The Echocardiographers’ Guide

DEDICATION

This book is dedicated to Maureen Plappert CVT (dec.) – my wife, friend and partner in echocardiography for 26 years, with all my love. Ted Plappert

To Ted and the late Maureen Plappert whose dedication and expertise have been invaluable to patients and physicians alike. I have been privileged to work with them for more than 25 years at the University of Pennsylvania Medical Center and the Brigham and Women’s Hospital at Harvard Medical School during which time they have made pivotal contributions to many ground-breaking national and international clinical trials. Martin St John Sutton

PA USA BS FRCP .The Echocardiographers’ Guide Ted Plappert CVT Martin G St John Sutton MB Center for Quantitative Echocardiography Hospital of the University of Pennsylvania Philadelphia.

UK Tel. NW. photocopying. North Yorkshire Printed and bound in Great Britain by CPI Bath . number 1072954.uk/medicine All rights reserved. electronic.tandf.medicine@tandf. Informa Healthcare is a trading division of Informa UK Ltd. Abingdon.co. London W1T 3JH. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication. Oxon OX14 4RN. Neither the publishers nor the authors can be held responsible for errors or for any consequences arising from the use of information contained herein. FL 33487. A CIP record for this book is available from the British Library. Registered in England and Wales.: E-mail: 44 (0)1264 332424 tps. or transmitted. we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. Registered office: 37/41 Mortimer Street. or otherwise.co. Library of Congress Cataloging-in-Publication data available on application ISBN-13: 978 1 84184 489 3 ISBN-10: 1 84184 489 6 Distributed in North and South America by Taylor & Francis 6000 Broken Sound Parkway. 90 Tottenham Court Road. stored in a retrieval system.com Composition by J&L Composition. For detailed prescribing information or instructions on the use of any product or procedure discussed herein. No part of this publication may be reproduced. Although every effort has been made to ensure that drug doses and other information are presented accurately in this publication. in any form or by any means.: 44 (0) 207 017 6000 Fax.© 2006 Informa UK Limited First published in the United Kingdom in 2006 by Informa Healthcare. 4 Park Square. Milton Park. London W1P 0LP. Tel. Hampshire SP10 5BE. please consult the prescribing information or instructional material issued by the manufacturer. without the prior permission of the publisher or in accordance with the provisions of the Copyright.uk Website: http://www. the ultimate responsibility rests with the prescribing physician. Designs and Patents Act 1988 or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency.tandfsalesorder@thomson.com Distributed in the rest of the world by Thomson Publishing Services Cheriton House North Way Andover. mechanical.: 44 (0) 207 017 6699 E-mail: info. (Suite 300) Boca Raton. USA Phone: Fax: E-mail: 1 (800) 272-7737 or (561) 994-0555 within continental USA 1 (800) 374-3401 or (561) 361-6018 outside continental USA orders@crcpress. recording. Filey.

CONTENTS Acknowledgments 1 2 3 4 5 6 7 8 9 10 11 12 Physics and instrumentation The normal Doppler echocardiographic examination Evaluation of left ventricular systolic function Evaluation of right ventricular function Evaluation of diastolic function Coronary artery disease Valvular heart disease Cardiomyopathies Diseases of the pericardium Diseases of the aorta Cardiac masses Congenital cardiac malformations vi 1 13 35 43 51 61 75 117 135 147 155 163 181 Index v .

Monica Pugh. and Susan Thomas for their technical expertise. and Tim Koder. vi . to Drs Hind Rahmoudi. for editorial assistance. Hirotsugu Hamamoto. Thanks are due to Silvia Bush. Eva Hungler. Kelly Cornish. Kenneth Ruddell. Darryl Fenton. Ginny Englefield. Karen Eberman. Special thanks to Maureen Plappert. and Shinya Kanemoto for assistance with the illustrations and to Alan Burgess. Lise Fishman. Shumin Gao.ACKNOWLEDGMENTS The authors are indebted to the sonographers and cardiologists of the echocardiography laboratory and Center for Quantitative Echocardiography of the Hospital of the University of Pennsylvania for their assistance in preparing this textbook. Toni Emmi.

energy is lost as some of the sound wave is redirected. The time from the peak of one cycle to the peak of the next is the wavelength. Sound waves can be displayed graphically as local variations in acoustic pressure against time (Figure 1. is related to the density of the medium and is greater through dense materials. Wavelength is related to frequency: Wavelength propagation velocity/frequency The speed at which sound passes through a medium.1 PHYSICS AND INSTRUMENTATION CONTENTS q Sound q Transducers q Other Imaging Modalities q Two-Dimensional Images q Doppler SOUND Sound consists of mechanical waves. The acoustic impedance of a material is the product of its density and propagation velocity and is measured in rayls (one rayl is equal to one kilogram per square meter per second).e. The magnitude of the reflection will depend on the magnitude of the difference in acoustic impedances. Sound propagates by alternately compressing and expanding the particles of the medium.5 dB/cm to 1. sound needs a medium through which to propagate. a portion of the sound energy will be reflected back to its source. When a sound wave encounters a boundary between two media with different acoustic impedances. Most of the energy loss is through heat resulting from the compression of the medium.1 dB/cm/MHz in soft tissue. If the Pressure Time Figure 1.1 A sound wave is graphically represented as phasic variations in acoustic pressure (y-axis) against time (x-axis). Sound intensity (power per cross-sectional area) is attenuated as it travels through a medium. One wavelength (see double arrow) is measured as the time from the peak of one cycle to the peak of the next cycle. Energy loss is measured in decibels per centimeter per megahertz and ranges from 0. When a sound wave strikes a smooth interface between two materials with different acoustic impedances at a 90 angle. i. its propagation velocity. Unlike electromagnetic waves. 1 . Attenuation increases as frequency increases.1).

THE ECHOCARDIOGRAPHERS’ GUIDE

angle of incidence is not 90 sound may not be reflected back to the source. The angle of incidence will equal the angle of reflection. When the angle of incidence is not 90 and the acoustic impedances of two media at the interface are different, the propagating sound wave will be refracted, that is, it will change direction as it passes through the interface. When the interface between the two media is smooth and mirror-like (specular) more sound energy will be reflected, and when the interface is irregular, sound energy will be reflected in a number of directions. If the wavelength is large relative to the reflector, sound will be scattered in all directions.

TRANSDUCERS
Transducers convert one type of energy to another. Ultrasound (US) transducers rely on the piezoelectric properties of certain crystals, such as lead zirconate titanate ceramics, to convert electrical activity to mechanical vibration and mechanical vibrations back to electrical activity. When a piezoelectric crystal in a transducer is stimulated electrically it vibrates, producing an acoustic signal. When a piezoelectric crystal is mechanically deformed by ultrasound energy returning to the transducer it produces an electrical signal. The principal components of a simple single-crystal transducer are: a piezoelectric crystal; damping material behind the crystal; a lens; and an impedance matching layer in front of the lens (Figure 1.2). The damping material limits the vibration of the crystal, effectively turning it off after a few cycles and keeping the generated pulse train short. A short pulse length improves axial resolution, which is the ability to distinguish individual structures along the axis of propagation of the sound wave. Axial resolution is equal to one half the pulse length and does not change as the sound wave travels through the medium. The pulse length is equal to the product of the frequency and the number of cycles in the pulse train. Increasing the frequency increases the axial
2

Figure 1.2 A simple ultrasound transducer is composed of a piezoelectric crystal (blue), with an acoustic lens (red), and an impedance matching layer (green) in front and damping material (yellow) behind.

resolution, but increasing the frequency also increases the attenuation. When selecting a transducer it is therefore necessary to balance the requirements for penetration and resolution. The three-dimensional shape of an unfocused US beam resembles a cylinder in the near field that then diverges in the shape of a cone. The diameter of the crystal and its frequency determine the length of the near zone. The amount of beam divergence distal to the focal zone is determined by the crystal diameter. A focused beam is narrow and shaped like an hourglass. The beam can be focused by using an acoustic lens or a curved crystal. Lateral resolution is the ability to distinguish individual structures lying perpendicular to the axis of propagation of the sound wave and is optimal when

PHYSICS AND INSTRUMENTATION

the beam is at its narrowest. Two adjacent objects, side by side, will be resolved if they are farther apart than the width of the beam. The acoustic matching layer has an acoustic impedance value that lies between that of the crystal and skin. Its purpose is to minimize strong reflections at the skin surface so that the US beam will penetrate to the tissues. Part of the transmitted US energy is reflected back to the transducer each time the beam encounters an interface between two tissues with different acoustic impedances while the remainder of the beam continues to penetrate. Transducers spend only a fraction of a percent of the time transmitting the sound pulse. The rest of the time the transducer is in the receive mode ‘listening’ for a reflected signal. When reflected US is received at the transducer, mechanical deformation of the crystal results in an oscillating electric or radiofrequency (RF) signal. The distance from the transducer to the reflector can be calculated because the speed of sound in soft tissues is a constant (1540 m/s). When the reflected signal (echo) is received by the transducer it is amplified. Echoes returning to the transducer are differentially amplified as a function of their time of flight, i.e. late returning echoes get more amplification to compensate for attenuation. This differential amplification is performed automatically by the US system and manually by the operator through a time gain compensation (TGC) control. The returning signal is complex, consisting of oscillating waves with positive and negative components. The US system smoothes the waves and discards the negative components. To shorten the signal and emphasize the leading edge, the first derivative of the signal is calculated and the negative portion of the signal is again discarded. The signal may be amplified or if the signal is below a certain threshold determined by the system and the operator it will be ignored (reject control) (Figure 1.3). Returning echoes are displayed as dots along a line that represents depth in the chest. The brightness of each dot is propor-

E

A
Amplitude

B

C

D

Time Figure 1.3 (A) The raw radio-frequency signal returned to the transducer. (B) The signal is smoothed and the negative portion discarded. (C) The first derivative of the remaining signal is determined and (D) the negative portion is again discarded. (E) The signal is amplified.

tional to the echo intensity, which depends on the amount of reflected US, and is a function of the difference in acoustic impedances at each interface. This display of brightness per unit depth along one line is a B-mode scan line. An M-mode or motion mode display results from graphing returning echoes from successive transmitted pulses as a function of time. A sampling rate of 1000 Hz along a scan line can be achieved and provides M-mode with the temporal resolution required to evaluate even the fastest moving cardiac structures.

TWO-DIMENSIONAL IMAGES
For cardiac imaging the US beam is swept through an arc from a point on the chest wall. A single crystal transducer can generate two-dimensional images if the US beam is mechanically oscillated through a plane. The beam is directed in increments through an arc or sector of 90 and transmits and receives a B-mode scan line in less than 1 increments. As the angle of the beam for each scan line is known, a two-dimensional still image can be constructed from a series of scan lines. The speed of sound in soft tissue is 1540 m/s; therefore, it takes an emitted sound train 0.00013 s to travel to a depth of 20 cm. The round trip from the
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THE ECHOCARDIOGRAPHERS’ GUIDE

transducer to the reflector and back takes twice as long or 0.00026 s. This return trip can be made 3846 times in one second. Each round trip represents a B-mode scan line, and 120 such scan lines can be made in 0.03 s. If one two-dimensional image is constructed from 120 scan lines derived from incrementally changing the angle of the US beam to the transducer face, 32 such images can be obtained in one second, i.e. the twodimensional image can be updated 32 times in a second and cardiac motion can be seen in real time. The pulse repetition frequency (PRF) is the number of transmit/receive cycles performed by the transducer in one second. In the example above: 3846 round trips per second is the PRF, 120 scan lines per image is the line density, and 32 images per second is the frame rate. These factors along with the depth are all interrelated. If the depth is decreased the PRF increases, this can yield either an increase in the frame rate or an increase in the line density. If the line density is increased, then either the depth or the frame rate must decrease. Most real-time two-dimensional sector scans are now made with phased array rather than mechanical transducers. A string of crystal elements are arranged in a row. All of the crystal elements transmit for each scan line. The beam is steered by changing the timing of the excitation of the crystal elements. The beam can be focused by altering the timing of both the excitation (transmit focus) of the crystals and the receipt of returning echoes (Figure 1.4). More than
A B

one focal zone can be employed but each scan line must be rescanned for each additional focal zone resulting in a decrease in the number of frames that can be assembled per second. In the digital scan converter (DSC), B-mode scan lines undergo analog to digital conversion. Echoes are assigned numerical values in increasing order of intensity. The numerical value will determine the gray shade of a picture element (pixel) when the digital information from each frame is mapped to a rectangular image. The amplitude range of returning echoes is on the order of 100 dB, i.e. the strongest echo is 100 000 times stronger than the weakest. This range of echo intensities is compressed by the DSC to fit the 30 dB dynamic range of the display. Operator selectable compression algorithms may be linear or logarithmic and determine the schedule with which incoming echoes are mapped to shades of gray for display (Figure 1.5). For example, a nonlinear algorithm might be selected to increase the visibility of weak reflectors while decreasing the intensity of strong ones to prevent them from obscuring adjacent anatomy. The DSC also fills in missing information between scan lines by assigning a numerical value to what would be a black pixel (no data) based on the average values of neighboring pixels: a process called interpolation. Information from frames adjacent in time can also be averaged to provide temporal as well as spatial smoothing. The frame rate is not reduced but each frame will be made up of a variable amount of
C D

Figure 1.4 All elements in a phased array transducer are fired for each scan line. The timing of the excitation of the crystal elements determines the direction of the beam. (A) When elements on the left side of the transducer are fired first the beam is directed to the right. (B) When fired simultaneously the beam is directed straight ahead. (C) When crystals on the right are fired first the beam is angled to the left. (D) Minor variations in the timing of crystal excitation focus the beam.

4

no flow can be detected. which alternately sends out 5 . If the flow is toward the transducer the frequency shift is positive. When is 0 or 180 . Completely digital echocardiography labs have been made possible by advances in digital storage media and transfer speeds.PHYSICS AND INSTRUMENTATION Compression that leaves the transducer from the frequency that returns to the transducer yields a third frequency.5 Echoes returning to the transducer are mapped to gray shades according to their intensities but the relationship is determined by the operator and need not be linear. The amount of ‘old’ information is determined by an operator-selected persistence factor. The propagation velocity is 1540 m/s. CW Doppler can measure high velocities but it samples all of the frequency shifts along an entire line. which is in the audible range and is proportional to the velocity of the moving target. which can be positioned through the region of interest of the real-time two-dimensional image. a small portion of the sound will be reflected back to the transducer. CW Doppler is used when the highest velocities are of interest. facilitating comparison of serial studies on a given patient. The best Doppler velocities are obtained when the flow is parallel to the beam. The reflected sound will have a different frequency than the transmitted sound. Subtracting the frequency Pulsed wave Doppler In contrast. and if away from the transducer it is negative. Images are transferred from the US systems to central computers (servers) were they are archived. The relation between the difference frequency and the velocity of the target is given by the Doppler equation: Propagation velocity Doppler shift ________________________ 2 transducer frequency cos Gray shades Black White Velocity Weak Echo intensity Strong Figure 1. The images are not degraded by digital to analog conversion. such as blood moving through the heart. the Doppler shift is the difference frequency and (theta) is the angle between the blood flow and the US beam. pulsed-wave (PW) Doppler uses a single crystal. the cosine of is equal to 1 and does not affect the relation but as the beam becomes increasingly less parallel to the flow the angle becomes increasingly important in the calculation of velocity. Comparator circuits in the US system perform these calculations. The multiple imaging windows available in cardiac scanning allow the beam to be aligned with flow and make angle correction for unnecessary. At 90 when the cosine of is 0. DOPPLER When US strikes a moving target. a difference frequency. Continuous wave Doppler Continuous wave (CW) Doppler requires one crystal to transmit sound waves constantly and one crystal to receive constantly. Images are easily recalled for viewing. The digital information must be converted back to analog form to be recorded on videotape and this results in a degree of image degradation. information from preceding frames.

Therefore. PW Doppler cannot resolve velocities when the Nyquist limit is exceeded. Flows toward the transducer (positive register) are displayed above the baseline and flows away from the transducer are displayed below the baseline (negative register). The systolic velocity below the baseline represents retrograde flow. and degree of turbulence of blood flows (Figure 1. Note that both the systolic and diastolic signals exhibit spectral broadening indicating turbulent blood flow. many frequency shifts are returned to the transducer. When this occurs. An excessively high positive frequency shift reflecting flow toward the transducer will be displayed graphically as negative. so that only frequency shifts that arise from an operator selected region of interest along the course of the line will be received. 64 for flow toward and 64 for flow away from the transducer. When red blood cells are moving at a relatively uniform velocity and direction the resulting graphic (spectral envelope) is thin. Unwanted low velocity signals originating from the movement of the cardiac structures lying near the baseline can be suppressed with a high pass ‘wall filter’. Time is on the horizontal axis and velocity is on the vertical axis with the zero velocity baseline in the center.6 Continuous wave Doppler signal with the sample line through the mitral valve in a patient with mitral stenosis and regurgitation. duration. This is known as spectral display or spectral Doppler. As the Nyquist limit is equal to half the pulse Figure 1.THE ECHOCARDIOGRAPHERS’ GUIDE US pulses and then listens for their return. flow away from the transducer. . rate of change of velocity. Spectral broadening along the velocity axis represents more disorganized blood flow. FFT resolves the returning Doppler shifted frequencies into their constituent parts and converts them to velocity signals that are plotted against time. The diastolic velocity signal represents antegrade flow across the mitral valve. 6 Examination of spectral Doppler waveforms gives the timing. The vertical distance between calibration markers (red dots) is 1 m/s and the horizontal distance between time markers at the top of the spectral display is 200 ms. Nyquist limit PRF/2 Red blood cells within the sample volume (PW) or along the sample line (CW) rarely have a uniform velocity or direction of motion. PW Doppler cannot measure high frequency shifts resulting from high velocity flows without ambiguity as to the direction of flow. This window of time corresponds to a window of depth. The system is gated or set to listen to returning signals from a window in time after the signal is transmitted.6). Velocities are sampled at 5 ms or 10 ms intervals and the resulting velocity components are assigned to 128 locations or bins along the vertical axis. Gray shades give the relative intensity of each velocity within the sample. The returning signal is complex and is resolved into a number of single frequency sine waves by fast Fourier transformation (FFT). or sample volume. high velocities are shown in the opposite register. This is termed aliasing. The maximum frequency shift that can be measured unambiguously by PW Doppler is termed the Nyquist limit and is a function of the PRF. Velocities above the baseline represent flow toward the transducer and velocities below the baseline. moving away from the transducer. velocity.

When the proximal velocity is 1 or less it can be ignored and the equation simplifies to: Pressure difference (mmHg) 4(velocity2) Intracardiac pressures can be calculated from Doppler flow velocities. In this way signals from two. If the sample volume is positioned at one half of the distance from the transducer to the true region of interest. signals from the true region of interest will be received at double the PRF.8). 7 . PW Doppler signal processing achieves range resolution by processing only those signals that return to the transducer within a window of time corresponding to the depth from the transducer of the sample volume.7). if the peak flow velocity across a stenosed aortic valve is 5 m/s. Sound returning from twice the depth of the sample volume initiated by the preceding pulse is received within the same window. In high pulse repetition frequency (PRF) Doppler frequency shift information from multiple sample volumes equidistant from the transducer is assessed. the pressure difference or gradient between the left ventricle and the aorta will be equal to 4(52) or 100 mmHg.PHYSICS AND INSTRUMENTATION repetition frequency and the PRF is greater at shallower depths. three or four times the distance to the primary sample volume can be received and analyzed but with a high PRF dependent only on the depth of the proximal sample volume. High-PRF Doppler High-PRF Doppler allows higher velocities to be assessed at the expense of some ambiguity as to their point of origin (depth of sample). between two chambers or across an obstruction to flow. In pulsed-wave (PW) Doppler only those signals returning from a single window in time after transmission of the ultrasound that corresponds to a discrete distance along the scan line (sample volume) are processed for display.e. i. aliasing will occur at higher velocities when sampled flows are close to the transducer. Moving the baseline up or down by assigning more velocity bins to flow toward or away from the transducer will allow the display of higher velocity signals without aliasing. For example. across a valve. most flow velocities are better assessed using either pure PW or CW Doppler (Figure 1. representing mitral regurgitation (MR).7 In continuous (CW) Doppler all of the frequency shifts along a scan line are translated into velocities for display. must have a velocity that reflects the pressure difference between the left ventricle (approximately 100–130 mmHg) and the left atrium (approximately 5–10 mmHg). are in close proximity. Velocity is related to the pressure difference by the modified Bernoulli equation: Pressure difference (mmHg) 4(velocity12 velocity22) where velocity2 is the proximal velocity and velocity1 the distal velocity is measured in m/s. Blood flow velocity is always related to the pressure difference between two points. The CW Doppler peak velocity of retrograde flow through the mitral valve in systole. A flow velocity of approximately 5 m/s is anticipated for MR (Figure 1. While high-PRF Doppler is occasionally useful in discriminating velocities at points of interest that CW PW High-PRF LV LA Figure 1.

