 mL/m 2 . It is not necessary to describe the peak instantaneous gradient; this just generates unjustifiable confusion with the (different) catheterization-derived peak-to-peak gradient, and is not the criterion for severity. Gradients, valve area, and LV function must be compared to previous determinations. If there is a difference in the gradient, ensure that the recording was obtained from a comparable sampling site.
It is important to enter annotations (e.g., apical, right parasternal, suprasternal) on all spectral Doppler recordings, to make appropriate comparisons possible. Gradients may be enhanced by numerous factors, only a few of which may be apparent when reading an echocardiogram. Factors that increase the aortic valve gradient include the following:

Bradycardia in the context of normal LV function or contractile recruitment
Causes of larger stroke volume ± lower peripheral resistance
• Anemia
• Fever
• Thyrotoxicosis
• Pregnancy
• Large dialysis fistulae
• Inotropic stimulation
• Peripheral vasodilation
Undersampling of the V 2 spectral profile is a common clinical problem, as the spectral profile boundary may be vague.
• If the sampling appears incomplete (i.e., not a full parabola), appropriate efforts must be made to try to obtain it.
• Equally important is that the report does not convey that the real gradient was only as low as it was sampled to be, when the sampling was clearly incomplete.
Fewer than 5% of cases of AS will have inadequate spectral profiles; the percentage is very much determined by the time and effort made to acquire the spectral recording.
Adequate spectral profiles are complete and plausible parabolic profiles.
If the peak velocity is to be marked with cross-hairs, the cross-hairs should not be placed on the peak of a spectral profile, because that may falsely confer an impression of the true peak to the reviewer. The cross-hairs should be placed off to the side of the presumed peak to allow the reviewing or reporting physician to establish independently that the peak was true, as a useful internal check.
If the profile initially does not appear complete, persistence in attempting better ones is required, as there is a (albeit diminished) return. Techniques that should be used include the following:
• Use of the “stand-off” probe
• Sampling from several parasternal, supraclavicular, and suprasternal sites
• Variable positioning of the patient
• Use of the most experienced sonographer
The published correlation of Doppler versus catheterization mean gradients averages 0.90, 3, 4 but importantly, 1 standard error of estimate (SEE) of Doppler gradient versus catheterization gradient is actually 10 mm Hg [SEE range, 6–12 mm Hg]. 5
Rahimtoola 5 emphasized consideration of the SEE by Doppler when describing AS severity (by gradient):
• Highly likely severe: mean gradient >70 mm Hg
• Probably severe: mean gradient >60 and <70 mm Hg
• Uncertain if severe: mean gradient <50 mm Hg
Recall that the pressure recovery phenomenon at aortic root level is seen with small aortic roots (dimensions <30 mm) and restrictive planar divergent orifices. Pressure recovery may add 15% to 30% to the gradient.
LVSWL, originally a catheterization-based parameter, can be approximated by echocardiography, and has been validated as a way to discriminate clinical end-points: an LVSWL ≤25 is the best predictor. 6 The concept expresses kinetic energy loss across the aortic valve in reference to the aortic pressure.

Continuity Equation–Derived Aortic Valve Area Issues
The idea of aortic valve area as a conceptual expression of AS is attractive, because it is intended to be a flow-independent description of AS severity, and it is widely accepted that flow does vary across stenotic aortic valves, reducing the predictiveness of gradient alone. Because flow across the aortic valve per cardiac cycle may vary, the gradient should be offered in the context of the stroke volume (index). Unfortunately, precise determination of the stenotic aortic valve area, by echo and also by catheterization, is neither as simple nor accurate as is believed. The calculation of AVA by echo and by catheterization actually is not “flow-independent” by either technique, because so many parameters are involved in the equations that the total introduced error becomes significant and sometimes problematic. Furthermore, plastic deformation of the aortic valve (i.e., greater opening under higher gradients and less opening under lower gradients) is known to occur.

Place less emphasis on the valve area alone; instead, emphasize the combination of area, gradient, and stroke volume. Unless these afford a congruent assessment of aortic stenosis severity, further consideration is needed.
Continuity-derived AVA is not flow independent. 7
The multiple variables used in the calculation of AVA may allow for introduction of considerable composite error.
The average published correlation of Doppler-derived AVA versus catheterization-derived AVA is r = 0.90. However, recall that the SEE of Doppler AVA versus catheterization gradients is, on average, 0.3 mm Hg [0.1–0.4 cm 2 ]. 5
Rahimtoola 5 suggests consideration of patient body size indexing of the AVA.
• Severe: <0.3 cm 2 /m 2
• Moderate: 0.3–0.59 cm 2 /m 2
• Mild: >0.6 cm 2 /m 2
Report AVA only to a single decimal place. A calculation accurate at best to ± 0.3 cm 2 cannot be realistically described to a second decimal place.

Peak Systolic Velocity
Calculations of gradient and area entail squaring and multiplying (4 × V 2 , 4 × V mean 2 , 0.785 × D 2 × V 1 /V 2 ), thereby conferring additive error to their calculation. Consequently, the case has been made in favor of measurement of the peak velocity alone, avoiding the error accrued from calculation of gradient and area. Peak velocity ≥ 4.5 m/sec is a reliable descriptor of severe AS, in the absence of noncardiac factors that may aggravate velocity. As a parameter, it is clinically useful, and as an example it serves as a reminder that calculated variables may diminish their own worth by the error accrued in yielding them. Peak systolic velocity is a robust means of describing the severity of AS.

Summary of Aortic Stenosis Descriptors
The important task is to determine which cases of AS are hemodynamically severe, and may benefit from surgery. There is little worth in debating moderate versus mild; both are in effect “nonsevere” and would not independently merit intervention. One significant exception is that AVR usually is performed in the scenario of CAD to undergo aortocoronary bypass grafting, in the presence of moderate AS (mean gradient ≥ 25 mm Hg), although the threshold for performing AVR in this scenario remains vexingly unclear.

Possibly severe in the presence of a normal stroke volume
• AVA < 1 cm 2 (for a person of average body size) or
• Indexed AVA < 0.5cm 2 /m 2 and a mean gradient ≥ 50 mm Hg
Severe in the presence of a normal stroke volume
• AVA < 0.75 cm 2 (for a person of average body size) or
• AVA < 0.3cm 2 /m 2 and a mean gradient ≥ 50 mm Hg

Other Issues
Although the focus of an echocardiographic study is on detailed examination and description of the valve and related hemodynamics, it also is necessary to assess for associations, complications, and concurrent diseases.
If the aortic valve is bicuspid, describe possible associations. Recall that a high-velocity AS jet may carry around the aortic arch—in other words, higher-velocity flow in the proximal descending aorta may not be coarctation generated, and represents only transmission of the AS jet. The diagnosis of coarctation of the aorta by echocardiograophy requires demonstration of a focal step-up of flow velocity.
Describe the dimensions and appearance of the root and ascending aorta. These are potentially important surgical details that may modify the approach to surgery. Furthermore, if a case is obviously severe, and the aortic annulus is small, the size of the annulus should be mentioned. An unusually small root will allow only a small prosthesis, which engenders a gradient little better than the AS it was supposed to relieve—an outcome known as “patient–prosthesis mis-match.” Although such a mismatch probably is not as significant a clinical problem as has been purported, it still has validity in some cases.
The presence of LV hypertrophy is expected. Its absence is conspicuously inconsistent with severe AS. The presence of wall motion abnormalities is important.

Concurrent Subvalvar Stenosis
Subvalvar AS may masquerade as valvar AS, or may be an unsuspected concurrent lesion. Concurrent subvalvar AS confounds accurate estimation of the aortic valve hemodynamics, and is not treated by AVR alone.

Subvalvar AS is revealed by the PISA (flow convergence) at a level well beneath the aortic valve (>1 cm beneath, but influenced by the Nyquist limit). Formerly, emphasis of detection was on pulsed wave Doppler sampling; however, as color flow mapping is essentially a flow map of pulsed-wave Doppler, clear color Doppler depiction of PISA well away from the valve is equivalent.
A two-fold focal step-up in velocity and a “dagger” or tooth shape of the profile are consistent with a intracavitary stenosis.
Provocative maneuvers (e.g., posture change, Valsalva maneuver, leg raise) may reveal the subvalvar gradient to be dynamic.
Zoom views are helpful to localize the step-up, and begin to resolve its nature, e.g., muscular, membrane, or tunnel, or from multiple causes.
TEE is superbly able to define the anatomy responsible for subvalvar obstruction; cardiac MRI is very good, and cardiac CT likely is as well.
Although one catheter study has suggested a 30% incidence of subvalvar gradients, 8 the incidence does not appear to be as high as that.
In the presence of subvalvar AS, the routine sampling of V 1 will fall into the flow convergence/flow acceleration or vena contracta of subvalvar stenosis. If the subvalvar velocity is >1.5 m/sec, the calculations of aortic valve area are skewed.

Low-Gradient Severe Aortic Stenosis

The definition of “low-gradient severe AS” is unresolved and variable, but may be approached as follows:
• Severe AS with an AVA ≤ 0.7 cm 2 with a mean gradient of ≤30 mm Hg due to reduced stroke volume. 9 Several papers have used an AVA of ≤1 cm 2 and a mean gradient of ≤40 mm Hg. 10
The challenge is to distinguish patients with end-stage AS with failing LV systolic function (responsible for the low gradient) from patients with moderate AS with poor LV systolic function, in whom a factor other than AS is responsible for the low gradient.
Low-gradient severe AS can be discounted by a convincingly normal stroke volume: if the gradient is low and the stroke volume is normal, then low-gradient severe AS is unlikely to be present.
Citing low EF% or “grade” to describe low-output AS is not adequate. The stroke volume should be shown to be low to establish that the per-beat output is low, and potentially responsible for the low gradient. There may be normal stroke volume with a low EF% LV (if dilated) and low stroke volume with an LV with normal EF% (if it is under-loaded or if there is severe MR). Therefore, LV grade is not synonymous with output.
EF% generally increases after AVR 10, 11 unless a perioperative infarction occurs, or the LV is intractably stiff. It appears that selected cases of low-gradient severe AS still benefit from AVR, 12 although the data in this field are preliminary. 13
In the presence of low output, both the Gorlin catheterization formula 11,14 and continuity methods are less accurate in the estimation of AVA.
When catheterizing suspected low-gradient AS, use of either two catheters or double-lumen catheters should be considered to eliminate phase shift artifacts, which can introduce a difference of >10 mm Hg in the gradient recording from a femoral side-arm.
Low-gradient AS should be reported as a possibility or probability, depending on how strongly it is believed to be present.
Valve resistance has been proposed as a means of establishing the severity of AS (>300 dynes/sec/cm −5 = severe disease) that is independent of flow output, but it has not been proved to be better than valve area calculation, 9 nor has it been popular. It appears less useful than LVSWL. 6
Determination of contractile reserve in low-gradient severe AS cases
• Consideration of pharmacologic stress (dobutamine up to 20 μg/min/m 2 )
• Determination of AVG and AVA in suspected cases of low-gradient AS (exercise or dobutamine) via echocardiography or catheterization to increase stroke volume by more than 20% and cardiac output (CO) to 4.5 L/min in non -coronary cases is reasonable. The gradient changes can be interpreted in the context of the change of the stroke volume across the valve.
• If stroke volume increases and the AVA increases outside the severe range, then the cause of the low gradient was low output (i.e., pseudostenosis), but the AS is not severe.
• If the stroke volume increases but the AVA remains within the severe range, then the AS is severe (and pseudostenosis is not present).
• However, AVR reduces mortality whether or not there is contractile reserve, and medical therapy is a poor option whether or not there is contractile reserve. Therefore, provocative testing should be done, although it has not been unequivocally proven to be helpful. 9, 13
• Rahimtoola 15 would caution that changes in stroke volume are labeled as an index of contractility and as the hemodynamic responses to dobutamine are complex.
In cases of suspected low-gradient severe AS, particular scrutiny should be afforded to the size of the aortic annulus/root. If the root is unusually small (e.g., 19–20 mm), then the size of prosthesis that would be implanted would confer a moderate gradient, which might be little different from the preoperative gradient.

Discordance of Catheterization and Echocardiographic Determination of the Severity of Aortic Stenosis
When catheterization and echocardiographic assessments of the hemodynamics of AS differ, either test may be in error, both may be correct, or both may be wrong. Whenever there is discordance, each test should be scrutinized for potential errors in recording, calculation, or interpretation.

Possible Reasons for Discordance of Catheterization and Echocardiographic Determination of the Severity of Aortic Stenosis

Recall that nonsimultaneous (echocardiographic and catheterization) estimates of gradient and area are obviously likely to differ more as stroke volume (cardiac output) and peripheral load is variable over time.
Recall that the published SEE of Doppler gradients versus catheterization gradients averages 10 mm Hg.
Recall that the published SEE of Doppler AVA versus catheterization gradients is about 0.3 cm 2 .
Recall that the following invariably reduce the accuracy of echocardiographic estimates of AVG and AVA:
• Measuring <3 beats of V 1 , and V 2
• Measuring <5 beats of V 1 , and V 2 if in afibrillation
• Not measuring (planimetering) the full width and symmetry of the spectral profile
• Use of a single measurement of LVOT if it was unclear
• Poor alignment for V 1 or V 2 sampling
• Uncertain location of V 1 sampling
• Subvalvar gradients
• Pressure recovery

Echocardiography Estimates Aortic Valve Area Lower Than Does Catheterization (A Common Scenario)

Echocardiography calculates effective orifice area (EOA), whereas the Gorlin formula calculates anatomic area. Hydrodynamic studies establish that EOA does not equal the actual orifice area (“anatomic” area), as flow converges into a smaller vena contracta. EOA is always less than the anatomic/actual oriface area.
If the V 1 is sampled too low (within the LV), the V 1 /V 2 ratio is too small and the AVA is calculated as too low.
LVOT may be mismeasured (i.e., too small) due to poor alignment.
Pressure recovery/localized gradient, especially with small aortic root sizes, may yield a higher local gradient than average peak or mean gradient. Catheterization cannot readily discern localized gradients, and echocardiography cannot always establish that a localized gradient has occurred.
A jet of mitral insufficiency may be sampled and misinterpreted as an AS jet. This is an avoidable and major error that most commonly occurs when the anteriorly directed jet from a posterior-leaflet flail wraps along the posterior wall of the aorta. The high velocity of MR jets would suggest severe AS. An MR jet is wider than an AS jet, because its ejection period usually includes (what would otherwise be) the isovolumic contraction and relaxation periods. Correct alignment to avoid MR can be guided using color Doppler.
Subvalvar stenosis accounted for most of the gradient, but was not identified on echocardiography.
The continuity calculation of AVA is significantly flow-dependent, 7, 16 and is prone to clinically significant standard error.

Echocardiography Estimates Aortic Valve Area Greater Than Does Catheterization

Under-sampling of AS jet
• Poor sampling alignment
• Poor signal intensity and lack of the true central peak
LVOT dimension measured as too large

Echocardiography Estimates Aortic Valve Gradient Greater Than Does Catheterization

There is the pressure–recovery phenomenon of a localized jet (typically seen in a small aorta—STJ dimension < 30 mm).
MR sampled in lieu of AS jet
Subvalvar or intracavitary stenosis accounted for most of the gradient calculated by echocardiography, but the valvar stenosis was not discriminated; catheterization discriminated between the presence of a subvalvar/intracavitary gradient and the valvar gradient and recorded a lower transvalvar gradient.