5 m/s. Turbulence can be represented by the addition of yellows and greens (variance map) (Figure 1. respectively. An array of hundreds of pulsed wave sample volumes are superimposed over the two-dimensional image. A black band represents zero flow.8 Peak systolic velocities of continuous wave Doppler signals through the aortic valve in a patient with aortic stenosis (AS. red toward) where shades of blue represent flow away from the transducer and shades of red represent flow toward the transducer. When the Nyquist limit is exceeded aliasing occurs. Reds become blues or blues become reds. The number of scan lines. A black band represents zero velocity or no flow. Colors are ‘painted’ or mapped into the sample volumes along each scan line to represent flow velocities. Doppler color flow Doppler color flow mapping allows blood flow to be visualized in real time. and variance around the mean representing turbulence are captured from each sample volume. Shades of red and blue indicate flow toward and away from the transducer. Increasing intensities of blues and reds represent increasing velocities. An enormous amount of Doppler information must be processed for each colorcoded frame. mean velocity.9). right panel) and through the mitral valve in a patient with mitral regurgitation (MR. and the width of the color array also 8 Figure 1.9 A close-up view of a color Doppler variance map. the depth of the scan. . left panel) are equal at 4.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 1. Each scan line must be sampled (pulsed) from 4 to 20 times to provide color images. Autocorrelation techniques are used wherein each returning pulse is compared to the preceding pulse to determine blood movement between pulses. determine the frame rate for Doppler color flow imaging. Blood flow direction. Increasing the number of pulses increases the accuracy of the velocity information but decreases the frame rate. Shades of yellow and green (right side of the map) are added to each color Doppler sample volume to represent turbulence. becoming progressively brighter as flow velocity approaches the Nyquist limit of 64 cm/s. Assuming a normal aortic systolic blood pressure of 120 mmHg systolic and a left atrial pressure of 10 mmHg the left ventricular systolic pressure is 201 mmHg for the patient with AS (120 81) and 101 mmHg for the patient with MR (10 81). One standard velocity map is known by the acronym BART (blue away.

amplitude displays are non-directional and aliasing does not occur. color M-modes and twodimensional color maps of myocardial velocity can be generated as well as a number of derived graphics (Figure 1. It is therefore expressed as a percentage of the initial distance. rotated.10 The left panel is spectral Tissue Doppler display with the transducer at the apex. change of strain or rate of length change. low velocity. The strain rate can be calculated as: Velocity at one position Velocity at a second position –––––––––––––––––––––– Distance between the two positions Tissue Doppler imaging When assessing blood flow. Myocardial velocities are toward the transducer in systole and away from the transducer in diastole. low velocity flow is better appreciated. Doppler ultrasound is optimized for high velocity and low amplitude signals. baseline shift and scale controls are available. This format has a high temporal resolution and is valuable for the precise timing of flow events. entire threedimensional volumes of reflected US data can be captured and stored (Figure 1. manipulated on the screen. high amplitude signals are given preference. blues turning to reds and reds turning to blues in keeping with the apparent change in flow direction seen in PW Doppler. As in spectral Doppler. Strain rate is the rate of Strain rate Strain rate is synonymous with myocardial velocity gradient. but it is well suited to vascular imaging.10). When the scale is reduced. Figure 1. To assess myocardial motion. Instead of acquiring scan plans. The right panel is color tissue Doppler imaging. Spectral displays (PW). the density of moving red blood cells in the sample rather than for the velocity of blood flow. Tissue Doppler imaging (TDI) measures the velocity of tissue and the timing of its motion. In color Doppler aliasing is seen by color reversal. (strain D/D). i. sliced along their x-. The myocardium is displayed in red indicating motion away from the transducer in this diastolic frame. Motion of the heart in systole is predominantly from the base to the apex so that velocity signals are higher at the base and there is a base to apex velocity gradient. Frequency shift information is not used.PHYSICS AND INSTRUMENTATION Color Doppler is PW Doppler and will alias when the Nyquist limit is exceeded. It is sensitive to motion artifacts and its use in cardiac imaging is limited.11). Other imaging modalities Three-dimensional echocardiography Real-time transthoracic three-dimensional imaging has recently emerged. Three-dimensional color Doppler images can also be acquired. y. The three-dimensional volumes can be viewed in real time. Tissue characterization The pattern of US reflection from tissues is a function of their material properties 9 .or z-axis or along any user-selected axis and viewed in real time. Color Doppler mapping can also be superimposed on the single scan line of the M-mode display. The distance traveled by the sampled muscle segment or its displacement is obtained by integrating the velocity waveform.e. In color amplitude imaging or power Doppler the color codes for the intensity of blood flow. The term strain refers to the distance (D) traveled between two points (converging in systole and diverging in diastole) or distance change normalized to the initial distance between the two points.

This cyclic variation is lost or muted in the muscle tissue in some disease processes. The unprocessed radio frequency of the reflected (backscattered) signal is used. These contrast agents improve LV endocardial definition.11 An apical four-chamber slice through a three-dimensional volume. A peripheral injection of these agents will cause first the right heart chambers and then the left heart chambers to be opacified (Figure 1. When this solution is injected into a peripheral vein during an ultrasound examination it opaci- fies the right heart chambers with echoes. right atrium). The three-dimensional volume can be sliced along the x-. right ventricle. RA. The integrated backscatter varies cyclically between systole and diastole in normal myocardium.THE ECHOCARDIOGRAPHERS’ GUIDE including: the spatial distribution of density within them and the number and kind of interfaces between tissues with different densities.or z-axis or any user selected axis and viewed in real time.25 MHz for a large patient or Figure 1. These microbubbles are strong reflectors of ultrasound. There is a catheter (arrow) in the left ventricle (LV) (RV. Microbubbles will form in a saline solution agitated with a small amount of air. y. right ventricle. Tissue characterization is an attempt to identify different types of tissue by their patterns of reflection.12). enhancing signals from small regurgitant jets. Some tissues have distinct acoustic signatures.13). The immediate appearance of ‘bubbles’ on the left side of the heart indicates an intracardiac shunt (RV. It can also aid in the CW Doppler interrogation of tricuspid regurgitation. RA. right atrium. Microbubbles manufactured with human serum albumin or perfluorocarbons are available that are small enough to transit the pulmonary capillaries. Myocardial opacification can be achieved with these agents when either injected into a peripheral vein or directly into a coronary artery to assess myocardial perfusion (Figure 1. 10 . Contrast echocardiography The blood pools can be opacified by the injection of a contrast agent. Modern transducers transmit a broad range of frequencies.14). left atrium).12 An intravenous contrast injection has caused opacification of the right heart chambers and some contrast material is seen in the left atrium and ventricle. LA. Figure 1. The operator can image at 2. This technique is often used to identify intracardiac shunts (Figure 1.

left ventricle.14 A modified four-chamber view in an ovine myocardial infarction model.PHYSICS AND INSTRUMENTATION Figure 1. LA. AO. a transmitted frequency of 2 MHz would cause a harmonic frequency of 4 MHz to be received. RA. The reflectivity of normally perfused myocardium (circled in yellow) is enhanced. By imaging with a low transmitted frequency and receiving at double the transmitted frequency. Non-perfused muscle (circled in red) is not (LV.13 Manufactured microbubbles when injected into a peripheral vein opacify the right heart chambers and then transit the pulmonary circulation to opacify the left heart (RV. 11 .5 MHz for a smaller patient with the same transducer. penetration is enhanced and noise is reduced. Harmonic imaging is principally a noise reduction technique and may result in loss of signal and shadowing in the periphery of the image. right ventricle. 3. right atrium. For example. left atrium. LV. aorta). left atrium). These broadband transducers have led to the introduction of harmonic imaging. Contrast material was injected directly into the left main coronary artery. left ventricle. Figure 1. LA.

.

so that the interatrial and interventricular septa are oriented along a line that is approximately 30–45 from the sagittal plane. two-dimensional imaging. The long axis of the heart extends from the PMI (which can be palpated at the fifth or sixth left intercostal space between the midclavicular and anterior axillary line) to a point on the middle of the right clavicle. Ultrasound is absorbed by bone and scattered by the air in the lungs. at the supersternal notch. bring the apex closer to the chest 13 . In thin patients the heart may be retrosternal and difficult to image. The right ventricle (RV) is anterior to the left ventricle (LV) and the right atrium (RA) and RV inflow tract are predominantly retrosternal. inferior and lateral to the point of maximum impulse (PMI). Thorough knowledge of the instrumentation of the ultrasound system used is required but careful attention must be paid to patient positioning to optimize imaging and Doppler signals. It is more technically difficult to obtain optimal images in elderly patients with calcification of the costochondral junctions. The tomographic anatomy and Doppler flow signals that can be obtained from each window are described in detail below. This will help keep the examination focused on relevant clinical issues. is almost completely surrounded by the bones of the thoracic cage and the lungs. After the patient is greeted and the test explained. which integrates M-mode. a brief history should be obtained before beginning the examination.2 THE NORMAL DOPPLER ECHOCARDIOGRAPHIC EXAMINATION CONTENTS q Anatomy q The Parasternal Window q The Apical Window q The Subcostal Window q The Suprasternal Notch Views q The Right Parasternal Transducer Position This chapter will describe a method of performing a complete tranthoracic echocardiographic examination. and at the upper right sternal edge. THE PARASTERNAL WINDOW For parasternal imaging the recumbent patient is placed in the full left lateral decubitus position to allow the heart to hang down from behind the sternum as much as possible. inferior to the xiphoid process (subcostal). at the apex. ANATOMY The acoustic windows through which sound can propagate are located along the left sternal edge (parasternal). All technologists should follow a systematic protocol so that no important information is omitted. and in patients with obstructive pulmonary disease and hyperinflated lungs. and Doppler for each acoustic window. The left supraclavicular fossa is also useful for imaging the superior vena cava and adjacent structures. The heart. including the proximal great vessels.

aorta. The RV outflow tract crosses the LV outflow tract anteriorly. The sinuses of Valsalva in the aortic root and their termination at the sinotubular junction can be seen. Electrocardiographic (EKG) leads are attached and the signal is adjusted to obtain an upright QRS complex. The anterior and posterior walls of the aorta move anteriorly in systole as the LA fills. AO. When closed. then a higher intercostal space should be sought. superior to the atrioventricular (AV) groove (Figure 2. The long axis (LAX) image is optimized so that the interventricular septum (IVS) is horizontal on the screen with the apex at the left (Figure 2.3). Mmodes are a graphic representation in depth of penetration versus time of the structures sampled along the scan line. and increase the size of the window. LA. Both leaflets of the mitral valve (MV) and two cusps of the aortic valve (AOV) are dis- played. stay apart through ejection and come back together forming a box within the aorta.1 Parasternal long axis view from a normal subject (RVOT. left ventricle. Held expiration enlarges the size of the parasternal window. The head is elevated 30 to lower the diaphragm. The AOV cusps separate in early systole. If the IVS angles up from the right of the screen to the left. The long axis view The transducer is oriented along the long axis of the heart from the right shoulder to the left flank. The right coronary cusp of the AOV is seen in the anterior aortic root and it is usually the noncoronary cusp that is seen in the posterior aortic root. 14 . left atrium). the AOV leaflets are visualized as a line in the middle of the aorta. right ventricular outflow tract. Patients are instructed to place their left arm above the head and put their shoulders back to open up the intercostal spaces.1). LV. M-mode anatomy The M-mode cursor is first positioned through the aorta and LA (Figure 2.2). The descending thoracic aorta is located behind the left atrium (LA). A pillow for the patient’s head is essential. The left ventricular walls seen in this view are the posterior wall and the anterior IVS. Moving the transducer closer to the sternum and turning the patient to a more lateral position helps display the IVS in a horizontal orientation. The coronary sinus is often visualized as a small circular structure in the posterior atrioventricular sulcus. Figure 2.THE ECHOCARDIOGRAPHERS’ GUIDE wall. The transducer is in approximately the third or fourth intercostal space close to the left sternal edge.

2 Parasternal long axis view in early diastole. descending aorta). RV free wall thickness usually cannot be measured. measurements of the LV cavity are made from the leading edge of the left septal endocardial reflection to the leading edge of the posterior LV wall endocardium (Table 2. The posterior wall epicardial interface can be identified in systole when there is normally Figure 2. At the C point the MV is closed. The M-mode cursor is next directed through the MV leaflets (Figure 2. left ventricle. as the RV epicardium is too close to the transducer. a slight separation between the visceral and parietal layers of the pericardium.THE NORMAL DOPPLER ECHOCARDIOGRAPHIC EXAMINATION Figure 2. The MV leaflets separate again with atrial contraction. The beam first passes through the RV outflow tract then the IVS. The aortic root diameter is measured at the AOV opening and the LA size is measured at its maximum (late systole). aorta. They are farthest apart at the E point and partially closed at the F point. and then LV posterior wall. aortic valve. AO. The LV posterior wall endocardial reflection is identified as the line with the most rapid rise in systole. LA. At the D point the anterior and posterior leaflets separate. Dao. The A point is the second positive peak. The pericardium is a good reflector of ultrasound and will be the last remaining echo when the gain is decreased. LV cavity. AO. right ventricle. The black arrow indicates the coronary sinus (RV. By convention.3 M-mode echocardiogram showing the aorta and left atrium. left atrium. aorta. left atrium). The M-mode cursor is then directed through the LV just below (apical to) the tips of the MV leaflets (Figure 2.1).4). Measurements are made at end-diastole. LV. The RA/RV view or RV inflow tract view The anterior tricuspid valve leaflet is the largest and most excursive and divides the 15 . which is defined as the peak of the QRS complex and at end-systole defined as the point of maximum posterior excursion of the left side of the IVS. LA. Separation of the right and noncoronary cusps of the aortic valve forms the box-like pattern within the aorta in systole. AOV. and usually shows a presystolic dip caused by atrial contraction. The aortic valve closure line is seen as a horizontal stripe in the center of the aorta. The vertical distance between depth markers (red dots) is 1 cm and depth markers are generated at 1 s intervals (RVOT. right ventricular outflow tract.5).

Early diastolic filling velocity rises to an E point. This is the only view that routinely shows the posterior leaflet of the TV.2 0.8 1.1 0. Figure 2. the A point caused by atrial contraction.4 Figure 2. the continuous wave (CW) Doppler sample line is aligned through the direction of flow of the color signal (Figure 2. often helpful to move the transducer to a lower intercostal space to obtain this view. It is 16 . If TR is seen with color Doppler.0 0. The maximum velocity of the TR signal on the CW spectral display is related to the maximum pressure difference between the RV and the RA in systole by the modified Bernoulli formula: Pressure difference 4 (peak velocity2) For example. mitral valve). This positions the RV inflow nearly parallel to the beam and is especially useful for evaluating tricuspid regurgitation (TR). The coronary sinus can often be seen entering the RA in this view. Two leaflets of the tricuspid valve (TV).4 0. LV left ventricle). the RA. The long axis of the RV outflow tract and pulmonary artery can be visualized by rotating the transducer about 20 clockwise RV into inflow and outflow tracts. and a variable amount of the RV are visualized in the RA/RV view or RV inflow tract view (Figure 2. a velocity of 2. Mitral valve D.6).9 0.8). MV.3 2. low velocity.1 Normal M-mode values in cm (mean SD) Left ventricular internal end-diastolic dimension (LVIDd) Left ventricular internal end-systolic dimension (LVIDs) Interventricular septal thickness at end-diastole (IVSTd) Interventricular septal thickness at end-systole (IVSTs) Posterior wall thickness at end-diastole (PWTd) Posterior wall thickness at end-systole (PWTs) Left atrium (LA) Aorta (AO) 4.THE ECHOCARDIOGRAPHERS’ GUIDE Table 2.5 0. and C points are labeled on the second cycle (see text) (RV. right ventricle. filling slows in middiastole and then reaches a second peak. Normal antegrade flow through the TV in diastole is biphasic. A.4 M-mode echocardiogram of the mitral valve.9 1. E.3 3. and often respiro-phasic. The normal range for the percent change in LV diameter is 28–41%.7). left ventricle.2 0. LV. From the LAX plane the transducer is rotated 10–15 counterclockwise and angled inferiorly and medially to show the RV inflow tract. The severity of the TR is approximately proportional to the spatial extent of the color disturbance. F.3 0. The E wave is always higher in normal subjects.2 0. TR appears as a color Doppler flow disturbance in the RA in systole (Figure 2. right ventricle.5 M-mode echocardiogram of the left ventricle at the tips of the mitral valve (RV.4 0.8 3.5 m/s represents a pressure difference of 25 mmHg between the RV and the RA in systole.

right ventricle. LV. right atrium.THE NORMAL DOPPLER ECHOCARDIOGRAPHIC EXAMINATION Figure 2.6 Right ventricular inflow tract or RA/RV view. right ventricle. the downward pointing arrow indicates the thebesian valve. right atrium).8 Continuous wave Doppler signal of tricuspid regurgitation with a peak velocity of 3 m/s representing a right ventricle to right atrial pressure gradient of 36 mmHg. The anterior and posterior tricuspid valve leaflets are visualized. which is rarely seen. Figure 2. at the mouth of the coronary sinus (RV. Mild tricuspid regurgitation is often seen in normal subjects (RV. left ventricle. 17 . Figure 2. The vertical distance between calibration markers is 1 m/s. CS. The upward pointing arrow indicates a Chiari network. RA. RA.7 Right ventricular inflow tract or RA/RV view with color flow Doppler mapping in systole demonstrating mild tricuspid regurgitation as a blue signal in the right atrium. coronary sinus).

9 A parasternal long axis view of the right ventricular outflow tract (RVOT) and pulmonary artery (PA). Figure 2. SAX imaging is begun in the intercostal space in which the MV is seen with the transducer most perpendicular to the chest wall (Figure 2. left ventricle). The Figure 2.10). The plane extends from the patient’s right flank to the left shoulder. The short axis view From the LAX the transducer is next turned 90 clockwise into short axis (SAX) orientation.THE ECHOCARDIOGRAPHERS’ GUIDE from the parasternal LAX of the LV and angling superiorly and to the left (Figure 2.9). In SAX the LV cavity is round and the walls. which are uniformly thick. If the LAX view displayed the IVS as horizontal then in the SAX view it will be round. LV. move inward as they thicken symmetrically in systole. The pulmonic valve is indicated by an arrow (LV. The mitral valve is open in the early diastolic panel on the right taken at the time of the E point of the mitral valve M-mode and closed in the systolic panel on the right (RV. 18 . Transducer position and angulation are kept constant while the transducer is rotated.10 A parasternal short axis view at the level of the mitral valve. left ventricle). right ventricle.

The transducer is now angled back through the SAX of the MV and upward to the right shoulder to obtain a SAX at the base of the heart showing the aorta in circular cross-section with the LA posterior (Figure 2. moving the transducer 1 cm lateral and angling medially helps to visualize the AOV leaflets. left ventricle).12). SAX images at the level of the high papillary muscles (Figure 2. lateral (Lat. LV. the left coronary cusp is posterior and to the right of the image and the noncoronary cusp is posterior and to the left. the posteromedial papillary muscle is at about 8 o’clock and the anterolateral papillary muscle at 4 o’clock.11 A parasternal short axis view at the high papillary muscle level (RV. designated as: anterior. This can cause the false appearance of a posterior wall motion abnormality.). inferior.11) and then the low papillary muscles are recorded. posterior septal (PS).). LV wall motion and thickening should be uniform. From the SAX at AOV level. The right coronary cusp is anterior. Color coded wall segments are in clockwise order from the anterior interventricular sulcus (the junction of the right ventricular and left ventricular free walls anteriorly): anterior (Ant. and anterior septal (Figure 2. The anterior and posterior IV sulci are located where the RV free wall meets the LV free wall. The commissure between the right and left coronary cusps marks the Figure 2. and anterior septal (AS). posterior septal.13). The papillary muscles should be positioned symmetrically within the circular LV cavity. posterior (Post. The transducer is angled slightly and slowly to the apex.THE NORMAL DOPPLER ECHOCARDIOGRAPHIC EXAMINATION Figure 2. Slight clockwise rotation of the transducer frequently brings the wingshaped left atrial appendage (LAA) into view. 19 . inferior (Inf. posterior.). lateral. right ventricle.12 Anatomic preparation sliced in short axis at the level of the papillary muscles. The wall segments are in clockwise order from the anterior IV sulcus. The anterior MV leaflet opens toward the anterior IVS and divides the LV into inflow and outflow portions.). beam must not be allowed to wander superiorly into the left atrium in systole.

right atrium. Figure 2.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 2. right ventricle. pulmonary artery. descending aorta). left (L) and noncoronary (N) are seen. 20 The transducer often fits into the intercostal spaces in short axis better than in long axis because of its shape. aorta. The three leaflets of the aortic valve. right ventricle. pulmonary artery).13 A parasternal short axis view at the level of the aortic valve (AOV) and left atrium (LA). PA. AO. If so.14 A parasternal short axis view at the base of the heart demonstrating the pulmonary artery from the pulmonic valve (arrow) to the bifurcation (RV. insertion point of the right pulmonic valve cusp and the commissure between the right and noncoronary cusps marks the insertion of the septal leaflet of the tricuspid valve. Dao. PA. it can be manipulated closer to the sternum. the right (R). RA. allowing for a better M-mode sweep. Angling the transducer up and to the left shoulder slightly from the SAX of the AO . The intra-atrial septum arises from the midpoint of the noncoronary cusp. The left atrial appendage (LAA) is a wing-like extension of the left atrium (LA) (RV.