Echocardiography Estimates Aortic Valve Gradient Lower Than Does Catheterization

Under-sampling of AS jet (e.g., poor alignment, poor signal intensity)


Cardiac Catheterization Assessment of Aortic Stenosis

Usual Technique

Pulmonary artery catheter(s) for right-sided pressures and thermodilution-estimated CO
Performance of O 2 uptake for Fick calculation of cardiac output as a cross-check for CO calculation
Single femoral sheath (less risk and cost than two punctures/sheaths) for side-arm pressure recording, and introduction of a catheter into the aorta, then into the LV for:
• LV to aortic (femoral) pressure gradients, and
• Ejection time interval (systolic ejection period [SEP]): the average width (time) of the gradients
• However, use of the “systemic” arterial pressure from the femoral sheath side arm is less accurate than using either a second catheter or a double lumen catheter to more appropriately and accurately measure pressure in the ascending aorta. 17
Verification of pressure waveforms (discussed in the following section)
The Gorlin equation is employed. It requires the following variables: CO, SEP, heart rate, gradient. The equation uses variables that are readily obtained at cardiac catheterization.

Gorlin Equation
The Gorlin equation is as follows:

where CO = cardiac output, SEP = systolic ejection period, HR = heart rate, and MG = mean gradient.

Historically, the Gorlin equation constant was developed for mitral stenosis, not aortic stenosis, as flow dependence with mitral stenosis is less than for AS. 18
The Gorlin equation purportedly estimates anatomic area (not EOA), because it was validated against surgery and autopsy (for mitral stenosis). 18

Gorlin Formula Issues

CO Issues

CO is not reproducible within 15% regardless of technique.
Thermodilution estimate of CO is rendered less accurate by significant tricuspid regurgitation, which may not be known to be present.
Estimation of CO by the Fick principle is not likely more accurate, in the real world, but does offer a “cross-check.”
3 mL/kg is an estimate of oxygen consumption, and has its own variance

Gradient Issues 19

Ideally, two catheters, or a double-lumen catheter, would be used to record the gradient, but this tends not to be real-world practice.
The use of a femoral pressure tracing in lieu of an ascending aortic pressure tracing raises several issues that must be addressed: 19
• There is an associated time delay in its upslope of the femoral arterial tracing that must be adjusted/corrected for.
• “Time correction” (~40–50 msec) to make the up-slopes of the femoral and LV tracings coincident in an attempt to eliminate the inherent likelihood of overestimation of gradient. However
• Not using a time correction leads to overestimation of the gradient by about 10 mm Hg. 20
• Using a time correction leads to underestimation of the gradient by about 10 mm Hg, 20 because the femoral upslope is faster and the peak is taller (especially in older, hypertensive patients)
• Therefore, there is no perfect means to be always within 10 mm Hg. Although this is not a major issue in a usual clear-cut severe case of AS, a 10-mm Hg difference is meaningful in suspected low-gradient severe AS.
• When femoral tracings are in doubt, a centrally placed second catheter should be used.
It has been suggested that there is a high incidence of subvalvar stenosis concurrent with valvar stenosis; however, only a Millar catheter can discern this accurately. 8
Gradients will vary with atrial fibrillation, and more beats than usual (ideally, 10) should be averaged. 19
Drift of the “zero” baseline of either transducer

Systolic Ejection Period
The SEP can be measured to either the LV–aorta pressure crossover, or to the incisura/anacrotic “notch” of the aortic pressure tracing. When recorded more distally, the “hangout” interval between the two can be significantly greater. 17

Heart Rate
Heart rate must be averaged to account for sinus variation or arrhythmia, and especially for atrial fibrillation.

A “Constant”

A composite discharge cofficient C or K and a combined empirically derived constant (includes correction of conversion of mm Hg to cm H 2 O)
The constant (1.0) differs according to different CO outputs 14, 21 and is, therefore, clearly a variable.
• This renders the equation less accurate if CO is less than normal (<4 L/min), especially if it is <3 L/min; i.e., the equation is clearly flow-dependent. 7, 14, 19, 22 Unfortunately, low flow is common in cases of advanced valvular disease.


Catheterization-Responsible Reasons for Discordance

Catheterization Estimates Aortic Valve Area Greater Than Does Echocardiography

Catheterization estimates anatomic area that is theoretically larger than echocardiographic estimates of EOA.
Measured gradient using the femoral side-arm is less than the central real gradient because of higher femoral systolic pressure.
Averaged beats (especially if in atrial fibrillation) are less than the true average.
Zero drift

Catheterization Estimates Aortic Valve Area Less Than Does Echocardiography

Incorrect (incomplete) adjustment of femoral and LV waveforms
Measured beats (especially if in atrial fibrillation) are not representative of (are greater than) the average.
The presence of the catheter itself through the aortic valve orifice is not likely to reduce the AVA significantly.
Zero drift correction error
AI across the aortic valve leads to thermodilution estimate of CO, underestimating actual per beat aortic valve flow.

Catheterization Estimates Aortic Valve Gradient Greater Than Does Echocardiography

Sufficient time correction of the femoral side-arm pressure waveform was not applied.
Femoral waveform was used in lieu of aortic root waveform.
(Usually unsuspected) subvalvar gradient is added to valvar gradient.
Catheterization recordings of greater gradients than were obtained by echocardiography are not likely due to the presence of the catheter itself narrowing the stenotic area; the catheter is unlikely to confer a pressure difference >5 mm Hg. Larger catheters may cause larger gradients: Carabello reported a 10 mm Hg (peak) difference on pullback in tightly blocked valves. 23
Especially likely to occur if in atrial fibrillation (where higher heart rates reduce AS gradients) during echocardiography and in sinus rhythm during catheterization
Zero drift correction error

Catheterization Estimates Aortic Valve Gradient Less Than Does Echocardiography

Pigtail holes straddle the aortic valve.
Especially if in atrial fibrillation (where higher heart rates reduce AS gradients) during catheterization and in sinus rhythm during echocardiography
Zero drift correction error

The Most Common Predictors of Echocardiography: Catheterization Discordance in Aortic Valve Area

Difference in cardiac output 16
Difference in mean gradient 16

Summary

The echocardiographic assessment of AS must be hemodynamically focused and comprehensive.
Knowledge of the many details of echocardiography and catheterization determinations of AVA and gradient is essential to navigate cases of discordance.
The gradient of AS is a “per-beat” function.
The indications for aortic valve replacement and for balloon valvotomy are presented in Boxes 2-1 and 2-2 . The optimal role of the “new kid on the block,” percutaneous and transapical valve replacement, is not yet clearly defined.

BOX 2-1 Aortic Valve Replacement: ACC/AHA 2006 Recommendations

Class I

1. AVR is indicated for symptomatic patients with severe AS. (Level of evidence: B)
2. AVR is indicated for patients with severe AS undergoing CABG. (Level of evidence: C)
3. AVR is indicated for patients with severe AS undergoing surgery on the aorta or other heart valves. (Level of evidence: C)
4. AVR is recommended for patients with severe AS and LV systolic dysfunction (EF < 0.50). (Level of evidence: C)

Class IIa
AVR is reasonable for patients with moderate AS undergoing CABG or surgery on the aorta or other heart valves. (Level of evidence: B)

Class IIb

1. AVR may be considered for asymptomatic patients with severe AS and abnormal response to exercise (e.g., development of symptoms or asymptomatic hypotension). (Level of evidence: C)
2. AVR may be considered for adults with severe asymptomatic AS if there is a high likelihood of rapid progression (e.g., age, calcification, and CAD) or if surgery might be delayed at the time of symptom onset. (Level of evidence: C)
3. AVR may be considered in patients undergoing CABG who have mild AS when there is evidence, such as moderate-to-severe valve calcification, that progression may be rapid. (Level of evidence: C)
4. AVR may be considered for asymptomatic patients with extremely severe AS (aortic valve area < 0.6 cm 2 , mean gradient > 60 mm Hg, and jet velocity > 5.0 m/sec) when the patient’s expected operative mortality is ≤1.0%. (Level of evidence: C)

Class III
AVR is not useful for the prevention of sudden death in asymptomatic patients with AS who have none of the findings listed under the class IIa/IIb recommendations. (Level of evidence: B)
AS, aortic stenosis; AVR, aortic valve replacement; CABG, coronary artery bypass surgery; CAD, coronary artery disease; EF, ejection fraction; LV, left ventricle.
From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol . 2006;48(3):e1–e148.

BOX 2-2 Aortic Balloon Valvotomy: ACC/AHA 2006 Recommendations

Class IIb

1. Aortic balloon valvotomy might be reasonable as a bridge to surgery in hemodynamically unstable adult patients with AS who are at high risk for AVR. (Level of evidence: C)
2. Aortic balloon valvotomy might be reasonable for palliation in adult patients with AS in whom AVR cannot be performed because of serious comorbid conditions. (Level of evidence: C)

Class III
Aortic balloon valvotomy is not recommended as an alternative to AVR in adult patients with AS; however, certain younger adults without valve calcification may be an exception. (Level of evidence: B)
AS, aortic stenosis; AVR, aortic valve replacement.
From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2006;48(3):e1–e148.

BOX 2-3 Valvular Disease: Focused Update on Endocarditis: ACC/AHA 2008 Guidelines
Class IIa indication: Antibiotic prophylaxis is no longer indicated in patients with aortic stenosis for prevention of infective endocarditis
From ACC/AHA 2008 guideline update on valvular heart disease: focused update on infective endocarditis. J Am Coll Cardiol. 2008;52:676–685.

BOX 2-4 Appropriateness Criteria and Indications for Cardiac Imaging Modalities and Cardiac Catheterization for the Assessment of Aortic Stenosis

Transthoracic Echocardiography

ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 26

Native Valvular Stenosis with TTE

Routine surveillance (<3 yr) of mild valvular stenosis without a change in clinical status or cardiac examination
Appropriateness criteria: I; median score: 3
Routine surveillance (≥3 yr) of mild valvular stenosis without a change in clinical status or cardiac examination
Appropriateness criteria: A; median score: 7
Routine surveillance (<1 yr) of moderate or severe valvular stenosis without a change in clinical status or cardiac examination
Appropriateness criteria: I; median score: 3
Routine surveillance (≥1 yr) of moderate or severe valvular stenosis without a change in clinical status or cardiac examination
Appropriateness criteria: A; median score: 8

Chronic Valvular Disease—Asymptomatic with Stress Echocardiography

Mild aortic stenosis
Appropriateness criteria: I; median score: 3
Moderate aortic stenosis
Appropriateness criteria: U; median score: 6
Severe aortic stenosis
Appropriateness criteria: U; median score: 5

Chronic Valvular Disease—Symptomatic with Stress Echocardiography

Evaluation of equivocal aortic stenosis
Evidence of low cardiac output or LV systolic dysfunction (“low gradient aortic stenosis’’)
Use of dobutamine only
Appropriateness criteria: A; median score: 8

ACC/AHA/ASE 2003 Guideline Update for the Clinical Application of Echocardiography 27

Low-flow/low-gradient aortic stenosis: Class IIa
• Dobutamine stress echocardiography is reasonable to evaluate patients with low-flow/low-gradient AS and LV dysfunction. (Level of evidence: B)

ACC/AHA 1997 Guidelines for the Clinical Application of Echocardiography 28

Indications for Echocardiography in Valvular Stenosis

Class I
• Diagnosis; assessment of hemodynamic severity
• Assessment of LV and RV size, function, and/or hemodynamics
• Re-evaluation of patients with known valvular stenosis with changing symptoms or signs
Class IIa
• Assessment of changes in hemodynamic severity and ventricular compensation in patients with known valvular stenosis during pregnancy
• Re-evaluation of asymptomatic patients with severe stenosis
• Assessment of the hemodynamic significance of mild to moderate valvular stenosis by stress Doppler echocardiography
Class IIb
• Re-evaluation of patients with mild to moderate aortic stenosis with LV dysfunction or hypertrophy even without clinical symptoms
• Re-evaluation of patients with mild to moderate aortic valvular stenosis with stable signs and symptoms
Class III
• Routine re-evaluation of asymptomatic adult patients with mild aortic stenosis having stable physical signs and normal LV size and function

ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 29

Class I

• Echocardiography is recommended for the diagnosis and assessment of AS severity. (Level of evidence: B)

• Echocardiography is recommended in patients with AS for the assessment of LV wall thickness, size, and function. (Level of evidence: B)
• Echocardiography is recommended for re-evaluation of patients with known AS and changing symptoms or signs. (Level of evidence: B)
• Echocardiography is recommended for the assessment of changes in hemodynamic severity and LV function in patients with known AS during pregnancy. (Level of evidence: B)
• TTE echocardiography is recommended for re-evaluation of asymptomatic patients: every year for severe AS; every 1 to 2 years for moderate AS; and every 3 to 5 years for mild AS. (Level of evidence: B)

ACCF/ASE/ACEP/AHA/ASNC/SCAI/SCCT/SCMR 2008 Appropriateness Criteria for Stress Echocardiography 30

Stress study for hemodynamics (includes Doppler during stress)
Evaluation of equivocal AS
Evidence of low cardiac output
Use of dobutamine
Appropriateness criteria: A; median score: 8
Severe aortic or mitral stenosis
Appropriateness criteria: I; median score: 2

Transesophageal Echocardiography

ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 26

TEE as Initial or Supplemental Test—Valvular Disease

Evaluation of valvular structure and function to assess suitability for, and assist in planning of, an intervention
Appropriateness criteria: A; median score: 9

ACC/AHA/ASE 2003 Guideline Update for the Clinical Application of Echocardiography 27

Class I
• Use of echocardiography (especially TEE) in guiding the performance of interventional techniques and surgery (e.g., balloon valvuloplasty and valve repair for valvular diseases)

Cardiac Catheterization

The platform to perform percutaneous aortic valvulopathy and percutaneous aortic valve insertion

ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 29

Aortic Stenosis: Indications for Cardiac Catheterization 29

Class I
• Coronary angiography is recommended before AVR in patients with AS at risk for CAD. (Level of evidence: B)
• Cardiac catheterization for hemodynamic measurements is recommended for assessment of severity of AS in symptomatic patients when noninvasive tests are inconclusive or when there is a discrepancy between noninvasive tests and clinical findings regarding severity of AS. (Level of evidence: C)
• Coronary angiography is recommended before AVR in patients with AS for whom a pulmonary autograft (Ross procedure) is contemplated and if the origin of the coronary arteries was not identified by noninvasive technique. (Level of evidence: C)

Class III
• Cardiac catheterization for hemodynamic measurements is not recommended for the assessment of severity of AS before AVR when noninvasive tests are adequate and concordant with clinical findings. (Level of evidence: C)
• Cardiac catheterization for hemodynamic measurements is not recommended for the assessment of LV function and severity of AS in asymptomatic patients. (Level of evidence: C)

Low-Flow/Low-Gradient Aortic Stenosis

Class IIa
• Cardiac catheterization for hemodynamic measurements with infusion of dobutamine can be useful for evaluation of patients with low-flow/low-gradient AS and LV dysfunction. (Level of evidence: C)

Cardiac Computed Tomography

ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 31

Evaluation of Intra- and Extracardiac Structures

Characterization of native cardiac valves
Suspected clinically significant valvular dysfunction
Inadequate images from other noninvasive methods
Appropriateness criteria: A; median score: 8

Cardiac Magnetic Resonance

ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Magnetic Resonance Imaging 32

For characterization of native and prosthetic cardiac valves—including planimetry of stenotic disease and quantification of regurgitant disease
For patients with technically limited images from echocardiogram or TEE
Appropriateness criteria: A; median score: 8
For quantification of LV function
Appropriateness criteria: A; median score: 8

SCMR Consensus Panel Report; Indication for Cardiac Magnetic Resonance Imaging 33

For cardiac chamber anatomy and function in patients with valvular disease
For quantitation of valvular stenosis
• Class I

Nuclear

ACCF/ASNC/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging 34

Evaluation of LV Function

Assessment of LV function with radionuclide angiography (ERNA or FP RNA)
In absence of recent reliable diagnostic information regarding ventricular function obtained with another imaging modality
Appropriateness criteria: A; median score: 8
Appropriateness criteria: A; appropriate; I, inappropriate; U, uncertain.
AS, aortic stenosis; AVR, aortic valve replacement; CAD, coronary artery disease; LV, left ventricular; MPI, myocardial perfusion imaging; RV, right ventricular; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.
TABLE 2-1 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Aortic Stenosis MODALITY PROS CONS/CAVEATS Transthoracic Echocardiography

2D echocardiography
• 2D short-axis imaging of the aortic valve to determine the area is feasible in a minority of cases.
• Severe AS is generally associated with minimal apparent opening of the valve on short- and long-axis imaging. More than minimal opening is generally not associated with severe AS.     Doppler echocardiography

• Mean gradient determination by continuous wave Doppler, if sampling is well aligned, yields one of the best echocardiographic determinations of AS severity, and one that correlates well to catheter-derived determination of mean gradient.

• Mean gradient must be analyzed in the context of the total forward stroke volume (normal stroke volume index = 45 ± 13 mL/m 2 ).
• Potential problems with velocity measurement and gradient determination
• Inadequate alignment
• Prone to undersampling
• Pressure recovery within a small aortic root may yield a higher mean gradient than is appreciated by catheterization.
• Gradients are poorly suited to describe AS severity in low-flow states, and also in high-flow states.  

• Peak instantaneous gradient is not the “peak” (to-peak) gradient of catheterization

• Generates confusion about which peak gradient is referred to; seldom has a catheterization equivalent for comparison.
• Not the threshold for determining severity  

• A peak velocity of > 4.5 m/sec is a robust direct measurement of and index of severe AS.    

• V 2 :V 1 ratio > 4 is a fairly reliable index of severe AS.    

• The continuity relation to determine AVA (AVA = 0.785 x LVOT 2 diam x ), which is the effective orifice area rather than the “anatomic” area, affords a relatively, but not absolutely, flow-independent determination of AVA.

• Three variables used to solve for area impart, collectively, a fair amount of error.
• LVOT diameter measurement is the most problematic component as the measurement is squared, doubling the percentage error. Not fully flow independent; less accurate at low-flow states
• Less applicable for V 1  > 1.5 m/sec
• Must be analyzed in the context of the total forward stroke volume (normal stroke volume index = 45 ± 13 mL/m 2 )
• Prone to undersampling
• Pressure recovery within a small aortic root may yield a higher mean gradient than is appreciated by catheterization.
• Less suited to low-flow states Transesophageal Echocardiography

• TEE short-axis planimetry to measure the orifice area offers the best echocardiographic means to establish AVA by flow- and Doppler-independent means. Short-axis planimetry has been validated by generally small series that demonstrate high feasibility (93%), except when the orifice is “pin-hole.” Correlation with Gorlin determinations of AVA is excellent: r = 0.95; with 96% sensitivity and 88% specificity for AVA <0.75 cm 2 36

• Offers little over continuity equation
• Assumes that the orifice is planar, which often is not the case
• Resolving how far down side slits to include is very subjective.
• Calcium “blooming” falsely extends into orifice, diminishing its perception.  

• TEE gradient determination of AS from transgastric views is feasible and, in experienced hands, accurate.    

• Superb alternative test to accurately determine the LVOT diameter for continuity equation calculation, measuring in the long axis at about 130°. TEE determinations of the LVOT diameter tend to be slightly smaller than those of TTE (mean difference: –0.05 ± 0.09 cm; P  = 0.003. Diastolic TEE diameter tends to be slightly smaller than systolic: –0.03 ± 0.07, P  = 0.005). Intra- and interobserver variability for TEE determinations of LVOT diameter are 4 ± 3% and 3 ± 2%. 37    

• Similarly, a superb (probably the best) test to assess for subvalvar causes of stenosis.   Cardiac CT

• Tends to be utilized little in the routine assessment of AS to date, other than determining the diameter of the ascending aorta when this is unclear.    

• Valve morphology (bicuspid) may be established by gated cardiac CT. Note: systolic phase imaging is needed, rather than the usual diastolic phase imaging.    

• Accurate determination of the LVOT diameter by gated cardiac CT may be useful to supply a firmer determination of this important variable to echo continuity equation calculation of valve area.    

• AVA by short-axis imaging is feasible. ( Note: systolic phase imaging is needed rather than the usual diastolic phase imaging.) Small studies establish correlation with TTE planimetry (r = 0.88, P  < 0.001) and TEE planimetry (r = 0.99, P  < 0.0001) and reasonable accuracy (±0.2 cm 2 ). 38 As the technique evolves, AVA determination by cardiac CT may be more commonly employed.

• Planimetry may be performed, but valve calcification confers “blooming” and partial volume averaging artifacts that underestimate valve area. Without optimal use of filters/kernels, the encroachment of calcium blooming will diminish perceived orifice area.  

• Calcium scoring of the valve has some correlation with the severity of AS severity (in small studies).

• However, it is correlation without accuracy. 39 Massive calcification (>3700 AU) is consistent with severe stenosis. 38
• The covariates effects of age, gender, and renal dysfunction are not established.
• The effect of calcium on valve insufficiency has not been investigated.  

• Gated cardiac CT is an excellent means by which to appreciate subvalvar and LVOT lesions.      

• No functional aspects of AS can be established by cardiac CT. Cardiac MRI

SSFP sequences
• Direct measurement of AVA by short-axis SSFP imaging: SSFP sequences can accurately determine valve morphology (mean difference between observers: –0.03 ± 0.07, CI [0.02 – 0.04]; limits of agreement, 0.11 ± 0.16 cm 2 ).
• Calcium signal image voids are less a problem for CMR than is calcium blooming for cardiac CT.
• CMR three-chamber view SSFP cine sequences are a very good means by which to appreciate subvalvar and LVOT lesions.

• As with all planimetric methods, assumes that the orifice is planar.
• AS jet flow signal voids and calcium signal voids may confound measurement  

LGE sequences:
The extent of LGE appears to correlate with mortality risk in patients with AS. 40    

VEPC sequences:
Assessment of gradient is feasible using the VEPC technique, but validation is “early.” The encoding velocity must be increased to exceed that of the AS jet. Some correlation has been shown by small single-center series 41 (correlation of VEPC vs. planimetry: r 2  = 0.86, P  < 0.001; mean difference 0.05 ± 0.15 CI [0.02 – 0.08]; limits of agreement, –0.26 – 0.36 cm 2 ). 42 In general, more advanced methods (which are less available) are more accurate than conventional flow recording methods, which tend to be unruly. 43

• Validation exists, but the technique is very challenging, and often disappointing. Nuclear NA

• Perfusion imaging has not supplanted coronary angiography for the evaluation of angina in the clinical setting of AS. Chest Radiography

• Chest radiography corroborates the presence of left heart failure—the most pressing indication for valve replacement.
• Chest radiography is useful to identify some degree of associated dilation of the aorta and also calcification of the ascending aorta that may complicate surgery.

• Identification of aortic valve calcification, unless massive, is as difficult to appreciate on chest radiography as it is easy to appreciate on fluoroscopy. Cardiac Catheterization

• Catheterization determination of the mean transvalvavar gradient is a venerable and solid determination of the severity of AS, and is particularly accurate if double-lumen catheters are used to eliminate phase-delay artifacts imparted by use of the femoral side-arm to record pressure.

• Use of femoral side-arm recording as a surrogate of ascending aorta waveform may impart significant error, especially to low-gradient cases. As with echocardiography, often too few cardiac cycles are analyzed.  

• The catheterization “peak-to-peak” gradient is a quick and easy determination of the severity of AS.

• The peak-to-peak gradient does not equate with mean or peak instantaneous gradients. If the “pullback” is untidy due to motion artifact or PVCs, error is imparted to the cardiac cycles post-pullback. This description of gradient is not the traditional one (mean gradient) used to establish the severity of AS severity.  

• The determination of “anatomic” AVA by the Gorlin equation, if each variable is verified and critically approached, is the traditional gold standard of AVA calculation.

• It is not flow “independent,” and it is less accurate in low-flow states.
2D, two dimensional; AS, aortic stenosis; AU, absorbance units; AVA, aortic valve area; CMR, cardiac magnetic resonance; diam, diameter; LGE, late gadolinium enhancement; LVOT, left ventricular outflow tract; NA, not applicable; PVC, premature ventricular contractions; SSFP, steady-state free precession; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography; VEPC, velocity-encoded phase contrast; VTI, velocity time integral.

Figure 2-2 Left : V 1 and stroke volume. Right: V 2 , gradient and area calculation. Severe aortic stenosis with a mean gradient of 109 mm Hg; a stroke volume of (60 mL), normal for a smaller female; and an aortic valve area of 0.3 cm 2 . The patient’s body surface area was 1.6 m 2 .

Figure 2-3 Results from the same patient showing differences in V 2 sampling, depending on the type of probe used and the location of sampling. Left image: Imaging probe used sampling from the apex: mean gradient of 19 mm Hg; AVA 1.8 cm 2 Middle image: Imaging probe used from the right parasternal area: mean gradient of 14 mm Hg; AVA 1.8 cm 2 Right image: Nonimaging probe sampling from the right parasternum, achieving better depiction and more complete depiction of the profile: mean gradient of 78 mm Hg; AVA 0.9 cm 2 .

Figure 2-4 Differences in V 2 sampling in atrial fibrillation, according to R-R interval. The gradients vary widely depending on the length of the preceding R-R interval. Although the convention for echocardiography is to use the highest velocities for calculation of gradient and area, when the spectral profiles are as defined and as adequate as these, the average of five spectral profiles should be used for gradient, flow, and area calculations.

Figure 2-5 The effect of heart rate on aortic valve gradient. Upper left: Pulsed wave spectral profile of left ventricular outflow tract sampling when the patient presented in second degree (2:1) atrioventricular (AV) block at 35 bpm. Note the very elevated velocity time integral (VTI) (37 cm). Upper right: The same patient after undergoing permanent pacing at a heart rate of 65 bpm. Note the reduction of the VTI (to 28 cm). Lower left: Continuous wave Doppler profile in the same patient in second-degree (2:1) AV block at 35 bpm, with a peak gradient of 41 mm Hg. Lower right: Continuous wave Doppler profile across the valve when paced at 60 bpm, with a peak gradient of 20 mm Hg. Halving the heart rate doubled the gradient, because of normal contractile reserve. Conversely, doubling the heart rate would have reduced the gradient.

Figure 2-6 Low-gradient, severe aortic stenosis. Upper left: Two-dimensional (2D) end-systolic view of left ventricle (LV) before aortic valve replacement (AVR). Upper right: 2D end-systolic view of LV after AVR. Lower left: Left ventricular outflow tract (LVOT) flow indicating stroke volume before AVR. Lower right: LVOT flow indicating stroke volume after AVR. With AVR, there was a significant improvement in ejection fraction (Δ+35%) and stroke volume (Δ + 50%). The patient underwent uneventful AVR.

Figure 2-7 Subvalvar aortic stenosis (AS) in a patient with suspected valvar AS. Upper left: A linear ridge is seen in the left ventricular outflow tract (LVOT). Upper right: A proximal isovelocity surface area (PISA) is forming well before the aortic valve, before the ridge, consistent with subvalvar stenosis. Middle left: Posterior long-axis view shows a narrow ridge in the LVOT consistent with a membrane. Middle right: Zoom view of the LVOT from the apical four-chamber view shows a PISA forming before the membrane, well before the aortic valve, consistent with subvalvar flow acceleration (stenosis). Lower left: M-mode view of the aortic valve shows mid-systolic partial closure of the otherwise normal aortic valve. Lower right: Catheterization pull-back through the LVOT shows a 70-mm Hg fall in pressure within the LV, consistent with an intraventricular obstruction from a membrane.

Figure 2-8 Concurrent intraventricular obstruction and aortic valve stenosis. The upper images reveal left ventricular hypertrophy (LVH) with a small cavity. Color Doppler flow mapping depicts flow acceleration at the narrowest part of the LV cavity, where the posteromedial papillary muscle nearly opposes the interventricular symptom. The lower image of continuous wave Doppler sampling from the apex through both the interventricular gradient and the aortic valvular stenosis depicts the late-peaking dagger- or fang-shaped flow profile due to the intraventricular obstruction, and also the symmetrical parabolic contour of the aortic valve stenosis.

Figure 2-9 Concurrent intraventricular obstruction and aortic stenosis. Upper left: Pulsed-wave Doppler sampling in the mid-ventricle reveals the typical dagger- or fang-shaped late-peaking spectral flow profile of an intraventricular or dynamic obstruction. Upper right: Grayscale image with colored Doppler flow mapping reveals the site of obstruction in the mid-ventricle. Lower left: Continuous wave Doppler sampling from the apical position reveals superimposition of the spectral profiles of the intraventricular obstruction and also of the valve stenosis obstruction. Lower right: Spectral display of continuous wave Doppler sampling of the aortic valve selectively and without contamination of the intraventricular gradient reveals a complete and symmetrical parabolic profile of the aortic stenosis.

Figure 2-10 The effect of differing R-R intervals on aortic valve gradient. The patient is in atrial fibrillation. With longer R intervals, the gradient is higher; with shorter R intervals, the gradient is less. With very short R intervals, there is very little flow out the aortic valve and very little recorded gradient. Hence, tachycardia diminishes aortic valve gradients and bradycardia enhances them.

Figure 2-11 Transesophageal echocardiography (TEE) assessment of valvar aortic stenosis. Upper left: Long-axis view of the aortic valve, left ventricular outflow tract (LVOT), and aortic root. The valve is thickened and likely calcified in some places. Upper right: Transgastric sampling along the LVOT and across the aortic valve depicts both the subvalvar spectral profile and the transvalvar spectral profile. With careful sampling, and sufficient time, the peak gradient often can be well assessed by TEE. Use of the continuity equation with the LVOT dimension, V 1 V 2 sampled from the upper two images yielded an aortic valve area of 0.75 cm 2 Middle images: The aortic valve in cross-section in diastole ( left ) and systole ( right ). The aortic valve orifice can be appreciated, although it is not clear how far it extends along the commissures. It is necessary to sample at a number of heights to ensure that measurements are made at the narrowest level. Lower right: Outlining of the approximate aortic valve area/orifice yielded a measurement of 0.8 cm 2 .

Figure 2-12 Cardiac MRI steady-state free precession images along and across the aortic valve level. Upper images: Dephasing due to the flow acceleration yields lower signal and the appearance of darkened blood. The views that depict the left ventricle reveal a small cavity with left ventricular hypertrophy. Lower images : Short-axis view ( lower left ) with its reference image ( lower right ). Planimetry of the aortic valve is feasible but does require situating the level of imaging at the actual level of the stenosis.