16 (A) A parasternal short axis view at the level of the aortic valve (AOV) and left atrium (LA) with color flow Doppler demonstrating mild pulmonic insufficiency (PI) as a small color signal in the right ventricular outflow tract in diastole (RV. (B) Pulsed-wave Doppler signal demonstrating systolic forward flow (down from the baseline) and PI (up from the baseline).16). right atrium. The vertical distance between the calibration markers is 0. RV stroke volume can be estimated using the diameter of the RV outflow tract and the flow velocity integral (FVI) of the RV outflow tract systolic flow taken at the same spot.15). CW Doppler is rarely required to visualize the Figure 2. The velocity of the spectral signal of PI reflects the pressure difference between the PA and the RV in diastole. The PW Doppler sample volume is positioned just proximal A minor amount of pulmonary insufficiency (PI) is often present in normal subjects and can be seen by color Doppler as a small candle flame in the RV outflow tract in diastole. A thin envelope indicating laminar flow is displayed (Figure 2. The area under the curve of the RV outflow tract systolic flow (FVI) is multiplied by the cross-sectional area of the vessel obtained using the formula: Area Figure 2.15 Pulsed-wave Doppler signal with the sample volume positioned in the right ventricular outflow tract just proximal to the pulmonic valve. p (diameter/2)2 and LA. which can often be visualized beyond its bifurcation into right and left branches (Figure 2. Normal transpulmonic maximum systolic flow velocity is between 0.2 m/s. RA.9 m/s. with an approximate 5–10 clockwise rotation optimizes the pulmonary artery. PA.5 m/s and 0. right ventricle.THE NORMAL DOPPLER ECHOCARDIOGRAPHIC EXAMINATION to the pulmonic valve and the spectral display is obtained.14). When PI is detected by color flow mapping a pulsed-wave (PW) Doppler sample is positioned within the color disturbance and a spectral display is obtained (Figure 2. pulmonary artery). 21 .

They are in counterclockwise order from the lower left: the right superior. LA. It is often desirable to move the transducer even lower and more lateral than the perceived apical window and have the patient hold their breath at endinspiration. the moderator band. The atria are in the far field. right atrium. The M-mode cursor can be positioned through the right cusp of the pulmonic valve. The RV is more heavily trabeculated than the LV and a prominent linear structure.THE ECHOCARDIOGRAPHERS’ GUIDE peak flow velocity of PI even in the presence of pulmonary hypertension because this signal is close to the transducer.17). If the IVS angles up to the right of the screen then the transducer should be moved laterally until the IVS is vertically oriented in the middle of the sector. The posterior interventricular septum and lateral wall of the left ventricle (LV) are seen in this view (RV.17 Apical four-chamber view. The patient is in full left lateral decubitus position but may be turned back to the right slightly to accommodate the trans- ducer between the patient and the bed. This lowers the diaphragm and brings the heart into the ultrasound beam allowing visualization of the full length of the ventricles. If the ventricles are foreshortened. If the four-chamber image appears to be too round then the transducer should be moved lower on the chest. 22 . is seen angling across the RV cavity from a point on the right side of the IVS one-third of the distance from the apex to the apical RV free wall. systolic opening is away from the transducer. Figure 2. The left heart chambers are on the right of the screen and the right heart chambers are on the left. right ventricle. Three of the four pulmonary veins are often seen entering the LA. RA. the pulse repetition frequency (PRF) is high and aliasing only occurs at high velocity. left atrium). THE APICAL WINDOW From a SAX parasternal position the transducer is moved inferiorly and laterally to beyond the point of maximal impulse and angled to the patient’s right shoulder to obtain an apical four-chamber view (Figure 2. A presystolic dip caused by atrial contraction is seen in normal subjects. the apical myocardium will not be seen and wall motion at the apex will be overestimated.

The transducer must be swept through the orthogonal plane not to miss or underestimate these flow disturbances. The chordae tendinea originate from the tips of each papillary muscle and insert into the overlying commissure and into both leaflets of the MV.20).18 Apical four-chamber view in systole showing the entrance of three of the four pulmonary veins into the left atrium (LA). left ventricle.18). The insertion of the TV into the IVS is slightly more apical than that of the MV. the spatial extent of the turbulent color disturbance approximates the severity of regurgitation (Figure 2. This is termed the five-chamber view (Figure 2. Color flow mapping of the atria is used to detect and semiquantify MR and TR in systole. left atrium. 2. left ventricle. The LV lateral wall and posterior septum are seen in the four-chamber view with the anterolateral papillary muscle within the LV cavity. right atrium.19 The apical five-chamber view is obtained by angling the scan plane anteriorly from the apical fourchamber view (RV. the left inferior pulmonary vein (RV. AO. When MR or Figure 2. Segmental wall motion can be assessed and should appear symmetrical. and 3.THE NORMAL DOPPLER ECHOCARDIOGRAPHIC EXAMINATION the left superior. Posterior angulation often shows the coronary sinus in the posterior atrioventricular sulcus. right ventricle. RA. Figure 2.19). the left superior vein. the right superior vein. LA. LV. RA. They are: 1. No chordae originate from the septum and connect to the MV but the septal leaflet of the TV has chordal connections to the right IVS. aorta). 23 . right ventricle. The apical four-chamber view is ideal for Doppler interrogation of the mitral and tricuspid valves. Slight anterior angulation (elevation) of the transducer (about 5 ) shows the aorta exiting the LV. LA. LV. right atrium. Occasionally. and also the LA. and the left inferior pulmonary veins (Figure 2. even more anterior angulation will demonstrate the PA leaving the RV. left atrium). The ultrasound beam is parallel to blood flow entering the LV and RV.

TR is present CW Doppler is used to obtain spectral waveforms of these signals (Figure 2. right ventricle.5 m/s indicating a peak systolic left ventricular/left atrial pressure gradient of 81 mmHg. RA pressure can be estimated and when added to the RV RA pressure difference gives the RV pressure in systole.20 An apical four-chamber view demonstrating the approximate spatial extent of color disturbances of mitral and tricuspid regurgitation for each grade of severity (RV. The PW spectral Doppler Figure 2. In the absence of pulmonic stenosis.21 Continuous wave Doppler signal of mitral regurgitation with a peak velocity of approximately 4. LV. The peak velocity of the MR tracing gives the LV LA pressure gradient in systole. left ventricle). The second peak of the LV filling waveform is caused by atrial contraction and is maximum at the A point. the RV systolic pressure is equal to the pulmonary artery systolic pressure (PASP). Flow velocity can be underestimated if the beam is not parallel to the flow but it cannot be overestimated. Flow from the pulmonary veins to the LA occurs in systole when the base of the heart contracts toward the apex and in diastole with MV opening. The E wave is higher than the A wave in young to middle aged normal subjects (Figure 2. .22).5 m/s. the MV opens and early blood flow velocity reaches a peak at the E point. In mid-diastole flow and flow velocity approach zero in normal subjects with slow heart rates. If the CW signal of TR is obtained from both the RA/RV view and the apical fourchamber view the highest velocity is used to estimate PASP. The vertical distance between calibration markers is 0.21). 24 When LA pressure exceeds LV pressure. Figure 2.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 2.22 Pulsed-wave Doppler with the sample volume positioned at the tips of the mitral valve leaflets. The maximum velocity of the CW TR signal reflects the pressure difference between the RV and RA in systole. Diastolic transmitral flow is easily assessed from the apical four-chamber view and reflects the biphasic nature of LV filling.

The area under the curve is the FVI or stroke distance and is measured in centimeters.5 cm proximal to the aortic valve. The systolic wave is often biphasic and its two peaks are designated S1 and S2. The maximal flow velocity and especially the area under the LV outflow tract flow tracing are proportional to the LV stroke volume.2 m/s.THE NORMAL DOPPLER ECHOCARDIOGRAPHIC EXAMINATION display of flow in the pulmonary veins therefore shows two principal waves (Figure 2. DFT. D (diastolic) and A (atrial contraction) waves are labeled. The cross-sectional area is obtained from measuring the LV outflow tract diameter in IVCT IVRT LVET LVOT DFT 1 Velocity (m/s) 2 3 4 5 MR Figure 2. The vertical distance between the calibration markers is 0.2 m/s. 120 Pressure (mmHg) AO 80 LV LA 40 Figure 2. The difference is the isovolumic contraction time (IVCT) as LV pressure rises and the isovolumic relaxation time (IVRT) as LV pressure falls (LVET.23 Pulsed-wave Doppler signal obtained with the sample volume positioned within the right superior pulmonary vein.24). Stroke volume is estimated by multiplying the FVI by the cross-sectional area of the LV outflow tract. left ventricular ejection time.25 A graphic representation of the temporal relation between mitral regurgitation (MR) and left ventricular outflow (LVOT). S (systolic). The vertical distance between calibration markers is 0. Figure 2. diastolic filling time). 25 . The MR signal exists when LV pressure exceeds left atrial (LA) pressure while LV forward flow occurs when LV pressure exceeds aortic pressure. The systole peak flow is normally higher than the diastolic.24 Pulsed-wave Doppler signal with the sample volume in the left ventricular outflow tract approximately 0. With the transducer angled up to the five-chamber view the PW Doppler sample volume is positioned just proximal to the aortic cusps and a thin systolic envelope representing laminar flow out of the LV is obtained (Figure 2.23). Atrial contraction causes a small retrograde flow.

Transducer position and angulation are held constant.25). The difference in time between the two events is the IVRT (Figure 2. Their presence indicates that this plane encounters the SAX plane along its 12 o’clock to 6 o’clock axis. The anatomy visualized in this plane is identical to that seen in parasternal LAX (Figure 2. 26 . The aortic valve and RV outflow tract are also seen. left ventricle. LV forward flow ends at aortic valve closure when aortic pressure exceeds LV pressure but MR does not end until LA pressure exceeds LV pressure at the time of MV opening. AO. left atrium. This plane is identical to the parasternal long axis view (LV. IVCT and IVRT can be directly measured when the PW sample volume is positioned between the LV inflow and outflow tracts so that the signals of each can be seen. Figure 2. LA. The anterior septum and posterior left ventricular (LV) walls are seen in this view. MR begins when LV pressure exceeds LA pressure but LV forward flow cannot begin until LV pressure exceeds aortic pressure. The posterior wall of the LV and the anterior IVS are seen in this view. The difference is the IVCT period.26 Apical long axis or apical three-chambered view. Similarly.THE ECHOCARDIOGRAPHERS’ GUIDE the parasternal LAX and assuming a circular cross-section using the formula: Area p (diameter/2)2 The LV outflow tract diameter is measured by two-dimensional echo in the parasternal LAX as the length of a line drawn between the insertion points of the right and noncoronary cusps of the aortic valve in early systole. aorta).26). Note that any errors made in measuring the outflow tract diameters are squared in the area formula. The isovolumic contraction (IVCT) and relaxation times (IVRT) can be estimated by comparing MR duration with LV outflow tract flow duration. The apical long axis view The apical LAX view is obtained with 90–120 counterclockwise rotation from the apical four-chamber view.

the apical two-chamber plane at the 2 o’clock and 8 o’clock position and the apical four-chamber plane at the 4 o’clock and 10 o’clock positions (A. L. 27 . left The apical two-chamber view This view is obtained with clockwise rotation from the apical LAX or counterclockwise rotation from the apical four-chamber view (Figure 2. A portion of the descending thoracic aorta can be seen with medial and inferior angulation of the transducer from this view (Figure 2. AS.29). P.28 Diagrammatic representation of the relation of the parasternal and apical scan planes. Apical two-chamber view. posteroseptal. The LV appears circular and a small crescent of the RV cavity may also be seen Figure 2. lateral. The apical two-chamber view intersects the clock face of the SAX at about 2 o’clock and 8 o’clock (Figure 2. Apical Middle Basal PS L P AS I A AS AS PS A P I P L The apical short axis view This is a SAX view of the tip of the LV (i.THE NORMAL DOPPLER ECHOCARDIOGRAPHIC EXAMINATION Figure 2. The apical long axis plane intersects the parasternal short axis plane at the 12 o’clock and 6 o’clock positions.27). anteroseptal). PS. inferior. anterior. I. The anterior and inferior left ventricular (LV) walls are seen in this view (LA. It is obtained by bringing the transducer to the SAX orientation while at the apical imaging window and then moving up an intercostal space or two.27 atrium). The anterior and inferior LV walls are seen in this view.28). posterior. below the papillary muscles).e. This view is distinguished from the apical LAX in that no part of the RV or IVS is visualized.

29 Inferior and medial angulation of the transducer from the apical two-chamber view demonstrates a portion of the descending thoracic aorta (Dao) (LV. The apex points to the right of the screen.THE ECHOCARDIOGRAPHERS’ GUIDE THE SUBCOSTAL WINDOW The patient is turned to the supine position and asked to bend the knees to help to relax the abdominal muscles. focus. The depth. RV. A second Figure 2.31). The MHV is vertically oriented and well situated for PW Doppler interrogation (Figure 2. The plane of the subcostal four-chamber view is identical to the apical four-chamber view except that the full length of the ventricles is not usually appreciated.33). Held inspiration usually helps the image quality by lowering the diaphragm and bringing the heart closer to the transducer. The thickness of the RV free wall is best evaluated from this view (Figure 2. right ventricle). Systolic flow into the RA is predominant as the base of the heart moves toward the apex. The depth may have to be increased. left ventricle.30). The RV free wall. left atrium). The arrow indicates a trabeculation crossing the LV cavity (LV. The head of the bed is lowered so that the patient may lie flat. left ventricle. Angling the transducer to the patient’s right and somewhat posteriorly will show the IVC and middle hepatic vein (MHV) (Figure 2. Figure 2. (Figure 2. The subcostal four-chamber view is obtained with the transducer at either the right or left subcostal margin immediately below the xiphoid process and angled parallel to the sternum. IVS and interatrial septum (IAS) are now nearly perpendicular to the beam.32). and gain should be adjusted to optimize the near field of the image and a higher transducer frequency can be used.30 A short axis near the cardiac apex. LA. 28 .

LV.33 Pulsed-wave Doppler signal with the sample volume positioned in the middle hepatic vein. LA. right atrium).32 On angling the transducer to the patient’s right from a subcostal four-chamber view the inferior vena cava (IVC) and middle hepatic vein (MHV) are visualized (RA. RA. Figure 2. The vertical distance between the calibration markers is 0. right ventricle.THE NORMAL DOPPLER ECHOCARDIOGRAPHIC EXAMINATION Figure 2. right atrium. The anatomy sampled in this view is identical to that seen in the apical fourchamber view except that the apex is generally not seen in the subcostal four-chamber view (RV. left atrium). left ventricle.2 m/s.31 Subcostal four-chamber view. Figure 2. Flow into the inferior vena cava and right atrium is biphasic with a predominant systolic wave and a diastolic wave. 29 . There is a small retrograde wave caused by atrial contraction.

5–2.2).34 Subcostal short axis at the level of the papillary muscles (RV. they can be distinguished by their Doppler flow patterns.5–2.5 cm) with 50% inspiratory collapse IVC is dilated ( 2. Directing the transducer to the patient’s left permits visualization of the distal descending thoracic and proximal abdominal aorta. The transducer is then rotated 90 counterclockwise and angled laterally to obtain SAX images of the LV (Figure 2.5 cm) with 50% inspiratory collapse Nl IVC size (1. As the transducer is angled toward the midline. RA pressure can be estimated by examining the IVC (Table 2.37).34). The AOV can often be visualized in SAX.THE ECHOCARDIOGRAPHERS’ GUIDE Table 2.2 Right-atrial pressure (RAP) estimated by inspection of the inferior vena cava (IVC) RAP Small IVC ( 1. LV. Severe TR causes systolic flow reversal. Flow ceases or is reversed with atrial contraction.5 cm) with no inspiratory collapse 0–5 mmHg 5–10 mmHg 10–15 mmHg 15–20 mmHg wave during diastole occurs with tricuspid valve opening. Figure 2. The infundibulum is at a better angle to the beam than it is in the parasternal projection making this view ideal for the detection and evaluation of pulmonic subvalvular obstruction. left ventricle).35). the SAX of first the MV and then the basal structures is brought into view (Figure 2. Caudal angulation of the transducer shows the IVC and aorta in cross-section. When in doubt. 30 . so this imaging plane is good for the Doppler evaluation of pulmonary valvular stenosis and regurgitation (Figure 2.5 cm) with 50% inspiratory collapse Nl IVC size (1. The subcostal sweep is identical to the parasternal SAX sweep except that the images are rotated about 30 clockwise in the subcostal window. Flow across the pulmonic valve into the main PA is parallel to the beam. The aorta is to the right of the screen (the patient’s left) and is usually rounder then the IVC (Figure 2.36). right ventricle.

38). and color Doppler. LA. the patient is asked to hyperextend their neck. R. The transducer is positioned in the suprasternal notch and angled caudally. the left common carotid. CW. RA. Flow toward the transducer in the ascending aorta and flow away from the transducer in the descending aorta can be assessed by PW. right ventricle. THE SUPRASTERNAL NOTCH VIEWS Still remaining in the supine position.THE NORMAL DOPPLER ECHOCARDIOGRAPHIC EXAMINATION Figure 2. (B) The inferior vena cava (IVC) and superior vena cava (SVC) are seen entering the right atrium (RA). right ventricle. The ascending aorta is on the left of the screen. AO. The beam is angled at 50–60 to the coronal plane to show the aorta in its long axis (Figure 2. left pulmonary artery). They are from proximal to distal: the innominate.36 Subcostal short axis view at the base of the heart. pulmonary artery). The origins of the brachiocephalic vessels are also seen arising from the superior aspect of the transverse aorta. transverse aorta is in the near field and the proximal descending aorta is on the right. right pulmonary artery. and left subclavian arteries. L. The ascending aorta is anterior to the descending aorta and is on the right of the spine and the descending aorta is to the left of the spine.35 (A) Subcostal short axis at the base of the heart. PA. A pillow under the shoulders may facilitate this. aorta. left atrium. right atrium. . The SVC is not routinely seen from the subcostal view (RV. LA. The bifurcation of the pulmonary artery (PA) is seen (RV. These flows are separated by a band without color at 31 Figure 2. left atrium. Color Doppler shows red flow in the ascending aorta and the blue flow in the descending aorta.

38 Suprasternal notch view with the aorta in long axis. particularly in those with congenital abnormalities.37 (A) The abdominal aorta (Dao) is seen in its long axis. more often in children. Coarctation of the aorta usually occurs distal to the origin of the left subclavian artery at the site of the ligmentum arteriosum. The technologist must be aware of 32 . Figure 2. Two arteries are seen arising from the anterior surface of the Dao. allow visualization of the pulmonary veins entering the LA transversely. one at each corner. Inferior to the right PA in this projection is the LA. The left pulmonary veins are on the left and the superior pulmonary veins are closer to the right PA. This is a right aortic arch. (B) The abdominal aorta and inferior vena cava (IVC) are seen in short axis. descending aorta). and the left subclavian (c). They are the celiac trunk (1) and the superior mesenteric artery (2). the left common carotid (b). This projection is known as the ‘crab’ view. The ascending aorta is not well seen (Dao. A 90 counterclockwise rotation of the transducer displays the transverse aorta in circular section with the right PA beneath its long axis. Posterior angulation of the transducer in a more coronal orientation can sometimes. The aorta arches over the right PA whereas the brachiocephalic or innominate vein is anterior to the aortic arch.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 2. the ascending aorta is to the left of the spine and the descending aorta is on the right. In some patients. The brachiocephalic vessels arising from the superior aspect of the transverse aorta (Tao) are from proximal to distal: the innominate (a). The suprasternal notch view is useful for CW evaluation of transaortic flow in aortic stenosis and is the only view that permits Doppler evaluation of flow across a coarctation of the aorta. 12 o’clock where the flow is perpendicular to the transducer.

LA. The patient is directed to turn into a full right lateral decubitus position with the right arm placed above the head and the head of the exam table elevated 30 .40 Right parasternal long axis view of the ascending aorta (AO) (LV. The higher the intercostal space the more vertically oriented is the ascending aorta. Right parasternal SAX imaging offers special advantages for the evaluation of the IAS. The PW Doppler flow pattern is similar to that seen when the sample volume is in the MHV.40). In this view the IAS is more perpendicular to the beam than it is in the left parasternal window and it is closer to the transducer than in the subcostal four-chambered view. This is an extension of the left parasternal LAX view. as it will not be revealed by the recorded images.39). left atrium). It is frequently advantageous in evaluating the Interatrial Septum (IAS) and should be considered in all patients when left parasternal images are suboptimal. With the transducer at the upper right sternal edge. a LAX view of the ascending aorta from the AOV to the right PA is obtained (Figure 2. It is occasionally possible to obtain a whole SAX sweep from this window especially when the heart is malpositioned. 33 .THE NORMAL DOPPLER ECHOCARDIOGRAPHIC EXAMINATION the transducer orientation and note this condition. Rotation of the transducer 90 clockwise gives a SAX through the base of the heart. It can sometimes be followed to its junction with the RA. Figure 2.39 The superior vena cava (SVC) is seen in its long axis with the transducer positioned in the left supraclavicular fossa and angled parallel to the spine. Figure 2. Flow through the AOV can be aligned with the beam and this view is indispensable in the Doppler evaluation of aortic stenosis especially in elderly patients in whom the aorta is unfolded. Placing the transducer in the left supraclavicular fossa and angling the beam parallel to the spine shows the superior vena cava in its long axis (Figure 2. left ventricle. THE RIGHT PARASTERNAL TRANSDUCER POSITION This window is important in the evaluation of the aortic valve and ascending aorta.