Figure 2-13 Cardiac MRI steady-state free precession imaging at the aortic valve level in diastole ( left ) and in systole ( right ). The aortic valve morphology is bicuspid with a raphae in the 6 o’clock position. The crescent-like aortic valve orifice is apparent in systole and measured 0.8 cm 2 by planimetry.

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3 Aortic Insufficiency

Goals of Echocardiography in Aortic Insufficiency

To determine that aortic insufficiency (AI) is present
To determine the severity of AI
To determine the hemodynamics of AI
To determine the cause of AI
To assess and describe the left ventricle (LV) in detail
To describe the aorta
To describe other lesions, if present

Scanning Issues

Required Parameters to Obtain from Scanning

Cause of AI
• Aortic valve detail
• Aortic root detail
Severity of AI
• Color Doppler of the left ventricular outflow tract (LVOT) detects AI, but only poorly approximates severity
• Aortic flow reversal pattern: abdominal flow reversal is more useful than is thoracic flow reversal
• Further quantification if AI is worse than “mild” (i.e., moderate or severe): R Vol , R Fraction
LV
• Size: end-systolic dimension (ESD), end-diastolic dimension (EDD), end-systolic volume (ESV), end-diastolic volume (EDV)
• Systolic function: overall and regional
Echo Doppler assessment of AI severity should yield internal consistency. The choice of which parameter to use is lab dependent, but the logic of seeking concordance with volumetric quantification and peripheral (abdominal aortic) flow signs is clear.
Use of color Doppler mapping alone to determine the severity of AI is precarious, and should be discouraged.
The assessment of AI severity should incorporate multiple methods. Stronger methods include:
• Reversal of abdominal aortic flow
• Volumetric determinations (R Volume , R Fraction )
• Judicious use of color Doppler height and area “indexed” to the LVOT

Determination of the Cause of Aortic Insufficiency
The cause of AI usually is apparent from transthoracic echocardiography (TTE), although transesophageal echocardiography (TEE) often is needed to assess the mechanism and probable underlying disease. Fenestrations and some perforations are difficult to image even by TEE. Because some underlying diseases require independent treatment, it is important to recognize the etiology of AI to the fullest extent possible.

Root causes
Dilation of the root/sinotubular junction exerts traction on the commissures of the valve, tenting the cusps and reducing coaptation. Dilation usually leads to a centrally originating jet of AI, as the failure of coaptation is greatest centrally.
Aortic dissection and intramural hematoma * : Dissection and intramural hematoma of the root may lead to AI from several mechanisms. Dissection into the root will compromise the support of the adjacent cusp, which then prolapses, resulting in eccentric AI. Another mechanism seen in aortic dissection that may occur is prolapse of the intimal flap into the valve orifice, preventing it from coapting.
The number of possible aortic pathologies and their clinical importance is the basis of use of complementary imaging modalities such as CT and CMR to adequately assess the aorta in some cases of AI.
Valve causes
Thickening
• Age-related
• Hypertension
• Atherosclerosis
• Rheumatic
• Fibrocalcific
• Aortitis
• Fenestration
Myxomatous degeneration (approximately 10% of pure severe AI)
Endocarditis *
Traumatic *
Hypertension: patients with systolic hypertension commonly have mild leaflet thickening and mild AI. 1

Problems with Color Doppler Flow-Mapping “Quantification”
The principal contribution of color Doppler is to detect that AI is present, so that its severity can be determined by other means. Color Doppler flow mapping of the LVOT, LV, or proximal descending aorta is not reliably useful to establish the severity of AI, given the many eccentric and complex jets that are poorly represented by this technique.
LVOT color Doppler flow mapping is dependent on gain, angle, position, jet shape, and orientation, and is not a suitable means to evaluate very eccentric AI (e.g., from flail leaflets). It is not useful as an independent means to establish severity.
Color flow mapping of proximal descending aortic retrograde flow is not useful, because it is non-quantitative and is dependent on gain and image quality. It makes no independent contribution, and, therefore, its use should be discouraged.
AI color jet length into the LV is not useful to determine AI severity, because it cannot reliably distinguish moderate from severe AI.

Spectral and Volumetric Techniques

In general, spectral profiles should be displayed as two-thirds the height of the display, and wide enough so that two or three profiles are available for measurement.
Use of the continuity method for determination of regurgitant volumes is unsuitable if mitral regurgitation of any degree more than mild is present, or if a ventricular septal defect also is present.
It is far more useful to determine that there is retrograde flow in the abdominal aorta than to characterize flow in the proximal descending thoracic aorta. Every effort should be made to record subcostal views/pulsed-wave (PW) Doppler of the abdominal aortic flow profile. If the images obtained using standard echo probes are poor, an abdominal vascular probe is of considerable use to increase the quality of flow recordings.
Retrograde flow velocity time integral (VTI) > 15 cm in the proximal descending thoracic aorta often is used as a sign of severe AI, but the VTI of clearly severe AI often is twice that. The pattern of holodiastolic reversal is consistent with severe AI.
In the context of aortic insufficiency, the anterograde systolic LVOT flow is not the net forward cardiac output—it is the total forward flow (which includes the regurgitant flow).
Total forward stroke volume (if no MR) is described by Simpson’s EDV-ESV or LVOT stroke volume.

Other

Record the systolic and diastolic blood pressure.
If acute severe AI is suspected (as in endocarditis, type A aortic dissection, or trauma), M-mode and PW Doppler examinations of the mitral valve are performed to detect pre-closure signs.

Reporting Issues

Describe the cause of the AI and the severity together: For example, “Severe aortic insufficiency due to a flail leaflet, with a regurgitant fraction of 60%.”
Describe the LV function, both overall and regionally. The presence of overall or regional dysfunction increases the risk of AI.
If the AI is in the severe range, then describe the LV dimensions, as they are indices relevant to surgery.
Recall that color Doppler flow mapping establishes the presence/absence of AI, but does not independently establish severity.
Severe AI
• Severe hemodynamic effect: abdominal (= peripheral) diastolic flow reversal
• R Volume > 60 mL
• R Fraction > 60%
Compare all findings to previous studies.
As with the use of deceleration time (DT) or pressure half-time (PHT) to describe MS severity, their use to describe AI severity is easily confounded by anything that renders the LV compliance abnormal.
Describe the aorta in some anatomic detail. Echocardiography should detect signs of most root diseases relevant to AI.
AI peak velocity is quite variable and depends on blood pressure, the LV diastolic pressure, and the gradient between the two.
In the context of AI, do not report the total forward cardiac output (CO) as the net forward CO.
False-positives of abdominal aortic flow reversal are rare.
Avoid the term “trivial” for AI in general, because it is essentially a normal finding (if the valve is normal); and use of that term may generate confusion about whether or not the valve is pathologic. If the valve is morphologically abnormal, use of the term “mild” is consistent with the inference that the valve is functionally abnormal.

Notes on Echocardiographic Methods to Describe Severity of Aortic Insufficiency

Retrograde Holodiastolic Flow in the Abdominal Aorta
Retrograde holodiastolic flow in the abdominal aorta is sensitive (100%) and specific (96%) for level 3+ or 4+ AI. Consequently, it is one of the best signs to determine whether AI is severe. The potential false-positives include aortopulmonary shunts and patent ductus arteriosus 2 and also, possibly, aortic root to left atrial, right ventricular, or right atrial fistulae, all of which should be evident from color Doppler scanning. Abdominal diastolic flow reversal is analogous to the time-honored peripheral pulse signs used in physical diagnosis.

Retrograde Flow Profiles in the Proximal Thoracic Descending Aorta
Although it is more feasible to sample retrograde flow in the proximal descending aorta, it is of less worth to determine the severity of AI.
The amount of regurgitant flow in the descending thoracic aorta (sampled by PW just beneath the aortic isthmus) can be expressed by several echocardiographic means: the peak velocity of the diastolic regurgitant volume; the time velocity interval (TVI) of the regurgitant flow; the TVI of the regurgitant flow indexed to the systolic flow, or the TVI indexed to the diastolic filling period. As would be anticipated, given the multitude of parameters, it is, overall, less trustworthy as a sign.
The peak velocity of the regurgitant (diastolic) flow correlates with the regurgitant fraction (r = 0.82) and the regurgitant grade by angiography (r = 0.81). AI of 3+ by angiography correlates with a TVI of 22 ± 6 cm/sec SD, and 4+ by angiography with 34 ± 9 cm/sec). 3 End-diastolic flow velocity of 40 cm/sec or greater predicts a regurgitant fraction of 40% or more with a sensitivity of 89% and a specificity of 96%. 4
The integral of the spectral display of diastolic flow recorded from the proximal descending aorta (divided by the integral of the systolic flow) mapped in the proximal descending aorta correlates well with angiographic regurgitant fraction: r = 0.91 5 and r = 0.90; standard error of estimate (SEE) 9%. 6 However, the sign is inaccurate in the presence of aortic stenosis, 7 because the high-velocity systolic aortic stenosis jet continues around the arch in some cases. Neither the “cut-off” for the diastolic flow nor that for the diastolic flow integral/systolic flow integral that it constitutes has been conclusively established for severe AI. Some centers use 15 cm as the threshold above which AI is defined as severe. Obvious pan-diastolic flow above the baseline correlates well with the presence of severe AI, 6 as long as no aorticopulmonary shunt is present.

Color Flow Mapping of the Descending Aorta
Color flow mapping of the descending aorta adds little (if anything) to a standard assessment, and is only useful to set up spectral sampling.

Color Doppler Flow Mapping of the Left Ventricular Outflow Tract
Color Doppler flow mapping of the LVOT is useful to detect AI. Indexing improves correlation 8 with angiography (r = 0.88) and can classify the majority of central AI jets with thoracic (83%) and abdominal (86%) 9 aortic flow profiles. It is a poor technique to assess eccentric AI jets, however, and overall tends to be inaccurate. Indexing is performed to the height or area of the LVOT, to the aortic valve area, or to body surface area, and correlates with severity (r = 0.87). 10 Oblique jets are problematic, because they result in overestimation of severity. Jet length into the LV has been proved to be an in accurate means of describing AI severity, because jets of severe AI can be shorter than jets of moderate AI. Perry 8 proposed the categorizations shown in Table 3-1 .
TABLE 3-1 Categorization of AI Severity by Color Doppler Flow Mapping Indexed to the LVOT AI GRADE JET HEIGHT/LVOT JET AREA/LVOT I 1–24% <4% II 25–46% 4–24% III 47–64% 25–59% IV ≥65% ≥60%
AI, aortic insufficiency; LVOT, left ventricular outflow tract.

Vena Contracta Width and Area
The vena contracta imaged in the posterior long-axis view correlates well ( P < 0.0001) with Doppler effective regurgitant orifice (ERO; r = 0.89) and R Volume (0.90), and 2D methods (r = 0.90, r = 0.90), as well as with angiographic grading (r = 0.82; P = 0.01). 11, 12 A vena contracta width of ≥6 mm is 95% sensitive and 90% specific for diagnosing severe AI (ERO ≥ 30 mm 2 ), 11 and vena contracta area ≥7.5 mm 2 is 100% sensitive and specific for severe AI (R Volume > 50 mL). 12 Vena contracta width appears to be afterload independent. 12
Because small differences in vena contracta dimension measurement (1–2 mm) result in different grading, the technique is very demanding and image quality dependent, and its applicability can be disappointing. The advent of anti-aliasing software may improve the utility of this method.

Effective Regurgitant Oriface Method: Proximal Isovelocity Surface Area and Doppler
The proximal isovelocity surface area (PISA) ERO method correlates well with reference techniques ( P < 0.0001) but exhibits a trend to underestimate ERO due to cases where the AI jet is obtuse. 4 Doppler ERO correlates well with angiographic estimates of ERO (r = 0.97) when the aortic diameter is less than 4.8 cm. 13 Aortic pressure changes may influence the ERO, depending on whether the defect causing the AI is central (dynamic ERO: 51 ± 33% change with pharmacologic hypertension) versus a perforation in a leaflet proper (minimally dynamic orifice (9 ± 7%). 14 Aortic root area is strongly dependent on the aortic diastolic pressure and can vary widely with pharmacologic hypertension. 14

Regurgitant volume of AI (R Volume ):

where Diam = diameter, PA = pulmonary artery, and SV = stroke volume.

 
Regurgitant fraction of AI (R Fraction ):

 
The regurgitant fraction of AI can be calculated by left ventricular outflow as the total forward systolic volume (R Volume + net forward SV) minus anterograde flow anywhere there is no regurgitant flow (mitral level or PA). 3, 15, 16 R Fraction by Doppler correlates well with R Fraction by catheterization: r = 0.96. 3 Using this technique, 3+ and 4+ AI by angiography are associated with 53% and 62% R Fraction by Doppler. 3 The technique is less accurate with depressed left ventricular ejection fraction, and, as would be anticipated, in the presence of mitral regurgitation. 15

Suggested grading for AI:



Aortic Insufficieny Deceleration Time, Pressure Half-Time, and Slope
The PHT assessment of AI is feasible when the spectral profile can be obtained, and AI spectral profile DT and PHT correlate with angiographic AI severity (r = −0.79 and r = −0.89, respectively) 17 19 and are independent of the alignment of sampling. 17 Echo PHT correlates well with catheter-derived PHT, but factors such as systemic vascular resistance and aortic and LV compliance all affect AI PHT. Thus, unless the PHT is <300 msec where AI is always severe, the PHT method is not reliable for distinguishing different grades of AI. 20 Slope also correlates with left ventricular end-diastolic pressure (LVEDP; r = 0.80 18 and r = 0.84), 21 but in two studies 18, 21 the SEE has been reported to be 5 mm Hg. Therefore, this technique is unreliable in the presence of an abnormal ventricle, 22 or varying aortic load on the AI.

Calculation of Left Ventricular End-diastolic Pressure
The LVEDP may be approximated by subtracting the end-diastolic peak gradient from the EDP.
Doppler tends to overestimates LVEDP by catheterization using the AI end-diastolic gradient. 21 The sensitivity and specificity of Doppler-estimated LVEDP >15 mm Hg versus that of <15 mm Hg are 76% and 90%. repectively. 21

Aortic Insufficiency Deceleration Time
Measurement of AI DT is possible when the spectral profile is clear. Although DT correlates with angiographic grade (r = 0.85), Labovitz et al. 23 found that DT >2 m/sec establishes that AI is worse than mild, but DT is not nearly as helpful in distinguishing severe from moderate AI. The same authors found that PHT did not distinguish moderate from severe AI.

Mitral Valve Preclosure
Preclosure is an uncommon sign seen with some cases of acute, severe (“torrential”) AI, usually due to infective endocarditis, proximal aortic dissections, and trauma. Preclosure also may result from a long PR interval 24 or from complete heart block, both of which may occur with aortic valve endocarditis if there is a root abcess. 25 Pulsed-wave Doppler offers timing and the chance to record the valve leaflet “click.” 26 Although the sign is spectacular, it is disappointingly absent in many cases where it seems it should be present.

Fluttering of the Anterior Mitral Leaflet
Fluttering of the anterior mitral leaflet is an older (M-mode) sign that adds little, if anything, to the standard assessment of AI. The more the AI jet impacts the anterior mitral leaflet, the more likely the anterior leaflet is to vibrate (flutter), but some severe AI jets are directed toward the septum, not the anterior mitral leaflet. In addition, atrial fibrillation and especially atrial flutter, will reproduce this sign in the absence of AI. 27

Pulsed-Wave Mapping of Aortic Insufficiency in the Left Ventricle
Pulsed-wave mapping of AI in the LV is an obsolete means to assess AI, and has been entirely replaced by color Doppler flow mapping.