RV. As the transducer is moved. right ventricle. Rotating the transducer 90 allows SAX imaging with the RV free wall in the far field. the apex angles more and more to the left of the screen assuming a horizontal orientation with the LV lateral wall closest to the transducer (Figure 2. LA.41 Paraspinal four-chamber view. The presence of a large left pleural effusion (PL) enables visualization of the heart from the patient’s left midscapular area (LV. left ventricle.THE ECHOCARDIOGRAPHERS’ GUIDE ‘PARASPINAL’ IMAGING In the presence of a large left pleural effusion the transducer can be moved laterally from an apical four-chambered view to the left subscapular region. Figure 2. RA. right atrium).41). left atrium. 34 .

and LV mass to volume ratio. As preload increases. LV mass. The evaluation of ventricular systolic function must take into account the loading conditions. When afterload increases. Preload is the distending force on the ventricle prior to contraction. volume or wall stress. the pressure within the muscle. Afterload may be defined as end-systolic wall stress. which results in enhanced contraction (Frank–Starling mechanism) (Figure 3. and normalizes wall stress. The extent of ventricular remodeling can be assessed echocardiographically by Stroke volume LV end-diastolic volume Figure 3. left ventricle). Afterload is the resistance the ventricule must overcome to eject blood.3 EVALUATION OF LEFT VENTRICULAR SYSTOLIC FUNCTION CONTENTS q M-mode q Two Dimensional q Strain and Strain Rate q Doppler q Tissue Doppler Evaluation of left ventricular (LV) systolic function is a critically important application of Doppler echocardiography. in which sarcomeres are replicated in parallel. This increases wall thickness.1 The Frank–Starling relationship. stroke volume increases but a point is ultimately reached when further increase in preload does not affect output (LV. ejection fraction decreases. 35 . that is proportional to systolic cavity pressure and cavity radius. and major to minor axis diameter are almost constant in all mammalian hearts. mass to volume. in which sarcomeres are replicated in series resulting in a ventricle with increased cavity volume and normal wall thickness. Elevated end-diastolic wall stress is the stimulus for volume overload hypertrophy as in aortic and mitral regurgitation. atrial contraction.1). Increased peak systolic wall stress is a powerful stimulus for pressure overload hypertrophy as in chronic hypertension and aortic stenosis. LV ejection fraction and other ejection phase measures of ventricular function guide therapy and provide prognostic information but are load dependent. and inversely proportional to wall thickness. and ventricular chamber stiffness. Increasing preload within a physiologic range increases myocardial fiber stretch. The ratios of LV wall thickness to cavity radius. and it is influenced by a number of factors including intravascular volume. Preload can be estimated as end-diastolic pressure. Deviations from normal in any of these parameters are mediated through global or regional alterations in load.

If the ventricle is assumed to have the shape of a prolate ellipse with two equal short axis diameters and a long axis length equal to twice the short axis diameter. Quantitative evaluation of LV volumes and ejection fraction is more time consuming and relies on good image quality and conventional scan plane orientation.THE ECHOCARDIOGRAPHERS’ GUIDE the quantitation of ventricular cavity size. The cube formula overestimates the volumes in dilated ventricles.1). LVM 1. Mildly depressed systolic function is graded as between 40% and 50%. as the ventricle enlarges it becomes more spherical.e. moderately depressed from 30% to 40% and severely depressed as less than 30%.055 g/cm3) to yield muscle mass in grams. shape. mass. Short axis cavity area multiplied by the apical length would be the cavity volume if it was shaped like a cylinder. The visual assessment is generally expressed as ejection fraction. A normal LV ejects 55% of its end-diastolic volume in systole.0/(2. LV cavity volume A number of algorithms are available to convert measured LV cavity areas to volumes (Figure 3. Table 3. The % delta D divided by the LV ejection time is the mean velocity of circumferential fiber shortening (VcF) measured in ventricular circumferences per second. The 5/6 area length algorithm uses the cavity area from the short axis at the high papillary muscle level. The volume of the LV cavity is subtracted from the volume of the cavity plus the LV muscle and is multiplied by the density of muscle (1. Fractional shortening. The apical cavity length is measured from the midpoint of a line connecting the insertion points of the mitral valve leaflets in the apical four-chamber view to the apical endocardial border. but with ventricular enlargement the ventricle becomes increasingly spherical.4 LVID) (LVID3)) includes the correction factor developed by Teicholz et al. 36 . the increase in short axis diameter is greater than the increase in cavity length. An H/r ratio of greater than 0.055 ((PWT LVID (LVID)3) IVST)3 where PWT is posterior wall thickness and IVST is interventricular septal thickness. Multiplying this by 5/6 gives the volume of a bullet-shaped ventricle. and function. The normal LV is roughly bulletshaped. i. the percentage change in LVID from diastole to systole (% delta D). The formula: Volume (7.2.42 is diagnostic of pressure overload hypertrophy. As the LV dilates the 5/6 area length This equation simplifies to: Volume /3 LVID3 or approximately LVID3 This cube formula for LV volumes can be used for normal ventricles. provides an approximation of global LV systolic function when the ventricle contracts symmetrically. Wall thickness and left ventricular mass The relative wall thickness (H/r ratio) is defined as twice the posterior wall thickness divided by the LVID in diastole. ventricular volumes can be calculated by the formulae: Volume 4/3 LVID LVID/2 LVID/2 LV mass (LVM) can be calculated by M-mode using the cube or the Teicholz formulae for volumes. M-MODE LV size can be assessed from M-mode measurements of the LV internal diameter (LVID). Two-dimensional echo A trained echocardiographer can visually estimate systolic function accurately and reproducibly by observing the difference between LV diastolic and systolic cavity areas from multiple scan planes. However. which better reflects the axis ratio of the enlarged ventricle.

like the bullet formula. becomes less reliable when there are regions of akinesis or dyskinesis. The Simpson rule method of disks (MOD) makes no assumptions about LV shape. long axis. which assumes that the ventricle is a prolate ellipse of revolution.EVALUATION OF LEFT VENTRICULAR SYSTOLIC FUNCTION 5/6 Area length (0.e: Volume (biplane) (D2/2) Rp L/n (D1/2) algorithm will increasingly overestimate true volume. which is multiplied by L/n.2 The 5/6 area length algorithm assumes that the left ventricle (LV) is bullet-shaped. A single plane version uses the apical four-chamber area and length alone: volume 0. LV shape LV shape can be assessed as the ratio of cavity diameter and cavity length or as the ratio of the short axis cavity area to the apical cavity area. is not planar. The 0.1 Two-dimensional methods for quantitation of left ventricular volume Bullet 5/6 SAX cavity area LAX length Prolate ellipse 0. LV cavity volume can be divided by the volume of a sphere whose diameter is equal to the apical cavity length.85 (area1 area2/length).3). The apical area/length formula Volume 0. The LV volume is calculated by summing the volumes of all the cylinders (Figure 3. necting the opposing walls. Once the endocardial silhouette is traced.85 (area2/length). The annulus is farther from the apex in the two-chamber view. 37 .85 (area2/length) algorithm assumes that the LV has the shape of a prolate ellipse. i. The Simpson rule method This method does not make assumptions about ventricular shape and is the preferred method for LV volume calculation.85 Area2/length) Simpson rule (MOD) Figure 3. the base to apex length is automatically determined. This length (L) is divided into a number of segments of equal height (L/n) and lines perpendicular to it are drawn con- Both apical four-chamber and two-chamber single plane volumes correlate closely with biplane volumes. LV shape LV volume / 4/3p ((LAX length/2)3) All methods provide an index of sphericity. Apical lengths measured from the two-chamber view are consistently slightly longer than apical four-chamber lengths because the mitral annulus. R L/n (p (d/2)2) If biplane tracings are made. the ventricle is more spherical as the ratios approach unity. uses the apical fourchamber cavity area and either the apical long axis or two-chamber area together with the apical length. Table 3. the base from which the lengths are measured. The lengths of these lines are the diameters of cylinders with height L/n.85 LAX area1 LAX area2 /LAX length Simpson rule (single plane) R L/n (p d/2)2 Simpson rule (biplane) p (D1/2) (D2/2) L/n LAX. two diameters from orthogonal apical views are used to calculate the area of an ellipse. This method. and all of the volumes of the stack are summed.

the papillary muscles and trabecular structures are generally included with the cavity. Length Area . LV cavity area is multiplied by the LV cavity length from the MV annulus to the apical endocardium from an apical four-chamber view at enddiastole and by the constant 5/6 to yield cavity volume.0 cm is added to the length of the epicardium to represent the thickness of the 38 myocardium at the apex. The cavity volume is subtracted from the cavity plus muscle volume and the difference is multiplied by the density of muscle to yield LV mass.055 g/cm3). The LV lengths in Figures 3. 2-D LVM 5/6 {[(SAX total area (LAX cavity length 1.4(B) has a more spherical shape.4 Left ventricular (LV) mass is calculated using areas from the parasternal short axis view and LV length from the apical four-chamber view. When the length to the epicardium cannot be determined.0 cm)] (SAX cavity area LAX cavity length)} A B Figure 3.4(B) are equal but Figure 3.3 Simpson rule left ventricular (LV) cavity volumes are calculated by summing the volumes of disks whose diameter is the distance between apposing LV walls and whose height is equal to the cavity length divided by the number of disks (L/n). LV mass/hypertrophy LV mass is calculated from two-dimensional echo images as the difference between LV cavity volume and LV muscle plus cavity volume multiplied by the density of muscle (1.4(A) and 3. The area surrounded by the right septal edge and LV epicardium from the same short axis image is planimetered and this is multiplied by the LV cavity length from the MV annulus to the apical epicardium and by the constant 5/6.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 3.4). The LV epicardial border is only rarely clearly visualized in the apical images so the 5/6 area length method is the only two-dimensional method in general use for LV mass estimation (Figure 3. The LV cavity area is planimetered at end-diastole in the short axis view at the papillary muscle level. 1.

The force of systolic ejection is equal to the product of acceleration of blood and the mass of blood being The Tei index This is a Doppler method for assessing combined systolic and diastolic ventricular performance that relies on the measurement of temporal intervals. Figure 3. TEI index (IVRT IVCT)/LVET The isovolumic intervals need not be measured separately as cycle length minus the sum of LVET and the diastolic filling time will equal the sum of IVRT and IVCT. This ratio has proved to be useful in the serial assessment of patients taking cardiotoxic chemotherapy. Force and acceleration The peak velocity of the LV outflow tract flow velocity signal divided by the time from the onset of flow to peak velocity (the acceleration time) is the acceleration (cm/s/s) (Figure 3. DOPPLER Doppler echocardiography is essential for an understanding of valvular heart disease and the evaluation of LV systolic and diastolic function.6 Force is equal to mass multiplied by acceleration.055 g/cm3) is the mass of blood ejected during the acceleration interval. It is a reflection of the rate of increase of LV pressure ( dP/dT) in early systole. The Tei index is calcu- IVCT IVRT LVET LVOT MV DFT Figure 3. The Tei index is equal to isovolumic contraction time (IVCT) plus isovolumic relaxation time (IVRT) divided by LV ejection time (LVET). It is also equal to cycle length minus the sum of diastolic filling time (DFT) and LVET divided by LVET. using matrix array transducers or reconstructed from twodimensional images when their proper spatial and temporal orientation is known. The shaded area in the first cycle is the flow velocity integral (FVI) during the acceleration time. Acceleration decreases when systolic function is impaired. Analysis of three-dimensional echocardiographic images for LV volumes shows closer agreement with magnetic resonance imaging (MRI) than two-dimensional echocardiograms with lower interobserver variability. 39 .5 A graphic representation of the timing of LV inflow (MV) and outflow (LVOT). congenital heart disease. Acceleration is equal to the peak velocity attained divided by the acceleration time (At) and is represented by the arrow on the second cycle.EVALUATION OF LEFT VENTRICULAR SYSTOLIC FUNCTION Three-dimensional echocardiography Three-dimensional volumetric data can be acquired in real time or with electrocardiographic (EKG) gating.5).6). lated as isovolumic contraction time (IVCT) plus the isovolumic relaxation time (IVRT) divided by the LV ejection time (LVET) (Figure 3. This FVI multiplied by the cross-sectional area of the left ventricular outflow tract and by the density of blood (1. and following cardiac transplantation. patients with cardiomyopathies.

Various color maps can be used.7). rarely exceeding 20 cm/s so that aliasing is not encountered. the time required for the ventricle to increase the mitral regurgitant velocity from 1 m/s to 3 m/s is the time required to increase LV pressure by 32 mmHg. with brighter colors reflecting higher velocities. velocities increase from the epicardium to the endocardium and from the apex to the base.070 457 mmHg/s indicating moderately impaired LV systolic function. Myocardial velocity gradients can be shown. Using parallel digital processing and high pulse repetition frequency. which is primarily due to subendocardial muscle fiber shortening.9). The myocardial velocities of circumferentially oriented muscle fibers can be sampled from small segments of the lateral wall and septum from the parasternal SAX.055 CSA FVIAT) (peak velocity/acceleration time) This measurement is made prior to aortic valve opening and is therefore independent of afterload but it is sensitive to changes in preload (Figure 3.THE ECHOCARDIOGRAPHERS’ GUIDE accelerated. can be assessed from apical views. Myocardial velocities are low relative to blood flow. dP/dT 4 (32) 4 (12) ––––––––––––––––––––––––– Time from 1 m/s to 3 m/s Figure 3. a color encoded M-mode tracing or as twodimensional real time color Doppler (Figure 3. Force (1. In this example the time for the MR velocity to rise from 1 m/s to 3 m/s is approximately 70 ms. one color represents movement away from the transducer and another color represents movement toward the transducer. In systole the walls of the LV move toward the center of the chamber while the whole Mitral regurgitation dP/dT The rate of rise of pressure in the LV ( dP/dT) can be calculated from the slope of the continuous wave Doppler signal of mitral regurgitation ( dV/dT) as pressure is related to velocity by the modified Bournoulli equation where delta pressure 4 (velocity2). Contraction toward the center of the LV cavity or radial shortening can be evaluated from the parasternal LAX and SAX views. Pulsed wave (spectral) TDI measures myocardial peak velocity and color-coded TDI gives mean myocardial velocities. The mass of the blood is the stroke volume during the acceleration time which is equal to the product of the crosssectional area (CSA) of the LV outflow tract and the flow velocity integral from onset of ejection to peak velocity and the density of blood. Displayed velocities are the sum of local muscle contraction along the axis of the beam and motion of the entire heart. Frequency shift information from TDI is angle dependent so that only motion parallel to the beam can be measured accurately.7 The continuous wave Doppler signal of mitral regurgitation (MR) can be used to calculate left ventricular (LV) dP/dT. The normal value for dP/dT is approximately 800 mmHg/s. TDI signals depend on the frequency shift information of the reflected ultrasound and not its amplitude and TDI is applicable even when two-dimensional images are of poor quality. Tissue Doppler imaging Tissue Doppler imaging (TDI) information can be displayed as a spectral signal from a single pulsed-wave sample volume. As left atrial pressure is assumed to be constant during systole. Longitudinal contraction. frame rates of greater than 200 Hz can be achieved. 40 . dP/dT 32/0.

Both systolic and diastolic velocities are markedly reduced in the patient with RCM. mid-wall and epicardium of the same wall segment can be differentiated. and lower and more heterogeneous in the mid-ventricle compared with the base. heart moves toward the anterior chest wall. and increased time to peak velocity in the spectral tracing (Figure 3. The interventricular septum is blue in the early systolic frame indicating early systolic contraction. excellent correlations with radionuclide and contrast ventriculographic ejection fractions are demonstrated even in patients with wall motion abnormalities. Wall motion abnormalities subjacent to individual annular sampling sites are reflected on TDI by decreased peak velocities.8).8 TDI spectral waveforms from a normal subject and a patient with a restrictive cardiomyopathy (RCM). Longitudinal tissue velocities are sampled at the base from the apical window. The left panel was taken in early systole and the right panel in late systole. Digitally stored color TDI images can be analyzed off-line to yield velocity-coded color M-modes from straight or curved line samples and velocity versus time graphs from any individual point. When peak S2 waves from several walls are averaged. whole heart motion exaggerates posterior wall velocities but diminishes septal velocities. The spatial resolution of color TDI is sufficiently good so that velocity signals from the endocardium. Wall motion velocities are higher and less heterogeneous in the lateral and posterior walls compared with the septum. The lateral wall is blue in the late systolic panel indicating late and dyssynchronous contraction of the lateral wall. From the parasternal window. which is marked by two consecutive negative deflections caused by early ventricular filling (E ) and atrial contraction (A ). the motion of the base of the heart reverses in diastole. decreased systolic time velocity integrals.EVALUATION OF LEFT VENTRICULAR SYSTOLIC FUNCTION Figure 3. 41 . An initial positive systolic wave ‘S1’ associated with isovolumic contraction can often be appreciated. The vertical distance between calibration markers is 5 cm/s. The reproducibility of velocities in myocardium at the apex is low because the myocardial velocities are low and the direction of fiber shortening is not parallel to the beam. S1 is followed by a larger positive S2 wave reflecting the descent of the base of the heart during LV ejection. Figure 3. After a discernible isovolumic relaxation interval.9 Color TDI from the apical four-chamber view.

5 7. Other techniques are available for displaying TDI information including a mapping 9.00 0.3 9.0 3.0 9. The same technology can color code for the time to peak velocity with normal wall segments in one color and regions with delayed peak velocities in another color.7 1.44 0.5 3.87 0.2 0 2.19 0 150 300 450 150 300 450 600 750 900 1050 1200 12.0 12. color coding the results and superimposing them on the anatomic image.44 0. twodimensional strain and strain rate images can be analyzed off-line to obtain straight or curved line color M-mode displays or depict strain versus time and strain rate versus time from any point within the myocardium (Figure 3. This technique is an effort to quickly identify patients with dyssynergic contraction patterns who would benefit from cardiac resynchronization therapy. In TDI it is the myocardial velocity gradient.10 TDI signals analyzed off-line to obtain a velocity versus time plot (top panel) and strain (red) and strain rate (blue) versus time graphs (bottom panel).0 900 1050 1200 Velocity (cm/s) Strain rate (1/S) Strain rate Strain 600 750 Figure 3.31 0. Because the distances between samples are small the effects of motion imparted on the sample from adjacent myocardial segments and the effects of whole heart motion are minimized.THE ECHOCARDIOGRAPHERS’ GUIDE Strain and strain rate Strain is the deformation of a material caused by an applied stress. Strain and strain rate imaging are accomplished by assessing the velocity differences and their integrals between very small distances throughout the two-dimensional myocardial velocity field.7 5.87 1.75 1.0 6. technique.8 0. As with two-dimensional velocity color images.0 0. Strain rate is the difference in velocity between two points divided by the distance between the points. which is equal to the change in the distance between two points divided by the original distance between the two points. TDI can measure strain and the rate of change of strain noninvasively.10). Regional strain in the heart is an important determinant of cardiac remodeling.19 1. Strain correlates closely with peak dP/dT and strain rate imaging can clearly distinguish regions of hypokinesis and akinesis from normal.0 1.3 5.75 2.8 3. Integrating strain rate over time gives the strain.31 1.0 3.0 9. which codes wall segments with velocities within normal ranges with one color and slower moving segments with another color to focus attention on areas of myocardium that become hypokinetic during stress testing.2 7. 42 Strain (%) .0 6.

4 EVALUATION OF RIGHT VENTRICULAR FUNCTION CONTENTS q Right Ventricular Volume Overload q Acute Pulmonary Embolism q Right Ventricular Pressure Overload Right ventricular (RV) inflow and outflow tracts are separated by the crista supraventricularis. The right and left ventricles have similar volumes and ejection fractions but the thickness of the LV free wall is two to three times greater than that of the RV. while RV mass is normally one-sixth that of the left ventricle (LV). Because of its complex shape there are no simple geometric models for calculating RV volume and ejection fraction by two-dimensional echo. The pulmonary circulation is characterized by low pressure and low resistance. However. This method is known as TAPSE (Tricuspid Annular Plane Systolic Excursion) and it correlates well with radionuclide angiography RV ejection fractions (Figure 4. which is a ridge of tissue composed of three prominent muscle bundles: q the parietal band – situated between the pulmonic valve (PV) and tricuspid valve (TV) annuli and makes up the lateral and posterior RV outflow tracts q the infundibular septum – between the right and left ventricular outflow tracts q the septal band – travels down the interventricular septum and bifurcates into inferior and anterosuperior limbs. RV systolic function is generally assessed qualitatively from apical and subcostal fourchambered views and RV size is assessed both in absolute terms and with reference to left ventricular size. being triangular in its base to apex dimension and crescentic in cross-section. Tissue Doppler measurements of RV long axis contraction velocity measured from the RV free wall near the TV annulus can characterize RV systolic function. Shortening of the RV from base to apex in systole can be measured by directing the M-mode cursor from the apex to the medial tricuspid annulus. The shape of the TV annulus resembles the letter ‘D’ turned 90 clockwise. The normal area and transverse diameter of the RV from the apical four-chamber view are approximately two-thirds of the LV and the major length of the RV from the TV annulus to the apex is 1–2 cm less than the LV length. which carries fibers of the right bundle branch. The moderator band. The normal septal curvature is convex to the RV and concave to the LV. The septal leaflet is parallel to the septum and the posterior leaflet is parallel to the posterior or diaphragmatic RV free wall. three-dimensional echocardiography can accurately measure RV volumes. arises from the apical termination of the septal band and crosses the RV cavity to insert into the RV free wall close to the anterior papillary muscle of the TV.1). The shape of the RV is com- plex. 43 . The anterior leaflet is the largest and most excursive and forms a curtain between the RV inflow and outflow tracts.

RA and inferior vena cava (IVC) enlargement result from severe TR (Figure 4.10). which can be detected by pulsed and color Doppler (Figure 4.4). There is normally an increase in right heart flow with inspiration as RV afterload is decreased and systemic venous return is augmented. The normal septal curvature is reversed in both diastole and systole. and there is prolongation of the LV isovolumic relaxation time and decreased E wave and increased A wave peak velocities on the transmitral Doppler signal. TV annular dilatation occurs with increasing severity of TR as a consequence of RV enlargement. RIGHT VENTRICULAR PRESSURE OVERLOAD Figure 4.2). The TV papillary muscles are displaced (Figure 4.1 Tricuspid Annular Plane Systolic Excursion (TAPSE) is an M-mode measure (arrow) obtained from the apical four-chamber view that reflects global right ventricular systolic function. RV pressure overload may be acute (pulmonary embolism) or chronic from pulmonary disease.3).THE ECHOCARDIOGRAPHERS’ GUIDE RIGHT VENTRICULAR VOLUME OVERLOAD RV volume overload is caused by leftto-right shunt or tricuspid insufficiency. TR results in retrograde systolic flow in the IVC and middle hepatic vein. 44 The RV responds to afterload excess with RV hypertrophy. RV dilatation is associated with a more spherical cavity shape and paradoxical septal motion (Figure 4.6) with RV enlargement causing tricuspid regurgitation (TR). increased RV wall thickness and RV muscle mass (Figure 4.5). LV preload is diminished. mitral valve disease or more frequently from LV dysfunction.8). The right ventricle remodels in response to preload excess by cavity dilatation (Figure 4. The RV becomes more spherical in shape with pressure overload. The .7) and the IVC no longer reduces its diameter with inspiration (Figure 4. As the RV dilates it forms the apex and the moderator band is nearly perpendicular to the interventricular septum (Figure 4. Paradoxical septal motion decreases the LV diameter and the LV becomes ‘D’ shaped in diastole (Figure 4. Normal pulmonary artery pressure (PAP) in systole ranges from 15 mmHg to 30 mmHg and in diastole from 4 mmHg to 12 mmHg.9). which when severe results in a circular RV and crescentic LV in short axis and can cause LV outflow tract obstruction. The altered LV geometry together with reduced LV preload may decrease LV ejection fraction. Mean PAP is between 9 mmHg and 19 mmHg.

left heart failure. The RV is markedly enlarged and the interventricular septal motion is paradoxical. which elevate the pulmonary vascular resistance causing pulmonary hypertension (Figure 4. Eisenmenger syndrome refers to left-to-right shunts that reverse direction due to the development of severe irreversible pulmonary hypertension. Pulmonary hypertension is also caused by cardiac disease associated with increased left atrial pressure as in mitral stenosis. RV can generate suprasystemic pressures when the onset of the pressure overload is gradual. left ventricle. In pulmonary hypertension the pulmonary artery dilates and the plane of the pulmonic valve is displaced anteriorly and to the right. The right ventricle (RV) is markedly enlarged (LV. Septal motion is toward the RV in systole and toward the LV in diastole. RV wall thickness can be measured from the subcostal or parasternal windows and RV hypertrophy is present when the RV wall thickness is 0. RV systolic pressure is equal to pulmonary artery systolic pressure when there is no RV outflow tract obstruction. When this occurs the pulmonary valve can sometimes be imaged in short axis. The 45 . AO.3 M-mode of the right and left ventricles.2 Parasternal long axis view.5 cm (Figure 4. abnormalities of the vessels of the lungs and applies to a diverse group of conditions.13) and an estimate of the RA pressure. left atrium. In severe pulmonary hypertension the pulmonic valve can be anterior to the aortic valve. The term ‘cor pulmonale’ describes chronic right heart dysfunction caused by Figure 4. and chronically elevated pulmonary flow due to shunts such as atrial or ventricular septal defects or patent ductus arteriosus.EVALUATION OF RIGHT VENTRICULAR FUNCTION Figure 4. RV systolic pressure can be estimated with continuous wave Doppler from the sum of the maximum velocity of the TR jet (Figure 4.11).12). aorta). LA.

RV enlargement displaces the TV papillary muscles and causes TR (RA. left ventricle).THE ECHOCARDIOGRAPHERS’ GUIDE Figure 4. RV. left atrium. Figure 4. LA. LA. left ventricle.5 Parasternal short axis image of a patient with right ventricular (RV) volume overload. The RV is enlarged and the interventricular septum (arrow) exhibits paradoxical motion (LV. right ventricle. right atrium. RV papillary muscles (arrow) are not normally seen in this plane. PA.6 Parasternal short axis view of the base of the heart in a patient with right ventricular (RV) enlargement. pulmonary artery).4 Apical four-chamber view in a patient with severe right ventricular (RV) volume overload. 46 . The RV forms the apex and the moderator band (arrow) is perpendicular to the interventricular septum (LV. left atrium. RA. Figure 4. right atrium).

There is marked systolic flow reversal caused by severe tricuspid regurgitation. Figure 4.8 Subcostal view of a markedly enlarged inferior vena cava (IVC) resulting from severe TR. Figure 4. right atrium. A small pericardial effusion (PE) is seen adjacent to the right atrial free wall. right ventricle).EVALUATION OF RIGHT VENTRICULAR FUNCTION Figure 4. 47 . Moderately severe tricuspid regurgitation is seen in the systolic frame with color Doppler (RA. RV.7 RA/RV view in a patient with markedly dilated right heart chambers.9 Pulsed wave Doppler signal with the sample volume in the middle hepatic vein. The papillary muscle is prominent in the diastolic frame.

14). left ventricle). Pure RV pressure overload hypertrophy is rare. which is roughly equivalent to mean RA pressure. This is due to superimposition of volume overload from tricuspid regurgitation on RV pressure overload. The RV remodels in response to alterations in preload and afterload. RV dilatation almost invariably follows RV hypertrophy.11 A giant pulmonary artery (PA) in a patient with severe chronic pulmonary emboli. Pulmonary artery diastolic pressures can be estimated from the pulsed or continuous wave signal of pulmonary valve insufficiency. ACUTE PULMONARY EMBOLISM Most pulmonary emboli originate from deep vein thrombi in the pelvis or legs. There is a large laminated thrombus (*) and ‘smoke’ (AO. The RV hypertrophies in response to increased afterload but unlike the LV in pressure overload hypertrophy. There is also a small pericardial effusion (*) (LV. aorta). Peak or end-diastolic pressure gradients retrograde across the pulmonic valve are calculated from the Bernoulli equation and added to an estimated RV diastolic pressure. . Mid-systolic notching of the pulmonary 48 artery flow profile is a specific but insensitive sign of pulmonary hypertension as is mid-systolic notching of the pulmonic valve M-mode (Figure 4. Time to peak velocity (acceleration time) shortens with increasing pulmonary artery systolic pressure. pulsed wave Doppler signal of systolic velocity in the pulmonary artery normally peaks later than the systolic velocity in the LV outflow tract. Figure 4.10 Parasternal short axis view showing hypertrophy of the right ventricular (RV) free wall and trabeculations. A pulmonary artery acceleration time of 100 ms is associated with pulmonary hypertension.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 4.

EVALUATION OF RIGHT VENTRICULAR FUNCTION Figure 4. Right ventricular (RV) free wall thickness is greater than 1 cm in the diastolic subcostal short axis view indicating Figure 4.14 An M-mode of the pulmonic valve showing mid-systolic partial closure or the ‘W’ sign. 49 . Figure 4.7 m/s indicating an RV/RA pressure gradient of 55 mmHg.12 severe RVH.13 Continuous wave Doppler of tricuspid regurgitation with a peak velocity of 3. This is a specific but insensitive sign of pulmonary hypertension.

The ratio of RV to LV size predicts the degree of obstruction.16). aorta. 50 . Visualization of thrombus in the pulmonary artery (Figure 4.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 4. right ventricle). there is RV hypertrophy indicating a chronic or acute-on-chronic disease process. hypermobile. In acute severe pulmonary embolism the RV dilates and RV systolic function is strikingly diminished. When a pulmonary embolus obstructs less than 25% of the pulmonary vasculature there is little increase in RV afterload and heart rate and blood pressure will remain normal. RV infarction may show a similar pattern of RV wall motion but in RV infarction PAP is low and there is usually evidence of an LV inferior wall motion abnormality. the RV dilates and fails.16 A mobile right atrial (RA) thrombus (arrow) is identified in a patient with suspected pulmonary embolism (LV. serpiginous clot (thrombus in transit) in the RA are specific but insensitive markers of pulmonary embolism (Figure 4. Larger emboli present an acute afterload excess to the RV. Approximately 50% of patients with documented pulmonary emboli have normal echocardiograms. right ventricle outflow tract).15) or elongated.15 A thrombus is identified (arrow) at the pulmonary artery (PA) bifurcation in this parasternal short axis view (AO. A distinct regional pattern of RV systolic dysfunction in which the mid-wall of the RV is akinetic but the apical motion is normal (McConnell sign) has been used to identify patients with pulmonary embolism. A normal RV is unable to generate pressures greater than 40–45 mmHg acutely and if PAP exceeds this level. RVOT. When the RV is able to generate pressures in excess of 50 mmHg. RV. left ventricle. Doppler signals of TR and pulmonary insufficiency show moderate pulmonary hypertension. Septal motion is paradoxical and the LV is under filled and decreased in size. Figure 4.

when volume is low. Diastolic dysfunction is more common in women and is largely a disease of elderly people. Its reciprocal (dV/dP) is termed compliance. which result in heart failure symptoms of pulmonary congestion and dyspnea. i. Chamber stiffness and myocardial relaxation are the main determinants of diastolic function. which increases chamber stiffness. as volume increases. change in pressure results in a much greater change in volume than at end-diastole when pressure is high. the slope of the pressure–volume relation increases (Figure 5. Diastolic dysfunction is often attributable to changes within the myocardium that accompany the hypertrophic response to chronic pressure overload. a Pressure Volume Figure 5. increased systolic wall stress stimulates the synthesis of interstitial and perivascular fibrillar collagen in the extracellular matrix. 51 . Chamber stiffness is defined as the slope of the tangent to any point on the pressure–volume curve. Increased resistance to filling causes elevated filling pressures. The level of LVEDP is closely correlated with exercise limitation in patients with heart failure. Chamber stiffness (dP/dV) at any point on the diastolic pressure–volume curve is defined as the STIFFNESS AND RELAXATION Stiffness can be defined as the force (the change in pressure) required to produce a change in volume (dP/dV).1 A graphic representation of the diastolic pressure–volume relation.e. In early diastole. In addition to myocyte hypertrophy.5 EVALUATION OF DIASTOLIC FUNCTION CONTENTS q Stiffness and Relaxation q Spectral Doppler q M-Mode and Two-Dimensional Imaging Diastolic dysfunction can be defined as an inability of the left ventricle (LV) to attain a normal end-diastolic volume without an inappropriate increase in LV end-diastolic pressure (LVEDP). A given change in pressure results in a much greater change in volume when volume is low (red) than when it is high (blue). The diastolic pressure–volume relation is nonlinear.1).

Systolic dysfunction causes an elevation in left ventricular (LV) enddiastolic pressure and an increase in stiffness. which approximates aortic valve closure. Another important determinant of diastolic function is myocardial relaxation. LV pressures from the point of peak negative dP/dT. black represents diastolic dysfunction. 52 Log pressure AO . AO. Tau is the reciprocal of the slope of the B LV pressure (mmHg) 80 LV 40 LA Time Figure 5. An elevated LVEDP causes an increase in calculated stiffness even without a change of the end-diastolic pressure/ volume relation (Figure 5. aorta). stiffness is increased. to a point 5 mmHg greater than end-diastolic pressure. In both cases. left ventricle. Myocardial relaxation occurs principally during the isovolumic relaxation time (IVRT) between aortic valve closure and mitral valve opening. is a measure of relaxation that requires cardiac catheterization. while changes in the material properties of the myocardium. but there is no change in the pressure–volume relation. due to fibrosis or post-infarction scarring. the time constant of relaxation that describes the decay in LV diastolic pressure. and blue represents systolic dysfunction. It is shifted upward and to the right but lies on the same normal curve.THE ECHOCARDIOGRAPHERS’ GUIDE 100 50 50 100 LV volume (mL) Figure 5. The decrease in LV pressure is assumed to be mono-exponential and the pressures are transformed to a logarithmic scale so that their relation with time is linear (Figure 5. the time constant of relaxation is calculated from diastolic pressures measured at cardiac catheterization (red arrow). approximating the time of mitral valve opening. and its reciprocal is chamber compliance. Increases in preload move the pressure/volume intercept point upward on the curve. (B) These pressures are log transformed and plotted against time so that the relationship is linear (LV.3). Diastolic dysfunction with a change in the material properties of the myocardium displaces the pressure–volume relation upward and to the left. slope of a tangent to the curve. move the pressure/volume intercept upward and to the left.2 Three pressure–volume loops are shown: green is normal. LA. Compliance is a passive property of the myocardium that is also determined by A 120 Pressure (mmHg) preload.2). Tau. left atrium. Chamber stiffness is linearly related to pressure. a process requiring energy. are logarithmically transformed and plotted against time.3 (A) Tau.

Suction is strongest at the apex. The rapid filling phase of diastole begins when left atrial (LA) pressure exceeds LV pressure and the MV opens. The relative contributions of the separate phases of diastole to LV filling can be seen when LV volume is plotted against time (Figure 5. SF.EVALUATION OF DIASTOLIC FUNCTION log pressure versus time relation and is normally 30–40 ms. delays the onset of contraction causing shortening to persist beyond ejection. The excellent temporal resolution of Mmode echocardiography allows a qualitative assessment of the rate of increase in cavity size and rate of LV wall thinning. LV. . Atrial contraction then renews the LA/LV pressure gradient. Transmitral and pulmonary venous Doppler velocity waveforms plotted against time (RF. At end-systole muscle fibers are shorter than they are at rest and systolic compression of connective tissues stores potential energy which is released with LV relaxation.4 Left ventricular (LV) volume. rapid filling. The contribution of elastic recoil to diastolic filling is lost when systolic function is poor. LA Pressure E A M-MODE AND TWO-DIMENSIONAL IMAGING Evaluation of LV diastolic function begins with a visual assessment of LV filling with M-mode and two-dimensional imaging. usually caused by left bundle branch block (LBBB). 53 Transmitral Doppler S2 S1 D Pulmonary vein Doppler A Figure 5. slow filling. systolic function is a major AF SF LV volume RF AO LV determinant of relaxation. Atrial contraction contributes about 15–20% of LV end-diastolic volume in normal subjects. This results in dyssynchronous and prolonged relaxation. Diastasis follows rapid filling when LA and LV pressures approximate but this phase of diastole is absent at high heart rates. The peak rate of filling is directly related to the LA/LV pressure gradient. Increasing LV volume causes LV pressure to rise and the rate of filling to slow. AF. Flattening of the E–F slope on the MV M-mode in the absence of mitral stenosis or aortic insufficiency is associated with decreased LV compliance. thus. This elastic recoil causes a ‘suction’ that facilitates LV pressure decline during the isovolumic interval. Increased LV afterload delays relaxation and dyssynchronous contraction. If the P–R interval minus the A–C interval is greater than 60 ms the LVEDP is usually greater than 20 mmHg. left atrial (LA) and aortic (AO) pressure. filling provided by atrial contraction). but the added fiber stretch supplied by atrial contraction is an important determinant of systolic function via the Frank–Starling mechanism.4). Prolongation of the final closing slope (A–C) of the MV M-mode is associated with an increased LVEDP in the absence of first degree atrioventricular block. LV pressure continues to decline even after mitral valve (MV) opening as volume rises.

Diastasis follows and is marked by low or absent flow velocities although flow may continue due to inertial forces. The MV opens when LA pressure exceeds LV pressure and transvalvular velocity reaches a peak at the E point 54 which ranges from 70 cm/s to 100 cm/s in normal subjects. LA volume is larger at the time of atrial contraction and this results in a higher A wave. As early filling is decreased. Atrial contraction causes a second spike in the LA/LV pressure gradient. These are ‘normal’ findings in elderly people due to age-related changes in the myocardial extracellular matrix that slow diastolic relaxation. A restrictive filling pattern occurs when there is a high LA pressure and a nondistensible ventricle. The slope of the continuous wave Doppler signal of mitral regurgitation is a surrogate for LV dP/dT (rise in pressure) and indicator of LV systolic function (see Chapter 3). Hypovolemia or use of venodilators such as nitroglycerin lower LA pressure thereby delaying MV opening (the time at which LA pressure exceeds LV pressure) and prolonging IVRT. In atrial fibrillation the A wave is lost and the height of the E wave is determined by the length of the preceding cardiac cycle. It reaches a peak at between 45 cm/s and 70 cm/s in normal subjects. The early LA/LV pressure gradient is therefore relatively low and this is reflected in a diminished E wave maximal velocity. aging. Abnormal transmitral flow patterns have been described. the isovolumic relaxation time (IVRT) can be measured directly as the time from the end of LV outflow tract flow to the beginning of transmitral flow. IVRT is prolonged when LV relaxation is impaired but it is load dependent. and preload. similarly negative dP/dT accurately characterizes LV relaxation and correlates with tau. At rates of greater than 100 beats/min fusion of the E wave and A waves occurs resulting in monophasic diastolic filling. The duration of diastasis is determined by the heart rate. and prolongation of both the IVRT and deceleration times. whereas a long IVRT in combination with systolic dysfunction indicates a normal or near-normal filling pressure. There is reversal of the normal E/A ratio and deceleration time is prolonged. Mitral deceleration time is measured as a linear approximation of the time that it takes for velocity to return to the baseline from the peak of the E wave. will often reveal slow and prolonged filling associated with diastolic dysfunction but this assessment is difficult when the heart rate is elevated. Impaired relaxation prolongs IVRT as LV pressure falls slowly.THE ECHOCARDIOGRAPHERS’ GUIDE Careful observation of two-dimensional echo images. among them are heart rate and rhythm. Increasing age is associated with decreased E wave velocities. increased A wave velocities. When LV inflow and outflow signals are sampled simultaneously by either pulsed or continuous wave Doppler. There are many factors that affect the transmitral velocity waveform. SPECTRAL DOPPLER Spectral Doppler is the tool of choice for the evaluation of diastolic function. It is marked by a . The IVRT is not a true measure of relaxation. but a shortened IVRT indicates elevated LA pressure. LA enlargement is associated with elevated LVEDP.0–1.5. These findings are associated with a low pulmonary capillary wedge pressure ( 15 mmHg). the A wave occurs earlier and its maximum velocity is increased. The normal ratio of E wave to A wave velocity is 1. the rate of equilibration is provided by the down slope from the E peak. The presence of left ventricular hypertrophy (LVH) or regional heterogeneity of contraction suggests the presence of diastolic dysfunction. time for diastasis is reduced. Transmitral Doppler Spectral Doppler of transmitral flow reveals the instantaneous pressure gradient between the LA and LV throughout diastole and this signal has long had a role in assessing diastolic function. particularly short axis images of the LV. As the heart rate increases. LA and LV pressures then equilibrate.