Utility of Transesophageal Echocardiography in Aortic Insufficiency
For routine AI, TEE offers little to the assessment. TEE is able to resolve the mechanism of AI 28 and probably the disease causing AI in most cases where these issues are not apparent on TTE. There is no significant difference in the detection of AI by TTE and TEE: there is 80% concordance; and most differences are of one grade, with only 3% differing by two grades. 29

Summary

Echocardiography is useful to identify AI and to establish its cause, its severity, and the reparability of the valve.
Multiple diagnostic criteria should be used, with emphasis on the more robust ones.
Many cases of AI are due to disease of the aorta and require adequate assessment of the aorta by another complementary imaging modality.
In addition to identifying severity, echocardiography can garner some indices of surgical timing.

BOX 3-1 Aortic Valve Replacement or Repair for Aortic Insufficiency or Medical Therapy: ACC/AHA 2006 Recommendations

Indications for Aortic Valve Replacement or Aortic Valve Repair

Class I

1. AVR * is indicated for symptomatic patients with severe aortic regurgitation irrespective of LV systolic function. (Level of evidence: B)
2. AVR is indicated for asymptomatic patients with chronic severe AR and LV systolic dysfunction (ejection fraction ≤ 0.50) at rest. (Level of evidence: B)
3. AVR is indicated for patients with chronic severe AR while undergoing CABG or surgery on the aorta or other heart valves. (Level of evidence: C)

Class IIa
AVR is reasonable for asymptomatic patients with severe AR with normal LV systolic function (ejection fraction > 0.50) but with severe LV dilatation (end-diastolic dimension > 75 mm or end-systolic dimension > 55 mm). † (Level of evidence: B)

Class IIb

1. AVR may be considered in patients with moderate AR while undergoing surgery on the ascending aorta. (Level of evidence: C)
2. AVR may be considered in patients with moderate AR while undergoing CABG. (Level of evidence: C)
3. AVR may be considered for asymptomatic patients with severe AR and normal LV systolic function at rest (ejection fraction > 0.50) when the degree of LV dilatation exceeds an end-diastolic dimension of 70 mm or end-systolic dimension of 50 mm, when there is evidence of progressive LV dilatation, declining exercise tolerance, or abnormal hemodynamic responses to exercise. † (Level of evidence: C)

Class III
AVR is not indicated for asymptomatic patients with mild, moderate, or severe AR and normal LV systolic function at rest (ejection fraction > 0.50) when degree of dilatation is not moderate or severe (end-diastolic dimension < 70 mm, end-systolic dimension < 50 mm). † (Level of evidence: B)

Medical Therapy

Class I
Vasodilator therapy is indicated for chronic therapy in patients with severe AR who have symptoms or LV dysfunction when surgery is not recommended because of additional cardiac or noncardiac factors. (Level of evidence: B )

Class IIa
Vasodilator therapy is reasonable for short-term therapy to improve the hemodynamic profile of patients with severe heart failure symptoms and severe LV dysfunction before proceeding with AVR. (Level of evidence: C)

Class IIb
Vasodilator therapy may be considered for long-term therapy in asymptomatic patients with severe AR who have LV dilatation but normal systolic function. (Level of evidence: B)

Class III

1. Vasodilator therapy is not indicated for long-term therapy in asymptomatic patients with mild to moderate AR and normal LV systolic function. (Level of evidence: B)
2. Vasodilator therapy is not indicated for long-term therapy in asymptomatic patients with LV systolic dysfunction who are otherwise candidates for aortic valve replacement. (Level of evidence: C)
3. Vasodilator therapy is not indicated for long-term therapy in symptomatic patients with either normal LV function or mild to moderate LV systolic dysfunction who are otherwise candidates for aortic valve replacement. (Level of evidence: C)
AR, aortic regurgitation; CABG, coronary artery bypass grafting; LV, left ventricular.
From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2006; 48(3):e1–e148.

* AVR refers to both aortic valve replacement and repair..
† Consider lower threshold values for patients of small stature of either gender.

BOX 3-2 Appropriateness Criteria and Indications for Cardiac Imaging Modalities and Cardiac Catheterization for the Assessment of Aortic Insufficiency

Transthoracic Echocardiography

ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 30

Native Valvular Regurgitation with TTE

Routine surveillance of trace valvular regurgitation
Appropriateness criteria: I; median score: 1
Routine surveillance (<3 yr) of mild valvular regurgitation without a change in clinical status or cardiac examination
Appropriateness criteria: I; median score: 2
Routine surveillance (≥3 yr) of mild valvular regurgitation without a change in clinical status or cardiac examination
Appropriateness criteria: U; median score: 4
Routine surveillance (<1 yr) of moderate or severe valvular regurgitation without a change in clinical status or cardiac examination
Appropriateness criteria: U; median score: 6
Routine surveillance (≥1 yr) of moderate or severe valvular regurgitation without change in clinical status or cardiac examination
Appropriateness criteria: A; median score: 8

Chronic Valvular Disease—Asymptomatic with Stress Echocardiography

Mild aortic regurgitation
Appropriateness criteria: I; median score: 2
Moderate aortic regurgitation
Appropriateness criteria: U; median score: 5
Severe aortic regurgitation
LV size and function not meeting surgical criteria
Appropriateness criteria: A; median score: 7

Acute Valvular Disease with Stress Echocardiography

Acute, moderate, or severe mitral or aortic regurgitation
Appropriateness criteria: I; median score: 3

ACC/AHA 2003 Guideline Update for the Clinical Application of Echocardiography 31

Class I
• Assessment of the effects of medical therapy on the severity of regurgitation and ventricular compensation and function when it might change medical management
• Assessment of valvular morphology and regurgitation in patients with a history of anorectic drug use, or the use of any drug or agent known to be associated with valvular heart disease, who are symptomatic, have cardiac murmurs, or have technically inadequate auscultatory examination
Class III
• Routine repetition of echocardiography in past users of anorectic drugs with normal studies or known trivial valvular abnormalities

ACC/AHA 1997 Guidelines for the Clinical Application of Echocardiography 32

Indications for Echocardiography in Native Valvular Regurgitation

Class I
• Diagnosis; assessment of hemodynamic severity
• Initial assessment and re-evaluation (when indicated) of LV and right ventricular size, function, and/or hemodynamics
• Re-evaluation of patients with mild to moderate valvular regurgitation with changing symptoms
• Re-evaluation of asymptomatic patients with severe regurgitation
• Assessment of changes in hemodynamic severity and ventricular compensation in patients with known valvular regurgitation during pregnancy
• Re-evaluation of patients with mild to moderate regurgitation with ventricular dilation without clinical symptoms
• Assessment of the effects of medical therapy on the severity of regurgitation and ventricular compensation and function
Class IIb
• Re-evaluation of patients with mild to moderate mitral regurgitation without chamber dilation and without clinical symptoms
• Re-evaluation of patients with moderate aortic regurgitation without chamber dilation and without clinical symptoms
Class III
• Routine re-evaluation in asymptomatic patients with mild valvular regurgitation having stable physical signs and normal LV size and function

ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 33

Diagnosis and Initial Evaluation

Class I
• Echocardiography is indicated to confirm the presence and severity of acute or chronic aortic regurgitation. (Level of evidence: B)
• Echocardiography is indicated for diagnosis and assessment of the cause of chronic aortic regurgitation. (including valve morphology and aortic root size and morphology) and for assessment of LV hypertrophy, dimension (or volume), and systolic function. (Level of evidence: B)
• Echocardiography is indicated in patients with an enlarged aortic root to assess regurgitation and the severity of aortic dilatation. (Level of evidence: B)
• Echocardiography is indicated for the periodic re-evaluation of LV size and function in asymptomatic patients with severe aortic regurgitation. (Level of evidence: B)
• Radionuclide angiography or MRI is indicated for the initial and serial assessment of LV volume and function at rest in patients with aortic regurgitation and suboptimal echocardiograms. (Level of evidence: B)
• Echocardiography is indicated to re-evaluate mild, moderate, or severe aortic regurgitation in patients with new or changing symptoms. (Level of evidence: B)
Class IIa
• Exercise stress testing for chronic aortic regurgitation is reasonable for assessment of functional capacity and symptomatic response in patients with a history of equivocal symptoms. (Level of evidence: B)
• Exercise stress testing for patients with chronic aortic regurgitation is reasonable for the evaluation of symptoms and functional capacity before participation in athletic activities. (Level of evidence: C)
• MRI is reasonable for the estimation of aortic regurgitation severity in patients with unsatisfactory echocardiograms. (Level of evidence: B)
Class IIb
• Exercise stress testing in patients with radionuclide angiography may be considered for assessment of LV function in asymptomatic or symptomatic patients with chronic aortic regurgitation. (Level of evidence: B)

ACCF/ASE/ACEP/AHA/ASNC/SCAI/SCCT/SCMR 2008 Appropriateness Criteria for Stress Echocardiography 34

Asymptomatic severe AI or MR
LV size and function not meeting surgical criteria
Appropriateness criteria: A; median score: 7
Severe AI or MR
Symptomatic or with severe LV enlargement or LV systolic dysfunction
Appropriateness criteria: I; median score: 2

Transesophageal Echocardiography

ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 30

TEE as Initial or Supplemental Test—Valvular Disease

Evaluation of valvular structure and function to assess suitability for, and assist in planning of, an intervention
Appropriateness criteria: A; median score: 9

Cardiac Catheterization

ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 33

Indications for Cardiac Catheterization

Class I
• Cardiac catheterization with aortic root angiography and measurement of LV pressure is indicated for assessment of severity of regurgitation, LV function, or aortic root size when noninvasive tests are inconclusive or discordant with clinical findings in patients with aortic regurgitation. (Level of evidence: B)
• Coronary angiography is indicated before AVR in patients at risk for CAD. (Level of evidence: C)
Class III
• Cardiac catheterization with aortic root angiography and measurement of LV pressure is not indicated for assessment of LV function, aortic root size, or severity of regurgitation before AVR when noninvasive tests are adequate and concordant with clinical findings and coronary angiography is not needed. (Level of evidence: C)
• Cardiac catheterization with aortic root angiography and measurement of LV pressure is not indicated for assessment of LV function and severity of regurgitation in asymptomatic patients when noninvasive tests are adequate. (Level of evidence: C)

Cardiac Computed Tomography

ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 35

Characterization of native cardiac valves
Suspected clinically significant valvular dysfunction
Inadequate images from other noninvasive methods
Appropriateness criteria: A; median score: 8

Cardiac Magnetic Resonance

ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Magnetic Resonance Imaging 36

For characterization of native and prosthetic cardiac valves, including planimetry of stenotic disease and quantification of regurgitant disease
For patients with technically limited images from echo or TEE
Appropriateness criteria: A; median score: 8
For quantification of LV function
Appropriateness criteria: A; median score: A

SCMR Consensus Indication for Cardiac Magnetic Resonance Imaging 37

Class I
• For cardiac chamber anatomy and function in patients with valvular disease
• For quantitation of valvular regurgitation

ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 33

Diagnosis and Initial Evaluation

Class I
• Radionuclide angiography or MRI is indicated for the initial and serial assessment of LV volume and function at rest in patients with aortic regurgitation and suboptimal echocardiograms. (Level of evidence: B)
Class IIa
• Magnetic resonance imaging is reasonable for the estimation of AR severity in patients with unsatisfactory echocardiograms. (Level of evidence: B)

Nuclear

ACCF/ASNC/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging 38

Evaluation of LV Function

Assessment of LV function with radionuclide angiography (ERNA or FP RNA)
In absence of recent reliable diagnostic information regarding ventricular function obtained with another imaging modality
Appropriateness criteria: A; median score: 8

ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 33

Class I
• Radionuclide angiography or MRI is indicated for the initial and serial assessment of LV volume and function at rest in patients with aortic regurgitation and suboptimal echocardiograms. (Level of evidence: B)
Class IIb
• Exercise stress testing in patients with radionuclide angiography may be considered for assessment of LV function in asymptomatic or symptomatic patients with chronic aortic regurgitation. (Level of evidence: B)
Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain.
AI, aortic insufficiency; AVR, aortic valve replacement; CAD, coronary artery disease; LV, left ventricular; MR, mitral regurgitation; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.
Table 3-2 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Aortic Insufficiency MODALITY PROS CONS/Caveats Transthoracic Echocardiography

2D echocardiography
• 2D imaging is able to determine
• The mechanism of AI in many cases (aortic root causes, specific aortic valve causes)
• The repairability of the valve

• Some cases elude determination of cause, especially perforations and fenestrations.   M-mode    

• M-mode signs of AI are few, but preclosure of the mitral valve is an elegant sign of acute “torrential” AI.

• Often absent despite clinically severe AI
• False positives include
• First-degree AV block
• Junctional rhythm  

• Anterior mitral leaflet flutter

• Almost no correlation with severity of AI
• Seen also with atrial flutter   Color Doppler findings in AI    

Jet length into the LV

• Poor correlation with severity  

• Long-axis jet height in the LVOT:
Fair correlation with severity, as long as the jet is central and oriented down the long axis of the LVOT

• Unsuccessful with eccentric jets
• Gain dependent  

• Short-axis jet area in the LVOT
Good correlation with severity as long as the jet is central and oriented down the long axis of the LVOT

• Unsuccessful with eccentric jets  

• Vena contracta width
Good correlation with severity

• Machine factor dependent  

• Color Doppler flow mapping of the proximal descending aorta

• Of no use  

• PISA
An accurate means by which to quantify AI if all PISA equation components are measurable

• An optimal depiction of PISA is variably achievable by TTE   Spectral Doppler findings in AI    

• Deceleration time
Correlates with severity, but “cut-offs” are needed

• Profile may be incomplete and unmeasurable unless 3+ or 4+.
• Has difficulty distinguishing grades of AI
• Confounded if LV myocardial compliance is reduced  

• Deceleration slope
Low velocity/steep slope, low end-diastolic velocity is highly consistent with severe “torrential” AI    

• Abdominal holodiastolic flow reversal
An extremely useful sign—the single best sign that AI is severe

• May be difficult to record in obese patients, or if there is extensive midline gas
• Some nonspecificity (PDA, aortic-to-cardiac chamber fistula)  

• Proximal descending aortic holodiastolic flow reversaly
A useful sign

• Indexing to heart rate or diastolic time interval is needed
• Some nonspecificity (aortic-to-cardiac chamber fistula)  

• Calculation of LVEDP from diastolic BP end-diastolic velocity

• Places great faith in the diastolic BP recording, and dependence on a well-aligned and complete spectral recording of AI
• End-diastolic pressure has some correlation with average LA pressure, but is not equivalent to it.  

• Pulsed-wave Doppler mapping of AI within the LV cavity

• Obsolete—replaced by color Doppler flow mapping  

• Volumetric R Fraction and R Volume (LVOT VTI) stroke volume
LV stroke volume (EDV – ESV), is an excellent method if carefully done. Severe = R Volume > 60 mL, R Fraction > 60%

• Confounded if MR or a VSD is present because LV total stroke volume does not equal LVOT stroke volume Transesophageal Echocardiography

• The single best test to establish the etiology of AI and with which to plan valve repair
• Better able to yield PISA
• A very useful test to identify/exclude possible associations and complications, such as root abscess
• Can record low thoracic aortic flow as a surrogate of abdominal flow

• Has difficulty depicting valve fenestrations and/or some perforations
• Needs TTE to provide CW of AI for calculations
• Color Doppler flow mapping of the LVOT long-axis view of the aortic valve may over-depict the severity of AI if the jet is asymmetric and may under-represent the severity of AI if the jet is eccentric. Cardiac CT

• May identify the structural cause of AI (flail leaflets, perforations) if advanced techniques are used (such as blood pool inversion)
• Coronary CTA pre-AVR, in early and small studies, appears able to exclude the presence of CAD and the need for coronary angiography

• Cannot establish the severity of AI
• Offers functional assessment of the LV if helical scanning is used, but no functional assessment of the AI Cardiac MRI

SSFP sequences:
An excellent means to assess LV volumes and systolic function

• SSFP sequences suppress flow, void depiction of AI, and systematically under represent jets when compared to echo standards.   LGE sequences: NA          

VEPC sequences:
VEPC technique estimates of AI correlate with AI severity. 40,41

• VEPC techniques may be unruly and tend to underestimate the degree of AI. 42 Nuclear

RNA
• Lack of exercise increase in EF% in AI marks the onset of LV dysfunction and a worse prognosis.
• Given its low inter-test variability, RNA can be used to follow EF% in MR and identify a fall, and also to recognize impaired right ventricular function.

• Perfusion imaging has not supplanted coronary angiography for the evaluation of angina in AS.
• Lack of exercise increase in EF% in AI does not add incrementally to the measurements of resting EF% and end-systolic diameter. Chest Radiography

• Can establish the presence of left heart failure from AI
• Can identify enlargement of the ascending aorta associated with or causing AI   Cardiac Catheterization

• Pressure recordings are useful to corroborate hemodynamic severity    

• Contrast aortography is very useful to establish severity of AI.
• Seller’s classification
• 1+: Minimal regurgitation jet that clears the heart with each beat
• 2+: Moderate opacification of proximal chamber, clearing with subsequent beats
• 3+: Intense opacification of proximal chamber, equal to that of the distal chamber
• 4+: Intense opacification of proximal chamber, becoming more intense that the distal chamber. Opacification often persists over the entire series of images.

• Poor quality of injection (such as too high in the aorta) reduces accuracy of assessment.
• The lack of control for the size of the proximal injection chamber (aorta) may confound somewhat the assessment of AI.
• The Seller’s classification was developed to assess mitral insufficiency during left ventriculography; its use for AI is “borrowed.”  

• Coronary angiography has a standard role in the assessment of coronary anatomy presurgical management of AI.  
2D, two-dimensional; AI, aortic insufficiency; AS, aortic stenosis; AV, atrioventricular; AVR, aortic valve replacement; BP, blood pressure; CAD, coronary artery disease; CTA, computed tomographic angiography; CW, continuous wave; EDV, end-diastolic volume; EF%, ejection fraction; ESV, end-systolic volume; LGE, late gadolinium enhancement; LV, left ventricle; LVEDP, left ventricular end-diastolic pressure; LVOT, left ventricular outflow tract; MR, mitral regurgitation; NA, not applicable; PDA, patent ductus arteriosus; PISA, proximal isovelocity surface area; RNA, comparative radionuclide; SSFP, steady-state free precession; TTE, transthoracic echocardiographic; VEPC, velocity-encoded phase contrast; VSD, ventricular septal defect; VTI, velocity time integral.

Figure 3-1 Aortic valve causes of aortic insufficiency. Upper left and right: Rheumatic aortic valve disease. Note the thickening of both valves and doming. The jet is central. Lower left and right: Isolated myxomatous disease of the aortic valve. One leaflet is of normal thickness, whereas the other is thickened and “beaded” and has prolapsed. The jet is initially very eccentric, consistent with the flail leaflet.

Figure 3-2 Aortic insufficiency: proximal isovelocity surface area (PISA). Left: A5CV. The jet is more pronounced than the PISA. Flow mapping of the jet length and size in the left ventricle are minimally useful. Right: Zoom view of the PISA, with optimization of the color Doppler display. The PISA is well displayed, and its size is a useful index of the severity of the aortic insufficiency.

Figure 3-3 Aortic insufficiency (AI) from aortic root dilation. The abdominal aortic flow pattern reveals diastolic flow reversal, indicating severe AI.

Figure 3-4 Aortic root causes of aortic insufficiency (AI). Upper images: Transesophageal views. Upper left: Left ventricular outflow tract view shows an intimal flap in the aortic root. There is a proximal isovelocity surface area at the level of the aortic valve, but the jet is complex. Upper right: Short-axis view at the tips of the aortic valve leaflets shows that the intimal flap has extended down into the aortic valve between 5 o’clock and 12 o’clock. The aortic valve leaflets are compressed into a smaller elliptical orifice. Lower images: Transthoracic views—AI due to root dilation. The jet is central and well-formed.

Figure 3-5 Aortic insufficiency (AI): spectral profiles. Upper left: Chronic moderate (3+) AI. Note the well-defined complete profile, the high early and late diastolic velocities, and the shallow slope. Upper right: Acute severe AI. Note the lower early diastolic velocity, the steep slope, and the minimal late diastolic velocity, consistent with equilibration of aortic and left ventricular end-diastolic pressures. Lower left: Abdominal aortic flow. There is prominent reversal of diastolic flow, consistent with severe AI. Lower right: Proximal descending thoracic aortic flow. There is a large amount of pan-diastolic reversal of flow (velocity time integral [VTI] 39 cm), consistent with severe AI.

Figure 3-6 Acute severe aortic insufficiency (AI). Left: Questionable preclosure of the mitral valve leaflets. Right: The AI slope is steep, and the end-diastolic velocity is very low, consistent with (near) equilibration of the aortic and left ventricular end-diastolic pressures. Fluttering of the aortic valve leaflets is a common finding in AI as long as the jet impacts the mitral leaflets. Flutter per se does not indicate severity.

Figure 3-7 Acute torrential aortic insufficiency (AI) due to endocarditis and two flail cusps of the aortic valve. Upper left: Abdominal aortic spectral pattern. There is obvious flow reversal (beneath baseline). Upper right: Left ventricular outflow tract (LVOT) forward flow (total stroke volume) is markedly increased by the regurgitant volume. Middle left: Transesophageal echocardiographic (TEE) continuous wave investigation of the AI jet in the LVOT shows a steep slope and very low end-diastolic velocity. Middle right: Pulsed wave flow at the mitral level; there is no flow after the E wave, due to preclosure of the mitral valve. Lower left: TEE M-mode scan of the mitral valve. Note the closure before the QRS; this is known as “preclosure.” Lower right: TEE measurements of the mitral annulus to calculate net forward flow. Using the continuity method, given the lack of mitral regurgitation, the regurgitant volume of AI was 70%.

Figure 3-8 Parasternal long-axis view with color Doppler flow mapping and adjustment of the aliasing velocity to form a proximal isovelocity surface area above the aortic valve due to flow acceleration caused by aortic valve insufficiency.

Figure 3-9 The effect of R-R interval variation on aortic insufficiency velocity and on the ability to measure the slope. The end-diastolic velocities are lower with longer R-R intervals, due to greater depressurization of the aorta over time. With longer R-R intervals and a wider spectral contour, measurements are easier than with short and narrow spectral complexes, because short R-R intervals yield a small and often not linear top slope. The variation in slope measurement can be substantial.

Figure 3-10 Transesophageal recording of flow in the lower thoracic aorta using pulsed-wave Doppler. There is near holodiastolic flow reversal, consistent with severe aortic insufficiency.

Figure 3-11 Cardiac MRI velocity encoded phase contrast technique. The upper images are of the phase and magnitude sequences obtained just above the aortic valve. The lower display depicts the flow at this level of the aorta, which includes holodiastolic flow reversal. Automatic calculations yield a regurgitant fraction of 45% consistent of moderate to severe aortic insufficiency.

Figure 3-12 Cardiac MRI assessment of aortic insufficiency (AI). Upper images: Steady-state free precession sequences in systole ( left ) and diastole ( right ). In systole, dephasing of blood yields low-signal streaks arising into the aorta; similarly, in diastole, dephasing of blood due to the turbulence from the AI yields low-signal darker blood reentering the left ventricle. Lower image: Flow at the aortic root level, which includes homodiastolic flow reversal. The regurgitant fraction has been automatically calculated as 52%, close to or within the severe range of AI.

Figure 3-13 Preclosure of the mitral valve in a patient without aortic insufficiency (AI). This patient had complete heart block, and no AI. Left: The mitral valve is closed before the QRS. Right: M-mode of the mitral valve revealing the duration of preclosure.

References

1. Vigna C., Russo A., Salvatori M.P., et al. Color and pulsed-wave Doppler study of aortic regurgitation in systemic hypertension. Am J Cardiol . 1988;61(11):928-929.
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31. Cheitlin M.D., Armstrong W.F., Aurigemma G.P., et al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation . 2003;108(9):1146-1162.
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35. Taylor A.J., Cerqueira M., Hodgson J.M., et al. ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 appropriate use criteria for cardiac computed tomography. J Am Coll Cardiol . 2010;56(22):1864-1894.
36. Hendel R.C., Manesh P.R., Kramer C.M., Poon M. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR Appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging. J Am Coll Cardiol . 2006;48(7):1475-1497.
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* Also causes of acute AI.
4 The Mitral Valve
The mitral valve is a large (4.5–6 cm 2 ), anatomically complex three-dimensional structure; hence it is more of an “apparatus” than a valve. It is not circular; hence, even its simplest geometry is not well described in terms of diameter. Maintaining its competence requires that all the components be in ongoing adequate spatial position throughout systole, as the ventricular volume reduces by half, as the ventricular diameter and length reduce, and as the annular area reduces. Some components of the mitral apparatus have fixed dimensions (leaflets and chordae), some actively shorten in systole to preserve the length–tension apparatus (papillary muscles and the left ventricle myocardium between the papillary muscle and the annulus), and some passively shorten (mitral annulus)
Through its lifetime, the mitral valve moves twice per cardiac cycle (in the absence of atrial fibrillation, marked first-degree atrioventricular block, or marked tachycardia), and thus opens and closes through an average of 210,000 cardiac cycles daily, or about 7 billion times in a lifetime of 80 years. Like the aortic valve, it is subjected to systemic pressures, but over a pressure gradient twice as high.
Each component of the mitral valve is susceptible to disease, and, as with aortic insufficiency, not only the severity, but also the cause of the insufficiency, must be sought in all cases of mitral insufficiency. Determining the basis of mitral dysfunction is important, because it may guide the approach to the disease (e.g., emergency surgery for papillary rupture, antibiotics for endocarditis, repair for many myxomatous lesions) and determine the feasibility of surgical repair versus replacement.
Disease may involve a single component of the valve (e.g., endocarditis perforating a leaflet), or several components of the valve (e.g., myxomatous disease lengthening leaflet components, chordae, and the annulus). Disease processes may result in competing effects on valve competence: for example, prolapse may reduce coaptation and displace the valve basally while cavitary dilation secondary to the mitral regurgitation (MR) from the prolapse offsets the prolapse by displacing the papillary muscle anchoring point of the apparatus apically. Some regurgitant orifices are relatively fixed (e.g., flail chordae/leaflets and perforations), and some are dynamic (e.g., mitral valve prolapse, in which the regurgitant orifice may vary in time and severity through systole, and MR due to dilation/remodeling of the left ventricle). The mitral valve is complex, and, as a result, so is mitral insufficiency. Better understanding of the inherent complexity of the mitral valve has improved surgical approaches and, especially, surgical results.

Anatomic Components

Two leaflets
The anterior mitral leaflet
The posterior mitral leaflet
An oblique commissure
Anterolateral portion
Posteromedial portion
Two papillary muscles
Anterolateral
• Typically with one trunk/one head
Posteromedial
• Typically with two trunks/two heads
Chordae tendineae
Primary, secondary, and tertiary
Inserting into
• The free edge of the mitral leaflets
• The body of the mitral leaflets
Ventricular myocardium
Under (“subtending”) the papillary muscles, situating the papillary muscle
In longitudinal relation to the leaflets
In radial relation to the leaflets

Mitral Leaflets
The surface area of the two mitral leaflets is nearly the same, but their shape is very different.
The annular length of the posterior leaflet is about twice that of the anterior leaflet, but the height of the anterior leaflet is more than twice that of the posterior leaflet. The area of the leaflets is about 2.5 times the area of the mitral valve annulus. The leaflets are in continuity with each other, apposing over several millimeters, to achieve coaptation and competence and a reserve of coaptation.
The posterior mitral leaflet is formed of three scallops: anterior, middle, and posterior. The distinction among these leaflets is somewhat arbitrary.
The leaflets are lined by atrialis tissue on the atrial side and ventricularis tissue on the ventricular side, and contain the spongiosa and fibrosa layers in between. Different disease processes affect the leaflets differently; for example, rheumatic heart disease affects primarily the fibrosa, whereas myxomatous degeneration affects primarily the spongiosa.

The Commissures
Anatomically, there is only a single commissure, but by convention, the lateral portion is referred to as the anterolateral commissure, and the medial portion is referred to as the medial commissure.
The commissure is the site of systolic apposition of opposing leaflet surfaces, and the site of diastolic separation of the leaflets.
Rheumatic mitral stenosis results from fusion of the commissure from the outside in toward the center, resulting is a small residual central orifice. The treatment for mitral stenosis is to restore motion (separation) of the leaflets by “splitting” the commissure, allowing for a larger diastolic orifice. Rheumatic calcification of the commissures diminishes the probability of a good split from catheter balloon valvuloplasty, and increases the probability that the split will occur through the body of the leaflet (following the path of least resistance), rather than along the commissures, resulting in MR.
The best operation for mitral valve repair of myxomatous disease is the quadrangular resection of the central P2 component of the posterior leaflet, with reapposition of the leaflet margins and insertion of an annular ring to avoid tension on the sutured leaflet margins. Surgical resection of the lateral (P1) or medial (P3) leaflets has a greater chance of compromising the commissure.

Chordae
Three generations (primary, secondary, and tertiary) of chordae insert onto the undersurface (ventricular surface) of the leaflets via branching arcades. An average of 12 chordae arise from each papillary muscle, and 120 insert into the mitral valve leaflets.
The leaflets are suspended optimally by the chordae. Chordae insert into the free edge of the mitral valve and also one third to halfway back along the leaflet body.
Rheumatic disease and myxomatous disease may involve the chordae:

Rheumatic disease results in shortening, thickening, stiffening, and fusion of the chordae.
Myxomatous disease may result in elongation, stretching, weakening, and rupture of chordae.

Papillary Muscles
The two papillary muscles are deemed anterolateral and posteromedial, although their position, morphology, and number are prone to variation. Both are located one third of the distance from the base of the left ventricle toward the apex.

The Anterolateral Papillary Muscle
The anterolateral papillary muscle is the more constant of the two, usually consisting of a single trunk that protrudes well into the ventricular cavity.