55 . E wave deceleration time correlates closely with LV filling pressure in the presence of systolic dysfunction but when patients with normal ejection fractions are Figure 5. These findings reflect a high LA pressure at MV opening. The A wave is low velocity due to either atrial dysfunction or a high LVEDP. Mitral regurgitation increases preload and E wave amplitude. the development of mitral regurgitation or worsening diastolic function. The top panel demonstrates the pattern of impaired relaxation with a low velocity E wave. low velocity A wave. and a prolonged deceleration time.EVALUATION OF DIASTOLIC FUNCTION shortened IVRT. and rapid filling of the LV that terminates rapidly. a short deceleration time and a small A wave.5). Thus classification of diastolic function as normal based only on the transmitral flow velocity pattern will often be erroneous. Changes in preload affect the E wave velocity. Patients with decreased systolic function and a normal appearing transmitral flow velocity profile should be considered to be pseudonormal with moderately elevated LA pressures (Figure 5. a high E wave. a high A velocity wave. This decreases the E wave maximal velocity. As LV filling pressures rise and the LV inflow Doppler pattern transitions from impaired relaxation to restrictive filling. a pattern mimicking normal occurs. hypovolemia and venodilators lower LA pressure. it is often a marker of increased LV filling pressures secondary to systolic dysfunction alone and does not always indicate an intrinsic alteration of myocardial diastolic properties. In this pattern E wave and A wave velocities and their ratio are approximately normal. A patient with a pseudonormal pattern of transmitral flow may convert to a restrictive pattern with volume infusion. the IVRT is neither shortened nor prolonged and deceleration time is within the normal range. As previously noted. This ‘pseudonormal’ pattern results from a combination of impaired relaxation and elevated filling pressures.5 Three pulsed wave Doppler transmitral flow velocity waveforms are presented. The middle panel shows a pseudonormal pattern and the bottom panel is an example of the restrictive pattern with a high velocity E wave. and short deceleration time. Worsening systolic function with an elevated LV diastolic pressure is reflected by a change in the transmitral Doppler flow pattern from delayed relaxation to pseudonormal or from pseudonormal to restrictive. Although this pattern is abnormal and associated with a poor prognosis in patients with infiltrative and dilated cardiomyopathies.

left atrium. When LV compliance is reduced. and a retrograde Ar wave caused by atrial contraction. In mitral regurgitation the S wave may be blunted. RA. The S wave may be biphasic. a D wave in diastole. their E and A waves will both decrease.6 Apical four-chamber view with color Doppler demonstrating flow in the pulmonary veins (RV. LV. Normal pulmonary venous flow consists of a forward S wave in systole. agerelated changes have been described. Patients with normal filling will have a hypovolemic response.THE ECHOCARDIOGRAPHERS’ GUIDE included. The reduction in preload from this maneuver causes a pseudonormal pattern of transmitral flow to revert to a pattern of impaired relaxation. but also when it is optimal (rapid relaxation). 56 Figure 5. . The D wave decreases and the Ar and S wave increase with advancing age. The D wave is associated with MV opening and LV filling prior to atrial contraction. The ratio of S velocity to D velocity is approximately 1. Pulmonary venous Doppler waveforms can be obtained in between 60% and 90% Pulmonary vein Doppler The pulmonary veins are visualized from the apical four-chamber view. By causing intrathoracic pressure to exceed the pressure in the great veins venous return and preload is decreased. Patients with a restrictive pattern that can be reversed by the Valsalva maneuver or by drug therapy have a better prognosis than patients with a fixed restrictive pattern. right ventricle. LA. It is helpful to identify pulmonary venous flow in this vessel by color Doppler and then to position the pulsed wave sample volume in the vein 1–2 cm away from the LA (Figure 5. Reversal of the S wave is a mark of severe mitral regurgitation. The Valsalva maneuver causes a restrictive pattern to revert to a pseudonormal pattern in some patients. the early phase (Se) attributed to LA relaxation and the later (Sl) associated with apical displacement of the MV annulus.3–1. resistance to forward flow into the ventricle is increased and the retrograde Ar wave will be enhanced in velocity and duration. Atrial contraction forces blood into the LV but also retrograde into the pulmonary veins. right atrium).5 in normals with the S flow velocity integral occupying 60–68% of the total flow velocity integral. and as with the transmitral flow. This illustrates the fact that a rapid E wave deceleration time may occur not only when diastolic function is severely impaired (high LA pressures with an abrupt termination of filling). pulmonary vein S and D waves may fuse at high heart rates. The S wave is higher in normal subjects than the D wave and when it is biphasic Sl will be higher than Se. The Valsalva maneuver can be used to distinguish patients with a normal pattern of transmitral flow from a pseudonormal pattern. As with the transmitral E and A waves. In the apical four-chamber view the right upper pulmonary vein is oriented so that flow into the LA is nearly parallel with the ultrasound beam. less frequently from high parasternal short axis views and the suprasternal notch.6). left ventricle. the relation becomes nonsignificant.

This corresponds to a low velocity E wave on the transmitral Doppler waveform and typifies the pattern of impaired relaxation. The amplitude and duration of the Ar wave will be increased if LV compliance is reduced and atrial function is preserved.EVALUATION OF DIASTOLIC FUNCTION of patients with transthoracic echo but it is often difficult to obtain an A wave from which amplitude and duration can be measured. In patients with the pattern of impaired relaxation on the transmitral Doppler waveform. (B) this is pseudonormal. The magnitude of the S wave is primarily related to LA compliance and therefore the pulmonary vein systolic fraction (the proportion of the total pulmonary venous flow velocity integral contributed by the S wave) is inversely related to mean LA pressure Figure 5. During the pseudonormal phase the Ar may be enhanced due to poor LV compliance. The velocity of the D wave is reduced. As LA pressure rises its compliance is diminished.7 Pulmonary venous pulsed wave Doppler signal.7). Figure 5. The size of the Ar wave depends on LV compliance and LA function. but worsening LV diastolic function can result in LA enlargement. 57 . and (C) is an example of the restrictive pattern with a high velocity D wave and low velocity S wave.8 Three patterns of pulmonary venous flow are presented: (A) the pattern of impaired relaxation with a low velocity D wave. mechanical failure of atrial contraction and a reduced Ar. the D wave of the pulmonary venous signal may be blunted corresponding to a low velocity transmitral E wave (Figure 5.

M-mode display will demonstrate an isovelocity line at the aliasing velocity. The time from maximum velocity at the annulus to maximum velocity at a given point within the LV is prolonged in the presence of diastolic dysfunction. The vertical distance between calibration markers is 5 cm/s. Color Doppler M-mode with the cursor directed through LV inflow displays a map of velocity against time and permits measurement of this time delay (TD) and the propagation velocity (Vp). An Ar A duration predicts an LVEDP 15 mmHg and this relation is maintained irrespective of systolic function. This can be demonstrated by comparing a pulsed wave spectral Doppler tracing of LV inflow taken with the sample volume at the annulus with one taken at the midcavity level. and it gives the rate of propagation of peak velocity of the early diastolic wave from base to apex. (B) is from a patient with a pseudonormal transmitral Doppler flow pattern.10 Tissue Doppler imaging with the sample volume near the mitral valve annulus adjacent to the LV lateral wall. As LVEDP increases. Three examples are shown: (A) is from a normal subject and the Vp is 50 cm/s. Several studies have shown good correlations between pulmonary capillary wedge pressure or LVEDP and systolic fraction. The E velocity is reduced but the transmitral Doppler flow appeared normal. (LAP) or LVEDP. This indicates that the transmitral Doppler was pseudonormal. and (C) is from a patient with a restrictive transmitral Doppler flow pattern.9 The color Doppler M-mode propagation velocity (Vp) is the slope of any isovelocity line (arrows). the resistance to blood flow into the LV during atrial contraction increases.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 5. Adjustment of the scale and baseline shift functions of the color 58 Figure 5. . which is the slope of any isovelocity line on this display. This shortens the duration of the transmitral A wave but prolongs the duration of the pulmonary venous Ar wave. Vp ranges from 45 cm/s Propagation velocity Blood flow entering the LV reaches its maximum velocity progressively later as the wave of filling propagates from the MV annulus to apex. a predominant D wave and an S/D ratio falling to below 1. Vp is measured as the slope of this line from the annulus to a point approximately 4 cm into the LV.0 (Figure 5.8). Transition from pseudonormal to reversibly restrictive and fixed restrictive physiology is marked by progressively lower S waves.

The E peak velocity is higher than the A velocity in normals and like the transmitral E wave. Maneuvers that increase preload such as volume infusion or leg lifting will cause a pattern of impaired relaxation on the transmitral flow to change to a pseudonormal pattern with no change in E . and the extent of segmental wall dysfunction. Normal values for E at the medial mitral annulus are from 10 cm/s to 15 cm/s and those at the lateral annulus are from 15 cm/s to 20 cm/s. 59 . Dividing E by Vp controls for the effects of relaxation and provides a better estimate of filling pressures than either variable alone.11 (A) Transmitral PW Doppler demonstrating the restrictive filling pattern. Vp is further reduced in patients with the restrictive pattern of transmitral flow demonstrating that the driving force of the high early transmitral pressure gradient is rapidly attenuated (Figure 5. E velocity is reduced in diastolic dysfunction but does not change with variations in preload.10). The relation between E/Vp and filling pressure is maintained in patients with atrial fibrillation. The ratio of the transmitral E wave velocity and Vp is related to pulmonary artery capillary wedge pressures.EVALUATION OF DIASTOLIC FUNCTION to 55 cm/s in normal subjects and decreases with age. cavity shape. Vp also varies with systolic function. (B) PW TDI with a low velocity E wave. Reduced E velocity with a normal transmitral flow profile indicates pseudonormalization (Figure 5.9). E decreases with age. Normal transmitral Figure 5. The E/E ratio (115/3 38) indicates an elevated LVEDP. The vertical distance between calibration markers is 5 cm/s. while Vp is determined solely by relaxation. emphasizing the interrelation of systolic and diastolic function. Vp is independent of the preload and correlates well with tau and peak negative dP/dT. The E wave velocity is determined by relaxation and LA pressure. indicating that it is principally determined by relaxation. Vp is reduced equally in patients exhibiting a pattern of impaired relaxation on the transmitral spectral Doppler tracing and patients with a pseudonormal pattern. Tissue Doppler imaging The normal pattern of diastolic myocardial velocity is biphasic with an early negative peak designated E and a later negative peak caused by atrial contraction termed A . The vertical distance between calibration markers is 20 cm/s.

pulmonary venous Doppler waveforms. Abnormal tissue Doppler imaging velocities have been used to differentiate physiologic hypertrophy in athletes’ hearts from that in pressure overload hypertrophy. An E/E ratio 8 accurately predicts a normal mean LV enddiastolic pressure (LVEDP) and an E/E ratio of 15 accurately predicts a mean LVEDP of 15 mmHg. As diastolic dysfunction progresses from impaired relaxation through to irreversible diastolic dysfunction. the LA pressure rises causing an increase in E but no change in E (Figure 5. The E/E ratio continues to increase with the appearance of a restrictive pattern of transmitral flow caused by further increases in LA pressure.11). A normal ratio of E/E is 8. However. Doppler findings in diastolic dysfunction are summarized in Table 5. transmitral E wave velocities increase.THE ECHOCARDIOGRAPHERS’ GUIDE Table 5.0 220 ms Lower 35 unless atrial failure 45 cm/s 8 cm/s Higher Moderately elevated MV Pulmonary Doppler vein Doppler Normal Impaired relaxation Pseudonormal Diastolic dysfunction (reversible) Diastolic dysfunction (fixed) TDI Vp Figure 5. The E/E ratio has also been used to predict LV filling pressure.12 Transmitral Doppler waveforms. The ratio does not change with impaired relaxation as both E and E are reduced.0.5 cm/s and an E /A ratio of 1. 60 . impaired relaxation.12. As diastolic function deteriorates. pseudonormal. while pulmonary venous S wave velocities. pulsed wave TDI E velocities and propagation velocity (Vp) are increasingly reduced.1 and Figure 5.1 Summary of diastolic function Normal Delayed relaxation Low 1 100 ms 220 ms Higher Lower Prominent 45 cm/s 8 cm/s 8 Normal Pseudo normal Restrictive High 2.0 60 ms 150 ms Blunted Higher Prominent unless atrial failure Lower Lower Higher High E E/A Isovolumetric relaxation time DT S wave D wave A rev Propagation velocity E E/E LA pressure High 1 100 ms 220 ms D S Low (up with age) 55 (45 in elderly) 10 (8 in elderly) 8 Normal 1. intermediate values of E/E are associated with a wide variation in mean LVEDP. tissue Doppler imaging (TDI) waveforms and propagation velocity slopes are sketched for normal. flow can be distinguished from pseudonormal by a combination of a tissue Doppler imaging E of 8. and irreversible and fixed diastolic dysfunction patterns.

which is also supplied by the LAD. the right bundle branch. CORONARY ANATOMY The ostia of the main right and left coronary arteries arise from their respective sinuses of Valsalva approximately twothirds of the way from the aortic annulus to the sinotubular junction. Posterolateral branches of the RCA continue beyond the PDA in the atrioventricular sulcus and give off a branch that loops back to supply the atrioventricular node. In the short axis view of the aortic valve the proximal 1–2 cm of the right coronary artery (RCA) may be visualized at the 12 o’clock position (Figure 6. the posteromedial papillary muscle. Here the circumflex artery gives off one to three obtuse marginal branches that travel from base to apex and nourish the left ventricular (LV) lateral wall and anterolateral papillary muscle. Anastomoses are present from birth and become collateral sources of blood flow when a stenosis limits competing flow into 61 . The left main coronary artery can often be seen in a short axis view of the aorta at the 3 o’clock position. which travels under the left atrial appendage to the left atrioventricular sulcus. The terminal branches of the circumflex anastomose with the PDA and posterolateral branches of the RCA. The RCA travels medially and inferiorly in the right atrioventricular sulcus beneath the right atrial appendage. and the posterior left bundle branch. experience in recognizing and semi-quantifying variations in regional function. the posterior one-third of the interventricular septum. In 90% of subjects. and the circumflex coronary artery. The RCA has a variable number of branches that travel from base to apex and supply the anterior and lateral aspects of the right ventricle. the RCA continues as the posterior descending coronary artery (PDA) in the posterior interventricular sulcus. and a detailed knowledge of coronary anatomy and its relations with the regional blood supply.1). The coronary artery that continues as the PDA is termed the dominant artery. The RCA supplies the basal and mid-thirds of the inferior and posterior left and right ventricular walls. It is usually between 5 mm and 20 mm long. In two-thirds of cases the left main bifurcates into the left anterior descending (LAD) coronary artery. In two-thirds of subjects the RCA also supplies the sinoatrial node.6 CORONARY ARTERY DISEASE CONTENTS q Coronary Anatomy q Wall Motion Abnormalities q Echocardiographic Evaluation of the Patient with Acute Chest Pain q Complications of Acute Infarction The successful use of Doppler/echocardiography in the evaluation of patients with known or suspected coronary artery disease (CAD) requires: the technical expertise to obtain high quality images. which lies in the anterior interventricular sulcus. the most prominent of which is the acute marginal branch.

The LAD descends in the anterior interventricular sulcus from base to apex and ascends in the posterior interventricular sulcus for a variable distance where its terminal branches anastomose with the PDA. The apical third of the LV and often a variable amount of the RV apex becomes akinetic in the majority ( 80%) of LAD infarctions. Although coronary artery flow distribution varies. slight clockwise rotation facilitates visualization of the LM. A WMA resulting from an occlusion of the circumflex when there is right dominance usually extends to the lateral wall and not inferiorly. When the circumflex becomes the PDA (10% of subjects) the left coronary artery is dominant. noncoronary cusp. Extension of an .3). a vessel.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 6. pulmonary artery. right coronary cusp.2). The length of the RCA is reciprocally related to that of the circumflex. L. Critical stenoses tend to occur at bends and branch points of the coronary arteries and occur mostly in the proximal half of the LAD. it is usually possible to identify the culprit vessel from the location of a WMA. and the circumflex supplies the basal. AO. In one-third of cases. while slight counter-clockwise rotation with superior angulation helps to show the RCA (R. The LAD may also supply the right ventricular (RV) anterior free wall and usually supplies the RV apex (Figure 6. the distal half of the RCA. A similar pattern of WMA is observed in occlusion of the circumflex occlusion in left coronary artery dominance. and the 62 mid-portion of the circumflex. Occlusion of the LAD results in akinesis of the anterior wall and anterior septum beginning at the level of obstruction and continuing apically along the course of the vessel (Figure 6. With the aortic valve in short axis. Regional wall motion abnormalities (WMAs) resulting from myocardial ischemia or infarction due to coronary artery occlusion occur in regions of myocardium in the distribution of the occluded coronary artery. the posterior interventricular septum and the LV posterior and inferior walls when there is right coronary artery dominance. The LAD gives off septal perforators that supply the anterior two-thirds of the interventricular septum and the entire apical septum and diagonal vessels (usually two but there may be more smaller vessels) that supply the LV free wall. PA. mid and often apical thirds of the posterior LV wall. left atrium. left coronary cusp. LA. Occlusion of the RCA causes WMAs of the basal and middle thirds of the RV posterior wall. the left main trifurcates into the LAD. circumflex. and an intermediate vessel that parallels the obtuse marginal vessels.1 The left main (LM) coronary artery is seen in the left panel (arrow) and the origin of the right coronary artery (RCA) is shown in the right panel (arrow). N. aorta).

The left anterior descending coronary artery (LAD) travels in the anterior interventricular sulcus and wraps around the apex ascending for a variable distance in the posterior interventricular sulcus. AO. left ventricle.2 Diagram of the coronary arteries. CIRC. aorta). The right coronary artery (RCA) usually gives off the posterior descending artery (PDA) (LM. 63 . Figure 6. The interventricular septum is thin and akinetic resulting from occlusion of the proximal left anterior descending coronary artery (LV.CORONARY ARTERY DISEASE AO LM CIRC LAD RCA PDA Figure 6. left main. LA. left atrium). circumflex.3 Parasternal long axis view.

Patients with AMIs are more likely to undergo LV remodeling Figure 6. infarction of the anterolateral papillary muscle is much less common than infarction of the postero- medial papillary muscle. left ventricle). Figure 6. A mitral valve annuloplasty ring is also demonstrated (arrow) (RV. RA. Thus. LV. left atrium). 64 .5). left ventricle. LA.4 Apical four-chamber view. right atrium. right ventricle.5 Parasternal short axis view showing posterior and inferior wall akinesis as a consequence of occlusion of the posterior descending artery (LV. WMAs involving the basal and mid LV lateral wall from stenotic lesions of the circumflex are rare ( 5%) (Figure 6. Patients may have either inferior (IMIs) or anterior (AMIs) infarctions.4). The basal and mid-portions of the lateral wall are akinetic resulting from occlusion of the circumflex coronary.THE ECHOCARDIOGRAPHERS’ GUIDE inferior WMA to any apical wall segment is infrequent ( 40%). Those with IMIs have a propensity for dysrhythmias and mitral regurgitation due to posteromedial papillary muscle dysfunction (Figure 6.

six from the middle third. Each wall segment. visualized from a 65 . This tethering affects endocardial excursion and wall thickening. The size of a WMA does not correlate exactly with infarct size. Size of WMAs/quantitation of regional dysfunction WMAs are scored using a 16-segment model of the LV. indicating scar tissue. and four from the apex. In such cases wall motion may be normal or only mildly hypokinetic. WALL MOTION ABNORMALITIES The principal goal of echocardiography in patients with CAD is the evaluation of regional variations in systolic function.6). can be considered old. There is also extensive calcification of the aortic valve and mitral annulus (LV. Similarly. There may be discordance between the size of a wall motion abnormality and regional myocardial perfusion for a variable time after successful reperfusion. LV dyssynchrony caused by pacing or native delays in electrical conduction may be difficult to distinguish from regional akinesis or hypokinesis. Images adequate for the analysis of regional variations in systolic function can be obtained in approximately 95% of all patients by skilled and experienced sonographers but interpretation is complicated by a number of factors. but a wall segment that is thin and highly reflective of ultrasound (echo bright). The LV is divided into thirds using the papillary muscles’ tips and bases as lines of demarcation (Figure 6. infarcted muscle can be pulled along by the vigorous contraction of adjacent segments but this does not affect its wall thickening. LA.6 Apical three-chamber view.7).CORONARY ARTERY DISEASE Figure 6. left ventricle. left atrium). A large mobile thrombus (arrow) is seen at the apex. Infarct size is overestimated when the normally perfused borderzone myocardium is tethered by the infarcted muscle. because there is less muscle mass at the apex. WMAs may be difficult to recognize in subendocardial infarcts when less than 20% of the transmural thickness is affected. The presence of an old infarction may confound the detection of a new WMA. and to form aneurysms with increased risk for mural thrombus (Figure 6. There is extensive posterior wall and apical akinesis. six segments from the basal third of the heart.

The scores for all 16 segments are then summed to give a global assessment of LV systolic function. This is possible from the apical imaging planes because as the ventricle contracts the mitral annulus moves toward the apex with negligible translational or rotational motion. left ventricle. The apical four-chamber (4 CH) view intersects the clock face of the short axis at approximately 4 o’clock and 10 o’clock and shows the lateral wall (L) and posterior interventricular septum (PS).e. right ventricle. The resulting linear measurements can be displayed graphically overlying a range of normal values for each chord. development of congestive heart failure and malignant arrhythmias. The apical three-chamber (3 CH) or apical long axis view intersects the clock face of the short axis at approximately 12 o’clock and 6 o’clock and shows the anterior interventricular septum (AS) and posterior wall (P). In Sheehan’s centerline method. but patients without WMAs typically have small infarctions and a favorable prognosis. Between 20% and 40% of patients with non-Q wave infarctions do not have a detectable WMA. Regional function can be assessed completely from the apical window alone or from a combination of apical and parasternal images. For an akinetic segment the two silhouettes are superimposable (Figure 6. The endocardial excursion from diastole to systole is measured along each chord. the centerline. left atrium). LV. Comparison of the two silhouettes reveals the endocardial excursion of each wall segment toward the centroid (center of gravity) of the LV. regional endocardial excursion is quantified by identifying the diastolic and systolic endocardial boundaries. The motion pattern of each left and right ventricular wall segment can be combination of parasternal and apical imaging views. Higher wall motion scores (WMS) are associated with worse clinical outcomes after an infarction predicting an increased risk of death. LA. such as pericarditis with pericardial effusion. Quantitative analysis of LV WMAs can be achieved by comparison of diastolic and 66 .8). RA. ECHOCARDIOGRAPHIC EVALUATION OF THE PATIENT WITH ACUTE CHEST PAIN The absence of a regional WMA at rest does not exclude the diagnosis of severe epicardial CAD or even total coronary artery occlusion in the presence of collateral vessels. The apical two-chamber (2 CH) view intersects the clock face of the short axis at approximately 2 o’clock and 8 o’clock and shows the inferior and anterior walls (RV. systolic endocardial silhouettes. The length of the akinetic segment can be measured and indexed to the percentage of the total endocardial perimeter or cavity length.THE ECHOCARDIOGRAPHERS’ GUIDE 4 CH PS 3 CH AS 2 CH A I Apical Middle Basal LA P L I A P AS RV PS L LA AO RA LA Figure 6. is determined and 100 equidistant chords are drawn perpendicular to it. aortic stenosis. moves paradoxically with systole). is graded based on endocardial excursion and wall thickening: 1 2 3 4 – wall motion is normal or hyperdynamic – the wall is hypokinetic – the wall is akinetic – the wall is dyskinetic (i. right atrium.7 Relation between the apical scan planes and the short axis plane. A line intermediate between the two boundaries. pulmonary embolism or aortic dissection (although the diagnosis of aortic dissection cannot be excluded by transthoracic echocardiography alone). Echocardiography can identify other causes of chest pain.

Left atrial or pulmonary capillary wedge pressure can be estimated using one of several Doppler or tissue Doppler techniques (see Chapter 4). LA. systolic endocardial excursion is the difference between the diastolic and systolic silhouettes. The akinetic wall segments do not move. In the panels on the right. COMPLICATIONS OF ACUTE INFARCTION Aneurysms LV aneurysms are regional dilatations/ deformations of the infarcted myocardium that bulge in systole but also have an abnormal contour in diastole (Figures 6. The walls of an aneurysm are thin. Parasternal images are often obscured.9.8 (A) From a patient with a large anterior infarction. and (B) from a patient with a large inferior wall infarction that extends to the apex. fibrosed and highly reflective of ultrasound (‘echo bright’).CORONARY ARTERY DISEASE Figure 6. Obtaining high-quality images is often technically challenging in patients in cardiogenic shock who are being mechanically ventilated and cannot be positioned optimally for the exam. Ejection fraction and LV end-systolic volume are major determinants of survival after an infarction. Images from the subcostal window are frequently fully diagnostic and should always be attempted in this setting. Endocardial boundaries are traced in diastole (red) and systole (blue). 6. is associated with an 80% 1-year mortality. They are more commonly associated with AMIs than IMIs and 90% involve the apex. Aneurysms usually develop within days to weeks of a transmural infarction. Pseudonormal and restrictive patterns of transmitral flow early after an AMI predict progressive LV enlargement and a greatly increased 1-year mortality. Early aneurysm formation. carefully evaluated. development of congestive heart failure and recurrent MI. their diastolic and systolic endocardial tracings are superimposed (LV. Pulmonary artery (PA) pressure can be estimated when tricuspid regurgitation (TR) is present. left ventricle. within 5 days of infarction.10). The presence and severity of mitral regurgitation should always be assessed by color Doppler post-infarction because even mild regurgitation is associated with increased 1-year mortality. Rolling the patient to their left side even a small amount and propping them up with pillows will greatly increase the yield from the apical imaging window. left atrium). Systolic bulging is mechanically 67 . Doppler also provides important homodynamic information. Off axis images (intermediate between the parasternal and apical windows) are often obtainable and provide substantial information.

left atrium). Figure 6. left atrium).THE ECHOCARDIOGRAPHERS’ GUIDE Figure 6. The aneurysm has an abnormal contour in diastole and expands slightly in systole (RV. The apex has an abnormal contour in diastole and the aneurysm expands in systole (LA. right atrium.9 Apical four-chamber view demonstrating a left ventricular (LV) apical aneurysm. RA.10 Apical two-chamber view demonstrating a left ventricular (LV) apical aneurysm. LA. 68 . right ventricle.

Cardiac rupture Rupture of the LV free wall is a leading cause of death following an acute infarction. Suspected thrombus must be distinguished from false chords and trabeculations. disadvantageous and the aneurysm and adjacent tissue is a substrate for ventricular arrhythmias.12). LA. Thrombi may have a broad (sessile) (Figure 6. Visualization of thrombus from at least two echocardiographic imaging planes is mandatory for diagnosis. It is more common in females. Mural thrombus is identified echocardiographically as a mass. which protrudes into the cavity. The center of a thrombus may liquefy and become echolucent. The appearance of a mural thrombus varies. and from artifacts. attached to but distinct from the endocardium. Thrombus WMAs.CORONARY ARTERY DISEASE Figure 6. from trabeculations. It is necessary to differentiate intracavitary clot.11). elderly people and hypertensive patients. left ventricle. and apical short axis views of the LV are particularly useful for this. 69 . which are linear and often reticulated (Figure 6. The risk for systemic cardioembolism increases when the thrombus protrudes into the LV cavity and when the thrombus is mobile. becoming more echo-dense as it ages. Thrombus is less frequent following IMI than AMI (Figure 6. right atrium. LV.13) or narrow (pedunculated) base of attachment and may be highly mobile. having neither fibrosis nor collaterals. whether aneurysmal or akinetic. are commonly the nidus for mural thrombus formation and associated systemic emboli. and do not move with the cardiac cycle. which can extend outside of the cavity. Cardiac rupture is rarely witnessed echocardiographically because it results in tamponade. The risk of systemic or cerebral emboli is increased in patients with apical aneurysms and poor systolic function even without echocardiographic documentation of thrombus. left atrium). Cardiac rupture usually occurs in the first week after a transmural infarction in a myocardial segment that was previously healthy. RA. right ventricle. A large laminated mural thrombus (*) lines the aneurysm (RV. which is visible in orthogonal imaging planes and moves with the cardiac cycle. occurring in 3% of cases and accounting for 10–15% of in hospital deaths post infarction.11 Apical four-chamber view from a patient with a large apical aneurysm.

protuberant thrombus (*) with a hypoechoic center that represents liquefaction of the core of the thrombus. A right ventricular (RV) pacing wire is also seen (arrow) (LV. right atrium. left atrium). 70 .12 An apical short axis view of the left ventricle (LV) demonstrating a mobile. LA.13 Apical four-chamber view in a patient with a large laminated apical mural thrombus.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 6. From the apical four-chamber view the transducer is brought to a parasternal short axis orientation and moved one or two intercostal spaces higher on the chest to acquire apical short axis images. Figure 6. RA. The focal zone should be brought to the near field and a higher transducer frequency can be employed (RV. right ventricle). left ventricle.

left atrium. The LV cavity is in direct communion with the pericardial space causing a localized outpouching. LV.CORONARY ARTERY DISEASE shock. and rapid demise.14 Apical two-chamber view of an apical pseudoaneurysm (P) lined with thrombus (*) (LV. left ventricle. Pseudoaneurysm Myocardial rupture may be contained by preexisting pericardial adhesions resulting in a pseudoaneurysm (Figure 6.15. Color Doppler flow mapping often reveals a characteristic pattern of flow Figure 6. The point of entry or neck of a pseudoaneurysm is narrow relative to its size and this usually allows it to be distinguished from a true aneurysm. left ventricle. AO. Figure 6. 71 . 6. LA. left atrium). Medial angulation of the transducer demonstrates an inferior wall pseudoaneurysm lined with thrombus (*) (RV. aorta).16). Occasionally.14). right ventricle. small subacute ruptures may be detected. which is contained by scarred myocardium rather than the parietal pericardium. Pericardial clot and an effusion that increases in size over time may signal impending complete cardiac rupture and the need for emergent surgical repair.15 Parasternal long axis view. LA. which is usually lined with thrombus (Figures 6.

LV. Ventricular septal rupture Rupture of the interventricular septum is predisposed by the same factors as free wall rupture and also usually occurs in the first week after an infarction. left ventricle. A large inferior wall pseudoaneurysm that expands in systole is shown. ‘Smoke’ is seen in the pseudoaneurysm (RV. which can embolize and also rupture causing sudden death. right ventricle.17). . right atrium. left atrium). Pseudoaneurysms can be small or large (several hundred milliliters) and deprive the systemic circulation of a significant amount of the stroke volume. Prompt surgical repair is mandated in almost all cases. descending thoracic aorta). Dao. into the pseudoaneurysm in systole and back into the ventricle in diastole and can establish the presence of a communication when it cannot be visualized with twodimensional imaging.16 Parasternal short axis views. VSDs in this location are imaged best from the apical 72 Figure 6.17 Apical four-chamber view with color Doppler demonstrating systolic flow at the apex from LV to RV through a post-infarction ventricular septal defect (RV. They usually contain thrombus. usually in close proximity to the moderator band (Figure 6. right ventricle.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 6. LVOT. RA. LA. When ventricular septal rupture accompanies an anterior infarction. The mortality rate is high (95–100%) without surgical repair. the site of septal rupture (VSD) is in the apical third of the ventricle. left ventricular outflow tract.

19) but may be difficult to visualize with two-dimensional echo and are often first recognized with color flow Doppler. Color flow Doppler demonstrates a large left-to-right shunt through the ventricular septal defect in systole (RV. left atrium). and subcostal four-chamber views. LV. right atrium. VSDs in the inferior wall are best seen from the paraster- nal (Figure 6.18) and subcostal short axis views (Figure 6.18 Parasternal short axis view at the level of the papillary muscles.CORONARY ARTERY DISEASE four-chamber.19 Subcostal four-chamber view. The diastolic frame shows a very thin inferior wall. There is a large defect in the basal posterior septum in the left panel. RA. The systolic frame demonstrates an interventricular communication (arrow) associated with inferior left ventricular (LV) wall and right ventricular (RV) free wall akinesis. VSDs in association with inferior wall infarctions occur at the base of the heart beneath the posteromedial papillary muscle near the junction of the septum with the RV free wall and may have a serpiginous course. left ventricle. Continuous wave Doppler of the flow across a VSD can be used to obtain the interventricular pressure gradient. Off axis imaging is often necessary to align the Figure 6. 73 . apical short axis. right ventricle. LA. Figure 6.

The magnitude of the left-to-right shunt (Qp/Qs) can be calculated by Doppler echocardiography.THE ECHOCARDIOGRAPHERS’ GUIDE beam with the flow. It is rarely associated with AMIs. which persists through inspiration and by RA enlargement with bowing of the interatrial septum to the left. Systolic flow reversal in the pulmonary veins and a heightened E wave on the transmitral diastolic waveform should also raise the suspicion of acute severe mitral regurgitation. RV filling pressure is elevated as shown by IVC enlargement. The continuous wave Doppler signal may demonstrate a steep slope from early to late systole reflecting rapid equilibration of LA and LV 74 . The ruptured head of the papillary muscle is often visible as a mobile mass attached to the leaflet that prolapses into the LA in systole and may mimic a valvular vegetation. TEE may be necessary for diagnosis as patients are often tachycardic. In acute mitral regurgitation the force of the regurgitant jet is not blunted by a large compliant LA as in chronic mitral regurgitation but is transmitted to the pulmonary vasculature. reduce cardiac output. Right ventricular infarction Right ventricular infarction complicates between one-third to one-half of IMIs and occurs in isolation in approximately 3% of all MIs. Paradoxical septal motion with preserved septal thickening results from an elevated RV end-diastolic pressure. The RV cavity is enlarged. the interatrial septum should be carefully examined. Right-to-left shunting through a patent foramen ovale may cause hypoxemia. such as diuretics and nitrates. The affected papillary muscle and usually the underlying myocardium are thin and echo-dense on two-dimensional echo. One of the mitral leaflets is often flail and ruptured chords attached to the leaflets exhibit a chaotic motion pattern. It results in acute severe mitral regurgitation and pulmonary edema that is usually fatal if the entire trunk of the papillary muscle is ruptured. Papillary muscle rupture Papillary muscle rupture occurs in approximately 1% of myocardial infarctions and usually affects the posteromedial papillary muscle. and septum flattened in diastole. the percentage change in RV cavity area reduced. and mechanically ventilated. pressures. It is important to recognize post-infarction RV dysfunction because the use of drugs that are standard in LV infarction. Tricuspid regurgitation due to cavity enlargement or papillary muscle involvement in the infarction has a low velocity due to poor RV systolic function and elevated RA pressure. A step up in the oxygen saturation of blood in the RV found at cardiac catheterization in a patient with an acute MI is strongly suggestive of a VSD but if color Doppler does not reveal flow across the interventricular septum. and cause hypotension in RV infarction. In RV infarction echocardiography demonstrates hypokinesis of the RV free wall associated with an inferior LV wall motion abnormality. The jet of mitral regurgitation is often eccentric and the severity of the regurgitation can be underestimated by color Doppler. Elevated LV diastolic pressures caused by the infarction may increase left-to-right shunting across a previously unsuspected small atrial septal defect or patent foramen ovale. in cardiogenic shock. The RV apex is usually supplied by the LAD coronary artery and its wall motion is usually normal or hyperdynamic when RV infarction complicates an IMI. may lower RV preload.

noncoronary. which do not extend all the way to the annulus. The anterior and posterior MV leaflets have approximately the same surface area but the posterior leaflet occupies approximately 60% of the perimeter of the annulus. THE MITRAL VALVE Mitral valve anatomy The annulus of the mitral valve (MV) is an integral part of the fibromuscular cardiac skeleton. the anterior leaflet is the longer and more excursive of the two leaflets. and hemodynamics. The pulmonic valve is twisted approximately 60 from the plane of the aortic valve (R. The normal mitral valve leaflets are 2 mm thick and are separated by two commissures. function. N. and is triangular in shape with a rounded (convex) free edge. being attached to and supported by the aortic annulus anteriorly and on the left and right by the two fibrous trigones. and hemodynamics. left. cardiac function. The anterior leaflet divides the LV into inflow and outflow tracts (LVIT and LVOT). regurgitant flow. A. anterolateral and posteromedial. right. Doppler echocardiography is ideally suited to assess obstruction to forward flow. posterior. The posterior annulus connects with the basal ventricular myocardium at the atrioventricular (AV) groove.7 VALVULAR HEART DISEASE CONTENTS q The Mitral Valve q The Aortic Valve q The Tricuspid Valve q The Pulmonic Valve q Endocarditis q TEE Versus TTE in Endocarditis q Surgical Treatment of Valvular Heart Disease The four cardiac valves normally open to allow unimpeded forward flow and close securely to prevent retrograde blood flow (Figure 7. S. whereas the posterior leaflet is nearly rectangular. P. L. The aortic (red) and mitral (blue) valves are in fibrous continuity while the pulmonic (green) and tricuspid (yellow) valves are separated by the infundibulum. septal). The annulus is shaped like the letter ‘D’ with the straight side of the D lying beneath the aortic valve. Conditions that impair these two functions alter chamber sizes. . anterior.1). in proportion to their severity. Two indentations 75 R A N P S A R L L A P Figure 7. However. and their consequent effects on cardiac architecture.1 Diagram of the spatial relations of the valves at the base of the heart.

2 Apical long axis view. 76 . Etiology MS is almost invariably the result of rheumatic fever but may rarely be congenital resulting from anomalies of the leaflets or subvalvular apparatus. and chordae from the anterolateral papillary muscle attach to the lateral half of both mitral leaflets. Chords (chordae tendineae) (Figure 7. left atrium. P2 is central. particularly elderly women.0 cm2. Figure 7. aorta). and lateral scallops.0 cm2 and MS is critical when the orifice is 1. central. Contraction of the papillary muscles in early systole brings the leaflets together and initiates valve closure. chordae tendineae (arrows) and mitral valve leaflets is demonstrated in the image from a normal subject (LV. AO. renal disease.3 Parasternal short axis view at the level of the mitral valve.5–2.3) is usually confined to the ventricular side of the posterior annulus Figure 7. There is extensive mitral annular calcification (arrow) that causes shadowing and partially obscures distal structures (RV. and P3 extends from the posteromedial commissure. Congenital MS is usually associated with chordal attachments from both leaflets to a single papillary muscle termed a parachute MV. The anterior leaflet has no chordal attachments to its basal portion as does the posterior leaflet. Mitral stenosis The normal diastolic mitral orifice is elliptical in shape with an area of 4–6 cm2. and aortic stenosis.2) from the posteromedial papillary muscle attach to the medial half of both leaflets. Mitral annular calcification (MAC) is a common finding in elderly people.THE ECHOCARDIOGRAPHERS’ GUIDE divide each leaflet into medial. MAC (Figure 7. left ventricle. It is also associated with systemic hypertension. right ventricle. LV. Mitral stenosis (MS) typically causes symptoms of exertional dyspnea when the orifice is reduced to 1. left ventricle). LA. The scallop extending from the anterolateral commissure is designated P1. The divisions are more prominent for the posterior leaflet. The continuity of the papillary muscles.

By carefully scanning through the funnel of the MV in the short axis plane the characteristic fish-mouth-shaped orifice can be recognized (Figure 7. The rheumatic process begins at the leaflet tips and extends to the body of the leaflets and the chordae. Paradoxical septal motion due to RV pressure and volume overload may be present or the interventricular septum (IVS) may dip leftward in early diastole reflecting relatively enhanced RV filling. Symptoms of MS are similar to those of left heart failure. Progressive narrowing of the MV orifice elevates left atrial (LA) pressure causing LA enlargement. Rheumatic MS results from fusion of the two leaflets at the commissures. which would cause the 77 .5). tricuspid regurgitation (TR). which is best seen in the parasternal long axis view. Gain settings should be high enough to visualize the whole orifice without drop-out. and paroxysmal nocturnal dyspnea but the LV is relatively unaffected by MS. fibrose.VALVULAR HEART DISEASE at the base of the posterior leaflet but can spread to the entire posterior annulus causing obstruction to left ventricular (LV) filling that is usually mild. and calcify over time. cicatrize. a flattened E–F slope and anterior motion of the posterior leaflet in diastole (Figure 7. orthopnea. Bright reflections representing calcification may obscure posterior structures.7). LV size is normal and diastolic filling is slow and prolonged. Thickening and fusion of the chordae close off interchordal communications and worsen the obstruction. and ultimately right heart failure with hepatic congestion and peripheral edema. The M-mode of the pulmonic valve (PV) shows loss of the A wave and may Figure 7. Pulmonary hypertension causes right ventricular hypertrophy (RVH). as thickening and calcification progress and diastolic leaflet doming is lost (Figure 7. The latter finding is due to fusion of the leaflets at their tips so that the posterior leaflet is pulled along with the anterior leaflet. which narrows the orifice producing a funnel with a minimal cross-sectional area usually at the leaflet tips. The leaflets thicken. Two-dimensional echo findings Commissural fusion produces doming of the MV. The minimal mitral orifice area can be visualized and planimetered in approximately 80% of all patients but this method is difficult to apply when there is extensive calcification or when there has been distortion of the valve following balloon valvuloplasty. but low enough to prevent ‘blooming’ of echoes from the valve. M-mode echo findings The M-mode of the MV in MS shows diminished early opening (D to E excursion). show mid-systolic closure in pulmonary hypertension. and increased the likelihood of atrial fibrillation and thrombus formation. Subvalvular involvement in the rheumatic process can be assessed from the parasternal long axis and apical views by shifting the plane medially and laterally to inspect the chordae and papillary muscles. Loss of atrial contraction impairs diastolic filling. Elevated LA pressure is transmitted to the pulmonary vasculature causing pulmonary hypertension.4 M-mode of the mitral valve in a patient with mitral stenosis. The LA is usually enlarged and the aortic valve may also be affected by rheumatic disease. The leaflets become more immobile. A ‘hockey-stick’ or ‘bent knee’ appearance is seen in diastole when the body of the anterior leaflet is still pliable (Figure 7.4).6). dyspnea on exertion.

which should be carefully evaluated.7 Parasternal short axis at the tips of the mitral valve in early diastole in a patient with mitral stenosis (RV. RVH and abnormal septal motion is expected and reflects the severity of pulmonary hypertension.6 Parasternal long axis view in a patient with mitral stenosis.8). right ventricle). respectively. orifice area to be underestimated. Doppler findings Pulmonary artery systolic and diastolic pressures should be assessed from the spectral Doppler velocity signals of tricuspid and pulmonic regurgitation. 78 . The Doppler flow velocity across the MV can be assessed from the apical window in almost all patients. The effects of MS on other cardiac structures and the effects of the rheumatic process on the other valves must also be assessed. left atrium.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. left ventricle. but are especially important in patients with MS. in all patients. Pulsed-wave (PW) Figure 7. The left atrium (LA) and right ventricle (RV) are enlarged (LV. LA enlargement will be present and LA thrombus may be seen but cannot be excluded by transthoracic echocardiography (TTE) alone. aorta). Relative chamber sizes are best seen in the apical four-chamber view (Figure 7. Figure 7. The mitral valve is thickened and immobile. Right heart enlargement. AO. LA.5 Parasternal long axis view in a patient with mitral stenosis (MS) demonstrating the ‘hockey-stick’ or ‘bent knee’ deformity that is present in MS while the anterior leaflet is still pliable (LV. Most patients with MS have some degree of mitral regurgitation (MR). The aortic valve is also thickened. left ventricle).