The anterolateral papillary muscle is imaged by
Transthoracic echocardiography
• apical four-chamber view
Transesophageal echocardiography
• Lower esophageal horizontal view
• Transgastric long- and short-axis views

The Posteromedial Papillary Muscle

The posteromedial papillary muscle usually is smaller, and often consists of multiple insertions into the left ventricle, and sometimes even of multiple separate trunks.
Most patients have either two “heads” or two adjacent “trunks” of the posteromedial papillary muscle.
Rupture of the posteromedial papillary muscle has the chance of involving one head or trunk, leaving the other intact, and resulting in less fulminant MR than would complete rupture of both heads or trunks, or of a solitary (e.g., anterolateral) papillary muscle.
The posteromedial papillary muscle is imaged by
• Transthoracic echocardiography: off-axis posterior long-axis view and apical two-chamber view
• Transesophageal echocardiography: transgrastric long- and short-axis views

The Mitral Annulus
The mitral annulus is a fibrous C-shaped structure (open toward the aortic valve) that anchors the mitral valve leaflets. The posterior mitral leaflet inserts into a dense arc of fibrous tissue, whereas the anterior mitral leaflet arises from a continuation of the aortic valve and the interatrial septum, which consists of much less of an annulus in the sense of a fibrous ring. The mitral and tricuspid leaflets undergo a systolic reduction of surface area of about 30%.
Increased mitral annular circumference is found in mitral valve prolapse, dilated cardiomyopathy, and Ebstein’s malformation.

BOX 4-1 Appropriateness Criteria and Indications for Cardiac Imaging Modalities and Cardiac Catheterization for Assessment of the Mitral Valve

Transthoracic Echocardiography

TTE is the initial diagnostic test for the detection and determination of the severity of MR or MS and its cause.
• In many cases, TTE alone is sufficient to establish presence, severity, and cause.
The portability and versatility of TTE are considerable assets for the evaluation of acute and severe cases of mitral insufficiency.
Contrary to prevailing opinion, not all mitral valve lesions are better evaluated by TEE—for example, mitral valvuloplasty scoring is better performed by TTE than it is by TEE, because subvalvar disease may be better appreciated by TTE than by TEE.
3D echocardiography has been developing for decades and is on the cusp of long-awaited feasibility and quality. One of its major applications will be evaluation of mitral valve disease, as the mitral valve’s 3D architecture has been one of the limitations to understanding and evaluating it.

ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 1

For Murmur or Click with TTE

Initial evaluation when there is a reasonable suspicion of valvular or structural heart disease
Appropriateness criteria: A; median score: 9
Initial evaluation when there are no other symptoms or signs of valvular or structural heart disease
Appropriateness criteria: I; median score: 2
Re-evaluation in a patient without valvular disease on prior echocardiogram and no change in clinical status or cardiac examinationAppropriateness criteria: I; median score: 1
Re-evaluation of known valvular heart disease with a change in clinical status or cardiac examination or to guide therapy
Appropriateness criteria: A; median score: 9

Adult Congenital Heart Disease

No specific mention of bicuspid aortic valves
Initial evaluation of known or suspected adult congenital heart disease
Appropriateness criteria: A; median score: 9

ACC/AHA/ASE 2003 Guideline Update for the Clinical Application of Echocardiography 2

Class I
• Assessment of the effects of medical therapy on the severity of regurgitation and ventricular compensation and function when it might change medical management
• Assessment of valvular morphology and regurgitation in patients with a history of anorectic drug use, or the use of any drug or agent known to be associated with valvular heart disease, who are symptomatic, have cardiac murmurs, or have technically inadequate auscultatory examination
Class III
• Routine repetition of echocardiography in past users of anorectic drugs with normal studies or known trivial valvular abnormalities

ACC/AHA/ASE 2003 Guideline Update for the Clinical Application of Echocardiography 2
No specific mention of bicuspid aortic valves

Recommendations for Echocardiography in the Evaluation of Patients with a Heart Murmur

Class I
• A patient with a murmur and cardiorespiratory symptoms
• An asymptomatic patient with a murmur in whom clinical features indicate at least a moderate probability that the murmur is reflective of structural heart disease
Class IIa
• A murmur in an asymptomatic patient in whom there is a low probability of heart disease but in whom the diagnosis of heart disease cannot be reasonably excluded by the standard cardiovascular clinical evaluation
Class III
• In an asymptomatic adult, a heart murmur that has been identified by an experienced observer as functional or innocent

ACC/AHA 1997 Guidelines for the Clinical Application of Echocardiography 2

Indications for Echocardiography in Mitral Valve Prolapse

Class I
• Diagnosis; assessment of hemodynamic severity, leaflet morphology, and/or ventricular compensation in patients with physical signs of MVP
Class IIa
• To exclude MVP in patients who have been diagnosed but without clinical evidence to support the diagnosis
• To exclude MVP in patients with first-degree relatives with known myxomatous valve disease
• Risk stratification in patients with physical signs of MVP or known MVP
Class III
• Exclusion of MVP in patients with ill-defined symptoms in the absence of a constellation of clinical symptoms or physical findings suggestive of MVP or a positive family history
• Routine repetition of echocardiography in patients with MVP with no or mild regurgitation and no changes in clinical signs or symptoms

ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 2

Mitral Valve Prolapse: Evaluation and Management of the Asymptomatic Patient

Class I
• Echocardiography is indicated for the diagnosis of MVP and assessment of MR, leaflet morphology, and ventricular compensation in asymptomatic patients with physical signs of MVP. (Level of evidence: B)
Class IIa
• Echocardiography can effectively exclude MVP in asymptomatic patients who have been diagnosed without clinical evidence to support the diagnosis. (Level of evidence: C)
• Echocardiography can be effective for risk stratification in asymptomatic patients with physical signs of MVP or known MVP. (Level of evidence: C)
Class III
• Echocardiography is not indicated to exclude MVP in asymptomatic patients with ill-defined symptoms in the absence of a constellation of clinical symptoms or physical findings suggestive of MVP or a positive family history. (Level of evidence: B)
• Routine repetition of echocardiography is not indicated for the asymptomatic patient who has MVP and no MR or MVP and mild MR with no changes in clinical signs or symptoms. (Level of evidence: C)

Transesophageal Echocardiography

TEE is a very useful adjunct to the evaluation of mitral valve disease.
The idea that TEE is always needed for the assessment of severe mitral valve disease is antiquated, as TTE has advanced steadily since the TEE validation papers of nearly 2 decades ago established the supremacy of TEE for evaluation of valve disease.
However, TEE still affords the combination of structural and functional assessment and feasibility in acute cases, which makes it the tried and proven workhorse of contrast ventriculography.


TEE as Initial or Supplemental Test—General Uses

Use of TEE when there is a high likelihood of a nondiagnostic TTE due to patient characteristics or inadequate visualization of relevant structures
Appropriateness criteria: A; median score: 8
Routine use of TEE when a diagnostic TTE is reasonably anticipated to resolve all diagnostic and management concerns
Appropriateness criteria: I; median score: 1
In addition, it is reasonable to use TEE as a first test when visualization of certain structures seen best by TEE is necessary to achieve the goals of the imaging test, including, but not limited to, evaluation of the mitral valve, atria, great vessels and/or prosthetic valve.

Cardiac Catheterization

Cardiac catheterization/contrast ventriculography is able to depict some mitral valve morphologic abnormalities such as prolapse and stenosis, but is very limited when compared to the ability of TTE/TEE to assess mitral morphology.
The ability of cardiac catheterization to yield recordings of absolute pressure and pressure waveforms gives it a unique place in cardiac diagnostic testing.

Cardiac Computed Tomography

The role of ECG-gated cardiac CT has yet to be established.
The acquisition of volumetric data is, however, conceptually ideal for the evaluation of several mitral valve disorders, provided that spatial resolution is adequate.
Recent advances in cardiac CT coverage of the heart and in temporal and spatial resolution may yield clinically relevant applications of cardiac CT for mitral valve disease.
The all-too-common comorbidity of mitral valve disease and atrial fibrillation may be less of a problem for cardiac CT, as acquisition times improve toward single-cycle (rhythm-independent) acquisition.

ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 3

Characterization of native cardiac valves
Suspected clinically significant valvular dysfunction
Inadequate images from other noninvasive methods
Appropriateness criteria: A; median score: 8

Cardiac Magnetic Resonance

CMR still affords less detail about mitral valve morphology than it does about left ventricular volumes and systolic function.
The combination of velocity-encoded phase-contrast assessment of proximal aortic flow and LV total stroke volume from chamber volumetric quantification can indirectly quantify the mitral regurgitant volume and fraction (assuming the absence of aortic insufficiency).

ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Magnetic Resonance Imaging 4

For characterization of native and prosthetic cardiac valves—including planimetry of stenotic disease and quantification of regurgitant disease
Patients with technically limited images from echocardiography or TEE
Appropriateness criteria: A; median score: 8
For quantification of LV function where there is discordant information that is clinically significant from prior tests
Appropriateness criteria: A; median score: 8

SCMR Consensus Indication for Cardiac Magnetic Resonance Imaging 5

For other (nonbicuspid) valves
Class III

Nuclear

Nuclear modalities offer little for the assessment of mitral valve disease other than a reliable and, moreover, reproducible assessment of LV ejection fraction.

Chest Radiography

Chest radiography affords the best means, short of catheterization, to establish the presence of left heart failure.
Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain.
LV, left ventricular; MR, mitral regurgitation; MVP, mitral valve prolapse; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

Figure 4-1 Mitral anatomy. The redundancy of the posterior papillary muscle anatomy is apparent. There are two adjacent posterior papillary muscles—one supporting the anterior leaflet, and the other supporting the posterior leaflet. Hence, the papillary muscle apparatus supports the commissure. Also seen in this image is the insertion of chordae into the mid aspect of the (anterior and posterior) mitral leaflets. Hence, the papillary muscle’s chordal apparatus supports/exerts tension (traction) on the mid leaflet as well as the leaflet tip.

Figure 4-2 Mapping of the components of the mitral valve by different echocardiographic views. Proximity of the mitral apparatus to the left atrial appendage establishes the A1 and P1 sections. Note how some tomographic views depict only one aspect of the mitral valve (e.g., the posterior long-axis view shows only the middle section—the A2 and P2 components), whereas other views, such as the two-chamber view, show two segments and two commissures. Additionally, a four-chamber view may show either A1/P1 or A2/P2 scallops, depending on the level of the plane.

References

1. Douglas P.S., Garcia M.J., Haines D.E., et al. A report of the ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR on the 2011 appropriate use criteria for echocardiography. J Am Coll Cardiol . 2011;57(9):1126-1166.
2. Cheitlin M.D., Armstrong W.F., Aurigemma G.P., et al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation . 2003;108(9):1146-1162.
3. Taylor A.J., Cerqueira M., Hodgson J.M., et al. ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 appropriate use criteria for cardiac computed tomography. J Am Coll Cardiol . 2010;56(22):1864-1894.
4. Hendel R.C., Manesh P.R., Kramer C.M., Poon M. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging. J Am Coll Cardiol . 2006;48(7):1475-1497.
5. Pennell D.J., Sechtem U.P., Higgins C.B., et al. Clinical indications for cardiovascular magnetic resonance (CMR): Consensus Panel report. J Cardiovasc Magn Reson . 2004;6(4):727-765.
5 Mitral Stenosis

Goals of Echocardiography in Mitral Stenosis

To establish that mitral stenosis (MS) is present
To establish the level of obstruction
• Valvar
• Subvalvar
• Other (e.g., myxoma)
To establish the hemodynamic parameters: gradient, area, cardiac index (CI), right ventricular systolic pressure (RVSP)
To establish suitability for valvuloplasty
• Mass score, calcification
To identify complications of mitral stenosis
• Pulmonary hypertension
• Atrial or appendage thrombosis
• Infective endocarditis
To identify concurrent valvulopathies/pathologies
• Mitral regurgitation (MR)
• Aortic insufficiency (AI)
• Tricuspid regurgitation (TR)
• Tricuspid stenosis with tricuspid regurgitation (TS/TR)
• Tricuspid stenosis (TS)
• Aortic stenosis (AS)

Scanning Issues

Required Parameters to Obtain from Scanning

Valve parameters
• Morphology, suitability for catheter balloon valvuloplasty (CBV)
• Mean gradient
• Area (same value by ≥2 methods)
• Proximal isovelocity surface area (PISA) variables: PISA radius, V Alias , V Peak
• MR severity
Right ventricle size and systolic function
Indirect pressure overload signs: left atrium (LA) size, RVSP
Left ventricular outflow tract (LVOT)–derived cardiac output and stroke volume. Note that in the presence of AI, the stroke volume measured in the LVOT is the total forward stroke volume, not the net forward stroke volume.
Height and weight for body surface area
Has there been a commissurotomy within the last 3 months?

Valid Methods for Mitral Valve Area Determination (Need ≥2 Concordant)

Continuity (if < mild AI)
Pressure half time (PHT), if no factors are present that alter left ventricle (LV) compliance, such as left ventricular hypertrophy, left ventricular wall motion abnormalities, LV dysfunction, recent CBV, or more than mild AI
Proximal isovelocity surface area (PISA)
Planimetry
Real-time three-dimensional (3D) echocardiography

Scanning Notes

Gradient

Emphasize the mean gradient.
Ensure that transmitral Doppler sampling is correctly aligned, and that continuous wave Doppler is being used with adequate gain settings.
If sinus rhythm is present, measure three spectral profiles.
If atrial fibrillation is detected, measure five spectral profiles.
Ideally, measure 10 spectral profiles.
Spectral profiles should be displayed at two-thirds the height of the display, and wide enough so that there are two or three per display.
If the gradient is not severe, but the area is, consider provocative maneuvers (e.g., sit-ups) to increase flow and (thereby the gradient).


Planimetry

Optimize the gain settings for planimetry—over-gain results in a falsely low estimation of mitral valve area (MVA) due to “blooming” of the margins.
Measure the area at the narrowest part of the funnel-like orifice of MS—this may be at the level of the leaflet tips or at the subvalvar level.
Be cautious if there was a prior commissurotomy—planimetry underrepresents area if the orifice has deep “splits” into the commissures (or leaflets), which are difficult so see by ultrasound, especially if they extend off the plane of imaging.

Pressure Half Time

Do not accept PHT estimates of MVA if any of the following are present:
• Left ventricular hypertrophy
• Left ventricular wall motion abnormalities
• LV dysfunction
• Recent commissurotomy
• More than mild AI
All are factors that reduce the accuracy of the PHT relation to MVA.

Proximal Isovelocity Surface Area


where r = PISA radius.
The PISA method is based on the assumption that there is a hemisphere of flow acceleration such as would occur with a planar orifice. This often is not the case in mitral stenosis, however, particularly when the greatest stenosis is subvalvar. To adjust for the effect of the orifice on the volume of the PISA, use of an angle correction factor has been suggested ( Fig. 5-1 ), multiplying the preceding calculation by α/180°. Not all echo systems carry angle measurement software.

where α = the measured angle of the “plane” of the orifice and r = PISA radius.
Transesophageal echocardiography (TEE) generally affords excellent depiction of PISA in mitral stenosis.

Reporting Issues
The mean gradient is the gradient seen, by the left atrium, on average, through diastole and is, as with AS, the only suitable expression of the physiologic pressure burden on the downstream chamber. Many MS profiles have an initial, brief, higher velocity/gradient that is not borne out through the rest of diastole. Therefore, emphasize the mean gradient, and avoid mentioning the peak gradient. It is clinically useful to offer the heart rate and rhythm, both of which are apparent on echocardiography, when stating the mean gradient: “The mean gradient was 13 mm Hg at an average heart rate of 75 bpm (atrial fibrillation).” When reporting, compare gradients, areas and RVSP, and rhythm to any previously recorded measurements.

Gradient Issues

If there is a difference in gradient between current and previous echocardiographic determinations, then review the following variables:
• History (has there been a commissurotomy?)
• Rate differences
• Rhythm differences
• Sampling differences
Recall that the accepted gradients for “severe” assume the absence of factors provoking higher output, such as the following:
• Tachycardia
• Anemia
• Fever
• Pregnancy
• Thyrotoxicosis
• Large dialysis shunt
The 95% CI for mitral valve gradient is 3 mm Hg (vs. wedge:LV recordings).
Direct left atrial pressure recording (LA:LV) typically leads to a lower mitral gradient, as it is without the phase delay of pulmonary capillary wedge tracings.

Area Issues

Place less emphasis on the valve area, which is invariably calculated (other than by the planimetry method) and, therefore, is subject to larger error.
Ensure MVA is concordant by at least two suitable methods.

Pressure Half Time Method

The PHT relation (220) was validated in a relatively small series and is best applied for MVA between 1 and 1.5 cm 2 ; r = 0.75. 1 The actual precision of the correlation is less than has been thought.
The 220 constant is actually different for both MVA <1 cm 2 and MVA >1.5 cm 2 ; therefore, use of the relationship at higher or lower areas is essentially an extrapolation of the known relationship, and assumes that a known variable (220) is a constant, which it is not.
In the presence of AI, there are two ventricular inflows determining the spectral inflow:diastolic relationship. The PHT relation, therefore, is less representative of MS alone, in the presence of more than moderate AI. Correlation and SEE for MVA by PHT (vs. Gorlin) for patients both without and with AI are as follows:
• r = 0.69, SEE = 0.44 cm 2 for patients with AI
• r = 0.91, SEE = 0.24 cm 2 for patients without AI. 2
PHT is less accurate in patients older than 65 years of age, because of effects of hypertension on the ventricular diastolic properties, leading to overestimation of MVA. 3
PHT is less accurate for 3 months after CBV, 4 because passive ventricular diastolic properties and atrial diastolic properties are adapting to the changes in load (i.e., less atrial/more ventricular).

Planimetry Method

When images are amenable to planimetry, it is an accurate technique. It requires attention to scan extensively along the short axis of the orifice, to ensure sampling at the narrowest part. This may be at the leaflet tips, or in the subvalvar zone, which is important not to miss.
Correlation for MVA by planimetry (vs. cardiac catheterization): r = 0.92 – 0.95. 5, 6
Planimetry of MVA is an AI-independent technique.
Planimetry is less accurate with prior commissurotomy, 3, 7, 8 because the split often is eccentric: it may lead out onto another plane of imaging and be missed, or may go into a bright commissure that is difficult to visualize.

Continuity Method

MVA by the continuity method is less accurate when the ideal reference site (the LVOT) has more than mild AI. The tricuspid reference site is harder to use, and is at least as likely to have TR. For all-comers, the correlation of continuity is very good: r = 0.91, SEE = 0.24 cm 2 , 2 especially in the absence of AI: r = 0.93. 2 However, in the presence of AI it is less: r = 0.84. 2

Proximal Isovelocity Surface Area Method

The utility of PISA depends on the clarity (quality) of the flow convergence signal. TEE regularly offers good-quality PISA. The most accurate PISA calculations are possible when the orifice is planar rather than within a curving and narrowing tunnel.
Correlation and SEE for MVA by PISA 9
• Versus planimetry: r = 0.91, SEE 0.21 cm 2
• Versus PHT: r = 0.89, SEE 0.24 cm 2
• Versus Gorlin: r = 0.86, SEE 0.24 cm 2
• PISA appears not to be influenced by AI. 9
• Versus surgical standard
Planimetry: r = 0.95, SEE 0.06 cm 2
PHT: r = 0.87, SEE 0.09 cm 2
PISA: r = 0.90, SEE 0.09 cm 2

Real-Time Three-Dimensional Echocardiography
The real-time 3D technique allows depiction of the mitral orifice on any plane, and thus should assist with the task of planimetry. Although studies are limited to date, real-time 3D echocardiography shows very good correlation with Gorlin (average difference of 0.08 cm 2 ), and low inter- and intraobserver variability (κ of 0.84 and 0.96, respectively), which in comparative studies was better than with other methods. 10

Descriptors of Mitral Stenosis Severity

After it has been established that MS is present, the next important task is to determine its severity. This involves a composite assessment of symptoms, physical findings, and hemodynamics. It must be recalled that MVA < 1 cm 2 always indicates severe MS, but larger patients or those with higher cardiac output (CO) needs are commonly “severe” above an area of 1 cm 2 and receive intervention for average MVAs of 1.2 or 1.3 cm 2 .
Distinguishing moderate from mild is really of little consequence, as both are “nonsevere” and would not prompt intervention.
“Severe” = mean gradient >12 mm Hg at rest, and an area of <1.3 cm 2 .
• A subset of clinically severe cases have MVA > 1 cm 2 (1.2–1.3 cm 2 ).
“Critical” = mean gradient > 12 mm Hg at rest, and an area of <1.0 cm 2
Moderate = mean gradient < 12 mm Hg at rest, and an area of ≥1.3 cm 2

Suitability for Valvuloplasty and Commissurotomy Issues

Suitability for commissurotomy is determined by the following:
• Mass score < 8
• No contraindications: no significant MR, no LA or left atrial appendage (LAA) clot
Use the mass score
Calcification, especially of commissures, is a marker of higher short- and long-term mortality with CBV.
Commissurotomy is generally unsuitable if there is MR >2+.
There is substantial risk of arterial embolism if there is clot within the body of the left atrium, because valvuloplasty wires invariably are in the body of the atrium. There is a smaller risk of embolism if clot is within the LAA, because the wires that must traverse the LA body may avoid the LAA. TEE is clearly superior to evaluate for the presence of LA and LAA clot.

Surgical Issues

Establish the degree of submitral (annular) calcification. There is a greater risk of periprosthesis (paravalvar) MR when submitral (annular) calcification is severe.
Determine the degree of AI: in severe MR, IABP should not be used if there is concurrent AI ≥2+.
Describe the RV in detail (RVH/systolic dysfunction/size), as well as the RVSP.
RA size is a reasonable descriptor of RV diastolic function, if neither TR nor atrial fibrillation is present.

Provocative Testing to Enhance Transmitral Gradients and Right Ventricular Systolic Pressure
Simple bedside maneuvers (e.g., a few sit-ups) or more sophisticated ones (e.g., supine bicycle, upright treadmill testing, or dobutamine) may be used to increase the heart rate and cardiac output, and thereby enhance the mitral gradient and RVSP. The role of such testing is unclear: in mitral stenosis the gradient would be expected to increase, and generally it does, about two-fold, when patients are subjected to a Bruce or modified Bruce protocol: from 9 ± 7 mm Hg at rest to 17 ± 8 mm Hg, as does the RVSP, from 41 ±1 9 mm Hg to 70 ± 32 mm Hg. 11 The optimal interpretation of the provoked hemodynamics is unclear. Advocates suggest that it better describes the basis of exertional symptoms and may be contributory when the resting hemodynamics are less striking than the (exertional) symptoms and findings.
Dobutamine stress echo (a gradient cut-off of 18 mm Hg) has been shown to predict clinical events (90% sensitivity, 87% specificity, and 90% accuracy) over a 5-year period, and increases the detection of medium- and higher-risk cases. 12 Dobutamine stress echocardiography may assist with the evaluation of patients whose symptoms are out of proportion to the calculated valve area, and who may benefit from “medical or invasive intervention.” 13

Notes on Mitral Stenosis

Etiologies of Mitral Stenosis

Congenital

Congenital valvular MS is rare.
Cor triatriatum sinister also is rare. It is a baffle-like ridge across the mid-LA that obstructs flow across the atrium, not at the mitral valve level.

Acquired

Rheumatic origin is by far the most common cause of MS (>99% of all cases).
Severe mitral annular calcification may cause mild/moderate MS but very rarely causes severe MS.
LA myxoma/thrombus is an uncommon cause of MS (<1%).
A mitral annuloplasty ring may overly narrow the orifice.
Malignant carcinoid, rheumatoid arthritis, systemic lupus erythematosus, and other tumors are very rare causes.

Pathophysiology

The normal mitral valve area is 4.5 to 6 cm 2 . A diastolic transmitral valve gradient occurs with loss of about half of the original area. There is increased left atrial pressure at rest with MVA of 1.5 cm 2 .
Two thirds (at least) of MS cases occur in women. Of all cases of rheumatic heart disease, 25% are pure MS and 40% are mixed MS/mitral insufficiency.
The course of disease proceeds as follows:
• There is a 5- to 15-year latent period after rheumatic fever before early findings (auscultatory abnormalities) become apparent.
• Usually, a decade of asymptomaticity (with auscultatory abnormalities) passes before symptoms develop.
• Over 5 years, most patients with NYHA Class 2 symptoms progress to Class 3 to 4.
• Ten-year survival of patients with NYHA Class 2 symptoms is about 80%; for patients with NYHA Class 3 symptoms, it is about 38%. A more rapid progression has been noted among certain groups, such as in the subtropical areas of India and the Philippines, and among the Inuit.

Role of Transthoracic and Transesophageal Electrocardiography in Mitral Stenosis

Transthoracic Echocardiography
Nearly all cases of MS can be hemodynamically assessed using TTE alone. Both apical and lower esophagus sampling sites are, however, ideally aligned for Doppler interrogation, and generally generate accurate estimates of gradient. However, if the plane of the mitral orifice is oblique (because of LA dilation), TEE may struggle to achieve optimal alignment for sampling.
Mitral valve scoring is better performed by TTE than TEE, because posterior long-axis and apical views show subvalvar (chordal) involvement better than TEE does. TEE images from the esophagus, acquired through thickened (and potentially calcified) leaflets, fail to clearly depict subvalvar disease. Transgastric long-axis views may afford adequate views of the important subvalvar apparatus.
TEE is better than TTE for the following:

Detection of LAA and LA thrombus, which is necessary information when contemplating CBV
Estimation of MR severity (TTE may underestimate MR severity)
The rare truly technically difficult study case
TEE is not superior for the evaluation of subvalvar disease. The thickened and often calcified leaflets impair subvalvar imaging from the esophagus. Transgastric views are helpful to circumvent this imaging problem.

Cardiac Catheterization for Assessment of Mitral Stenosis

Usual Technique

Pulmonary artery (PA) catheter(s) for right-sided pressures and thermodilution-estimated CO
Femoral arterial access for retrograde cannulation into the LV via the aorta
• LV to aortic (femoral) pressure gradients
• Diastolic filling period (DFP): the average width (time) of the gradients
Verification of pressure waveforms (see later discussion)

Gorlin Equation

The Gorlin equation is employed, using the following variables: CO, DFP, HR, gradient. These variables are readily obtained at cardiac catheterization.
Historically, the Gorlin equation constant was developed for MS, because there is less flow dependence with MS than for AS. 14
In a small initial validation (11 cases), variation of serial measurements averaged ±0.0 cm 2 , but ranged from +0.2 to –0.4 cm 2 . 15
In the initial series, autopsy standard was ±0.5 to ±0.1 cm 2 and the variation against autopsy was ≤0.2 cm 2 . 14
The Gorlin equation purportedly estimates anatomic, not effective, orifice, because it was validated against surgery and autopsy, but there is evidence that it does not truly reflect anatomic area.
The Gorlin equation is less accurate in the presence of the following:
• MR. Therefore, in the presence of mixed mitral disease, echocardiographic measures (2D, planimetry) are superior to Gorlin. 16
• Atrial fibrillation
• Tachycardia
• Other valve lesions
• Abnormal LV function
Gorlin works best in the context of normal LV systolic function.
Areas should be calculated from 10 beats. 16

Gorlin Equation Considerations



Cardiac Output Issues

By any technique, CO is not reproducible within 15%.
Thermodilution is rendered less accurate by significant TR, which may not be known to be present, and is fairly common in advanced mitral disease.
The Fick technique is not likely more accurate in the real world, but does offer a “cross-check.” 3 mL/kg is an estimate of oxygen consumption, and has its own variance.

Gradient Issues

Ideally, the mitral gradient is recorded by catheters directly on either side of the valve (LA catheter via transseptal puncture and LV catheter), but this is not actual practice, and would confer additional risk if performed universally. Instead of an LA catheter, a pulmonary capillary wedge pressure (PCWP) recording is generally used, because it is easier and carries lower risk, but it is subject to artifacts that tend to increase the measured gradient.
In most patients, the PCWP is the same as the left atrial pressure, but delayed by 40 to 120 msec. To attempt to account for this, the peak of the V-wave is shifted (“phase corrected”) onto the downslope of the LV pressure tracing.
When the data by PCWP tracings are in doubt, a transseptal puncture for direct LA pressure should be considered.
Gradients will vary with atrial fibrillation, which is common with MS, and more beats than usual should be averaged, ideally 10. 16

Variables and Constants

DFP is an accurately measured variable with little error.
HR must be averaged to account for sinus variation/arrhythmia and especially for atrial fibrillation.
“Constant” and “correction factor”
• A discharge coefficient C or K and a combined empirically derived constant (includes correction of conversion of mm Hg to cm H 2 O)
• The constant (1.0) differs for different CO, 17, 18 and is, therefore, a variable.
• There is an additional correction factor of 0.8, which renders the equation less accurate at CO lower than normal (<4 L/min), especially if it is <3 L/min—i.e., the equation is clearly flow dependent. 16, 19 – 21 Unfortunately, low flow is common in advanced MS

Catheterization–Echocardiographic Discordance of Hemodynamic Parameters of Mitral Stenosis
Some cases of MS have discordance with catheter-derived estimates. The most common scenario that begets case discussion occurs when the case is not (quite) severe by echocardiography, but is severe as assessed by the wedge technique at catheterization. In most cases, this type of discordance reflects only lack of familiarity with wedge technique errors.

Reasons for Discordance with Catheterization–Echocardiography
The 95% CI Doppler mitral valve gradient versus catheter (wedge technique) gradient is 3 mm Hg.

Echocardiography Estimates Mitral Valve Area Less Than Catheterization

Planimetry: over-gain results in smaller depiction of orifice
PHT: if DT is prolonged due to LV properties
Within the SEE

Echocardiography Estimates Mitral Valve Area Greater Than Catheterization

Under-sampling of MS jet (alignment, poor signal intensity, poor planimetry)

Echocardiography Estimates Mitral Valve Gradient Greater Than Catheterization

Within the SEE

Echocardiography Estimates Mitral Valve Gradient Less Than Catheterization

Under-sampling of MS jet (alignment, poor signal intensity, poor planimetry)

Catheterization Estimates Transmitral Gradient Higher Than Does Echocardiography

Use of PCWP (not direct LAP) is the most likely cause of overestimation of MVG by catheterization. Use of PCWP tracing overestimates LAP–LVP by 3.3 ± 3.5 mm Hg (53%). 22
Use of phase-“corrected” PCWP improves correlation, but still leads to overestimation: 2.5 ± 2.9 mm Hg (43%) in one study 22 and a lesser mean difference in another study (1.7 mm Hg), as well as lesser difference in area. 23
Use of direct LAP results in a negligible mean difference between Doppler and catheterization gradient: only 0.2 ± 1.2 mm Hg. 22

Mitral Valve Catheter Balloon Valvuloplasty

Contraindications to Mitral Valve Catheter Balloon Valvuloplasty
A number of factors may contraindicate mitral valve catheter balloon valvuloplasty: 24

Related to valve
• MR of 3+ or 4+
• Thrombus in LA—free-floating or within body of LA

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