Note that the left atrium (LA) and right heart chambers are enlarged but the left ventricle is underfilled. The peak velocity across the valve is approximately 240 cm/s indicating a peak gradient of 23 mmHg. A pericardial effusion is also seen (*) (RV. Figure 7. which varies with cycle length and presence of MR. The gradients alone.8 Apical four-chamber view in a patient with severe mitral stenosis and moderate tricuspid stenosis and regurgitation. however. do not necessarily reflect the severity of the stenosis.11).9) usually provides a clearer envelope but continuous wave (CW) Doppler will ensure that the peak velocities are included in the sample (Figure 7. Peak and mean pressure gradients across the MV can be calculated from peak and mean Doppler velocities using the modified Bernoulli equation (Figure 7.10). Since velocity is quadratically 79 . They are in part determined by the amount of blood flow. This patient is in atrial fibrillation and no A wave is seen. is a reliable measure of the rate of pressure equilibration. Doppler (Figure 7. The time required for the peak transvalvular gradient to decrease by one-half.9 Pulsed-wave Doppler with the sample volume at the tips of the mitral valve leaflets in a patient with moderate mitral stenosis. right ventricle. the pressure half-time (P1/2). where pressure 4 (peak velocity2).VALVULAR HEART DISEASE Figure 7. right atrium). RA. The rate of equilibration of LA and LV pressure is a more fiducial measure of MS severity and can be obtained from the spectral envelope of the transmitral Doppler flow velocity.

the presence of an atrial septal defect (ASD) will decompress the LA and cause the P1/2 method to underestimate the severity of the MS. can be used to measure MV orifice areas. LV LA Figure 7.414). The product of the area of the PISA and the velocity at the PISA is . Blood flow across the MV in diastole must equal blood flow through the LVOT in systole if there is no aortic or mitral regurgitation. related to pressure. The cross-sectional area of the MV can also be estimated from the continuity equation. the proximal isovelocity surface area (PISA) method.0 cm2 (Figure 7.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. 80 A pressure half-time of 220 ms equals a valve area of 1. The area of the hemisphere is calculated as 2p(r2). The MV area is equal to the LVOT stroke volume divided by the transmitral flow velocity integral. Blood flow accelerates as it converges toward a narrowing from a larger chamber. Similarly. Another application of the continuity equation. the P1/2 time will equal the time from peak velocity to peak velocity divided by the square root of 2 (1. The middiastolic slope is extrapolated back to the time of peak velocity and the pressure halftime is recalculated. the mid-diastolic slope is used. The color Doppler scale and baseline are adjusted so that the first PISA is clearly seen and the radius of the first isovelocity hemisphere is measured. The pressure half-time method underestimates the severity of MS in the presence of aortic regurgitation (AR).10 Continuous wave Doppler in a patient with moderate mitral stenosis. The velocity of the blood at all points on the hemisphere is equal to the first aliasing velocity taken from the color Doppler map.11 Left atrial (LA) and left ventricular (LV) pressure tracings in a patient with mitral stenosis. Competitive retrograde filling of the LV from the aorta increases LV diastolic pressure and quickens the rate of transmitral pressure equilibration. Blood flow within the funnel of the stenosed MV accelerates toward the limiting orifice in a series of concentric hemispheres whose velocity can be determined by color Doppler (Figure 7. LVOT stroke volume can be calculated as the product of the LVOT flow velocity integral and the LVOT cross-sectional area. The pulmonary artery (PA) stroke volume can be substituted for the LVOT stroke volume if there is important AR but the PA diameter can be difficult to measure accurately. The pressure half-time is independent of heart rate or coexistent MR and is related to the mitral orifice area by the formula: MVA 220/P1/2.13).12). A pressure gradient (red) exists as LA pressure remains significantly higher than LV pressure throughout diastole. When the E to F slope of the transmitral flow velocity spectrum is nonlinear.

The area of the proximal isovelocity surface area (PISA) the Nyquist limit velocity the mitral valve (MV) orifice area the peak transmitral velocity therefore.12 Pressure half-time method for determining the mitral valve area. left ventricle. leaflet thickening.414).VALVULAR HEART DISEASE Figure 7. The cross-sectional area of the proximal hemisphere is determined from the measured radius (2p(r2)). left atrium). Percutaneous balloon valvuloplasty is used to increase the MV orifice area by splitting the commissures. mobility and calcification.9 cm2 (220/241). The patient on the right reaches the pressure half-time (white arrow) in 147 ms and has a valve area of 1. The peak velocity of the continuous wave Doppler signal on the left is 207 cm/s and the peak velocity of the signal on the right is 160 cm/s. A score of 8 indicates a 81 MV LA Figure 7. The velocity at pressure half-time is 146 cm/s for the patient on the left (207/1.13 Blood accelerates as it approaches a narrowing in the flow stream. The color Doppler signal aliases each time the velocity crosses a multiple of the Nyquist limit and a series of concentric hemispheres of alternating colors are formed.5 cm2 (220/147). A numeric value from 1 to 4 in order of ascending severity is assigned for four characteristics of the MV. MV area PISA area Nyquist limit/peak mitral velocity (LV.14). LA. Transesophageal echocardiography (TEE) is necessary to rule out LA thrombus prior to the procedure and TEE or TTE is often used to assess results following each balloon inflation. The interatrial septum (IAS) is punctured and a balloon tipped catheter is positioned in the MV orifice and rapidly inflated. The patient on the left reaches the pressure half-time in 241 ms (white arrow) and has a valve area of 0. Echocardiography is used to predict the clinical outcome of percutaneous balloon valvuloplasty using a scoring system devised at Massachusetts General Hospital. The red vertical arrows indicate 1 m/s and the red horizontal arrows indicate 200 m/s. . subvalvular involvement. MVA 2p(r2) V(Nyquist)/V(peak) The PISA method assumes that the MV orifice is circular and that the PISA is a hemisphere and these assumptions are not always warranted.414) and 113 cm/s for the patient on the right (160/1. LV the volume flow rate and it is equal to the product of the peak transmitral velocity and area of the MV orifice (Figure 7. Shunting across the IAS is common immediately after the procedure but is not typically seen at late follow-up.

The MV frequently appears normal in MR but careful examination of the valve and its subunits often reveals the etiology of the MR. As the LV enlarges the mitral annulus dilates and the papillary muscles are pulled laterally and apically disrupting leaflet coaptation and further exacerbating the MR. Hemodynamically significant MR can result from any disease process that affects the structural components of the MV: the papillary muscles. good likelihood of success when there is little MR.1 cm2 (2p(r2)). wall stress increases. The LV in chronic severe MR may remain compensated for many years. MAC can inhibit LV posterior basal wall motion and impede posterior MV leaflet motion producing MR. However. In rheumatic heart disease. As LV systolic volume increases. and identify any associated lesions. and this deterioration can become irreversible. so that LA and left pulmonary pressures are acutely elevated resulting in pulmonary edema. left atrium).1 40)]/250) (LA. which is a low-pressure sink.9 cm (arrow). myocardium. The radius of the first isovelocity surface area is 0. Thus. in acute severe MR due to papillary muscle rupture. the effects of the volume overload are progressive. Transthoracic Doppler echocardiography can assess the etiology and severity of MR and the effects of MR on LV. however. and right heart chamber size and function. In chronic MR the LA progressively dilates forming a reservoir that can accommodate the regurgitant volume without transmitting systolic LV pressure back to the pulmonary vasculature. MR coexists with MS resulting from scarred rigid leaflets with commissural fusion and shortened chordae that prevents valve closure. The mitral valve area is equal to 0. LV systolic function deteriorates. LA. leaflets. Ejection phase indices of LV systolic function are inversely related to wall stress explaining the supernormal ejection fraction. The LV dilates and assumes a more spherical shape. or the annulus. The isovelocity surface area of the PISA is 5. Ischemic MR Ischemic MR can result from infarction or ischemia of a papillary muscle (usually the posteromedial) or of the LV wall that supports the papillary muscle.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. chordae. The Nyquist limit taken from the Doppler color map is 40 cm/s and the peak transmitral velocity is 200 cm/s. In chronic MR preload is initially increased while LV afterload and wall stress are low because the LV can eject (unload) partly into the LA. a normal ejection fraction in chronic severe MR indicates LV dysfunction. pulmonary artery systolic pressure (PASP). 82 Chronic MR In chronic severe MR.14 Apical two-chamber view showing the proximal isovelocity surface area (PISA). the LV initially increases its stroke volume to accommodate forward and retrograde flow.8 cm2 [(5. there is no time for the LA to dilate or adapt to the regurgitant volume. Mitral regurgitation Mechanisms Mild MR can be detected in 70–80% of normal people by color Doppler. MR may be acute and torrential (see Chapter 6) or .

83 . elongated. and prone to rupture. Cardiac resynchronization therapy coordinates papillary muscle contraction and significantly and immediately reduces MR severity in some patients. The diagnosis of MVP should not be made unless leaflet thickness is 5 mm and prolapse of either leaflet or their point of coaptation reaches 2. Dyssynchronous contraction of the papillary muscles and subjacent myocardium due to an intraventricular conduction defect affects the timing and coordination of valve closure and promotes MR. The papillary muscle may be scarred and atrophied and motion of one of the leaflets is often restricted in ischemic MR. right atrium. descending thoracic aorta). left atrium. Mitral valve prolapse (MVP) MVP is the most common cause of isolated MR occurring in 2–4% of the population. the chordae are stretched. Folds of leaflet tissue billow or prolapse into the LA in systole. Doppler color flow has shown that posterior MV leaflet prolapse causes the MR jet to be directed anteriorly while the MR jet from anterior leaflet prolapse is directed posteriorly. MR may also result from LV remodeling post-infarction or in dilated cardiomyopathy and it can be difficult to determine whether the MR caused the LV dysfunction or resulted from it. AO. The annulus is usually dilated.0 mm beyond the plane of the mitral annulus in the parasternal long axis view (Figure 7. The prolapse and regurgitation may be holosystolic or late systolic. The valve leaflets are thickened. left ventricle.15 Parasternal long axis view in a patient with prolapse of the posterior mitral valve leaflet (arrow) (LV.15). RA.VALVULAR HEART DISEASE intermittent causing episodic flash pulmonary edema. aorta. The extent of the MVP should not be determined from the apical four-chamber view because the Figure 7. Dao. redundant. MR resulting from cavity enlargement usually produces a central regurgitant jet. and hypermobile. In a subset of patients leaflet deformity is severe and the degree of MR and LV dysfunction are progressive. Contraction abnormalities of the myocardium subjacent to the papillary muscle are generally evident and these walls may be thinned and noncontractile. LA. Chordal rupture may produce flail leaflet segments and severe (acute on chronic) MR. The posterior leaflet is more commonly affected than the anterior leaflet but both leaflets and other cardiac valves may be affected.

Cardiac chamber sizes. and if leaflet motion is restricted. In severe MR the aortic valve leaflets drift closed in systole due to diminished forward stroke volume (Figure 7. multicolored. severe mitral regurgitation. Other causes of MR Other causes of MR include: infiltration of any portion of the valve apparatus with amyloidosis or sarcoidosis. The regurgitant jet in acute MR will be small relative to its regurgitant volume because of high LA pressure. collagen vascular disease. The left atrium is 10 cm in diameter. Prolonged exposure to the anorexigens phenteramine and fenfluramine ( 6 months) can result in encasement of the posterior leaflet in a substance similar to that seen in carcinoid heart disease. The regurgitant volume is determined by the pressure gradient between the LV and LA. the size and shape of the regurgitant orifice and the compliance of the LA. as the development of pulmonary hypertension is associated with increased surgical mortality. The spatial extent of the color can also be indexed to the LA area. Jets that collide with the LA wall tend to adhere to it (Coanda effect) losing energy . Evaluation of severity of MR M-mode imaging The LA is usually enlarged and expands in systole. The aortic valve leaflets begin to drift closed in mid-systole (RVOT.17). mosaic jet. Color Doppler flow mapping The color signal of MR will alias many times as the MR jet is driven by the pressure difference between the LV and the LA. Angling the beam through the orthogonal 84 Figure 7.16 M-mode echocardiogram of the aorta (AO) and left atrium (LA) in a patient with chronic. less than 20% mild and greater than 40% severe.16). redundant. The severity of the MR is graded on a scale of 1 to 4 depending on the spatial extent of the color disturbance. the shape and orientation of the jet. This results in a bright. and congenitally cleft mitral valve as part of an endocardial cushion defect and trauma (although trauma to the tricuspid valve (TV) is more common than to the MV). which is very easy to detect visually (Figure 7. causing an exaggerated anterior displacement of the aorta. right ventricular outflow tract). The apical views are best to visualize the subvalvular apparatus and to determine if the chordae are thickened. Two-dimensional imaging This can assess LA size and LV size and function. such as systemic lupus erythematosus or rheumatoid arthritis. the MR is considered to be moderate. The PA pressure should also be assessed. or azimuthal plane helps the operator construct a three-dimensional appreciation of the extent of the color disturbance. Color Doppler is exquisitely sensitive for detecting MR but jets may be eccentric so that multiple views should always be used. and coexistent valvular abnormalities must be ascertained.THE ECHOCARDIOGRAPHERS’ GUIDE MV annulus is saddle-shaped and closer to the apex in this view. When the color Doppler signal occupies 20–40% of the LA. LV size and function is assessed by measuring LV internal diameters and calculating fractional shortening.

The parasternal long axis view and the apical views offer opportunities for multiple measurements. MR is classified as moderate when the vena contracta width is between 0.17 Parasternal long axis view with color Doppler showing severe mitral regurgitation in a patient with mitral valve prolapse (LV. AO. aorta). Measurement of the vena contracta width.5 cm.18 Measurements (arrows) of the vena contracta width in a patient with moderate mitral regurgitation (MR) (left panel) and in a patient with severe MR (right panel) (LV. left atrium.18). Regurgitant volume is the difference between the stroke volume calculated from plainimetry of two-dimensional images of 85 . A CW Doppler signal of MR that matches the antegrade flow in intensity represents significant MR. Color Doppler grading of MR overestimates central jets and underestimates eccentric jets.19). because signal intensity is proportional to the number of scatterers in the regurgitant jet.VALVULAR HEART DISEASE Figure 7. left ventricle. Zoom mode should be employed and the minimum diameter measured in the frame that shows the maximum MR for each view. These measurements can be made in approximately 90% of all patients and can differentiate mild from severe MR but there is overlap between mild and moderate and moderate and severe MR (Figure 7. Spectral Doppler Spectral Doppler of the LV inflow tract (LVIT) demonstrates a high velocity E wave consistent with rapid LV filling. The continuous wave Doppler signal of MR becomes easier to obtain and its signal intensity increases as the severity of the MR increases. particularly those that hug the wall. Figure 7.3 cm and 0.5 cm. It is mild when below this range and severe if 0. correlate well with regurgitant orifice areas and angiographically determined regurgitant grades and is independent of load. Pulmonary vein Doppler The S wave of the pulmonary venous waveform is blunted or reversed when there is significant MR but this finding may be absent when the LA is large and compliant or difficult to interpret when the jet is eccentric and aimed directly at the pulmonary vein under interrogation (Figure 7. LA. left ventricle) in the process. jets may be multiple and usually vary through systole. In addition. the narrowest central portion of a color jet with the greatest velocity.

All methods used for determination of stroke volume are limited. The mitral valve regurgitant orifice area (ROA) is 0.20 Apical four-chamber view with color Doppler in a patient with mitral regurgitation. As blood in the LV converges toward the regurgitant orifice of the MV the flow velocity increases. The former stroke volume includes the regurgitant volume whereas the latter does not. A regurgitant fraction of 30–50% denotes moderate (2–3 ) MR.19 Pulmonary vein pulsed wave Doppler. The PISA method calculates volumetric flow as the product of the cross-sectional area (CSA) of the flow stream and the FVI recorded at the same location. the transmitral stroke volume can be calculated as the product of the mitral annular area. The S wave of this tracing is blunted by the mitral regurgitant flow. This zone of flow convergence consists of concentric hemispheres radiating from the Figure 7. The color Doppler scale is reduced to 25 cm/s to increase the size of the proximal isovelocity surface area (PISA).THE ECHOCARDIOGRAPHERS’ GUIDE Nevertheless. left ventricle.4 cm (arrow). Regurgitant fraction is calculated as regurgitant volume divided by total (forward plus regurgitant) stroke volume. The assumption that the MV annulus is circular may be true in some patients but not others. . 86 Figure 7.20). which is assumed to be circular and the FVI of the transmitral diastolic flow taken at the same location. and relies on the fact that volume flow through a vessel is constant and independent of the diameter of the vessel (Figure 7. The PISA radius is 1. This stroke volume also includes the regurgitant volume and can be substituted for the stroke volume derived from LV images. LA. The cross-sectional area of the PISA is 12 cm2 (2p(r2)). The peak velocity of the mitral regurgitation (MR) continuous wave Doppler signal is 5 m/s. PW Doppler methods are dependent on accurate measurements of diameters and small errors are magnified as the diameters are squared to obtain areas.6 cm2 ((12 25)/500) (PISA flow/MR peak velocity ROA) indicating severe MR (LV. the LV in diastole and systole and the stroke volume calculated as the product of the flow velocity integral (FVI) of the pulsed wave Doppler signal of flow in the LVOT and the LVOT cross-sectional area. left atrium). A stroke volume calculated from the PA diameter and FVI could be substituted for the LVOT Doppler stroke volume. less than 30% is mild (1 ) and greater than 50% is severe (4 ). Quantitation of LV volumes from twodimensional images is operator dependent and reliant upon good image quality. calculation of regurgitant fraction can classify MR as mild. moderate or severe with reasonable accuracy. Similarly.

The regurgitant flow is the product of the two. rightward and slightly posteriorly so that the direction of blood flow in systole is toward the right shoulder. The valve cusps separate in systole to form a nearly circular orifice. but the systolic orifice 87 An ROA between 20 mm2 and 40 mm2 indicates moderate (2–3 ) MR. which appears wherever the flow velocity exceeds a multiple of the Nyquist velocity. The products of the crosssectional area and velocity are equal for each shell indicating that the flow at each shell is constant. suprasternal. A raphe may cause the valve to appear tricuspid in diastole. The area of the shell. The regurgitant volume is equal to the ROA multiplied by the FVI of the MR by CW Doppler. The aortic valve can be easily visualized echocardiographically from the left parasternal window and flow assessed by Doppler from the apical. The nodules of Arantius are small mounds of fibrous tissue at the center of the closing edges of each cusp that facilitate complete closure. The coronary arteries arise from the right and left aortic sinuses of Valsalva close to the sinotubular junction. The shell of the innermost hemisphere has the smallest crosssectional area but the fastest flow velocity. and right parasternal windows. In diastole the three cusps appose in the center of the aortic lumen and prevent regurgitant flow. The plane of the aortic valve faces superiorly. the larger may contain a raphe. By adjusting the color Doppler baseline shift and scale functions. Flow at the PISA must be equal to flow through the orifice so that: VelocityPISA CSAPISA VelocityMR CSAMR THE AORTIC VALVE Aortic valve anatomy The aortic valve is in close proximity to all four cardiac chambers. Difficulties with this technique remain. This flow is equal to the regurgitant flow and can be calculated as the product of the velocity and area where area 2p(r2). The assumption that the concentric flow fields are hemispheric may not be justified when the jet is constrained by adjacent structures.VALVULAR HEART DISEASE regurgitant orifice. the velocity at the PISA is given by the Nyquist limit of the color Doppler map that is displayed on the screen. severe (4 ). The aortic sinuses of Valsalva are outpouchings of the aortic wall behind each cusp. red to blue or blue to red. The diameter of the aorta at the level of the sinuses is larger than at the annulus or sinotubular junction. PISA flow/MR peak velocity ROA FVIMR ROA Regurgitant volume Bicuspid aortic valve Bicuspid aortic valve (BAV) is the most common congenital cardiac abnormality occurring in approximately 1% of the population with a 2:1 male to female predominance. which is a fibrous ridge at the site of fusion between two congenitally conjoined cusps. the angle of the unimpeded flow convergence is measured (angle a) and the ROA equation is corrected for the degree of flow constraint by multiplying it by a/180 . . or the PISA flow divided by the peak velocity of the CW signal of MR is equal to the regurgitant orifice area (ROA). Using color Doppler a shell is identified as an arc of color change. its PISA is calculated as 2p(r2). Shells further from the regurgitant orifice will have larger cross-sectional areas and lower velocities. When the jet is constrained. An ROA below this range can be considered mild (1 ) and above this range. which form the three commissures and sinuses that terminate at the sinotubular junction. A BAV usually has two leaflets of nearly equal size with the commissure running obliquely from lower left to upper right in the parasternal short axis image but leaflet orientation is variable. when r is the radius of the hemispherical shell. The aortic annulus separates the LVOT from the aorta and gives off three spurs. the first aliasing velocity (the proximal shell) can be visualized and the radius or distance to the valve orifice measured. When the two cusps are of unequal size. The valve leaflets extend for a few millimeters between the closing edge and the free edge of each cusp.

LA. . In the parasternal long axis view the closure line in diastole is often eccentric in BAV. BAV is present in approximately 15% of proximal (type A) aortic dissections. left ventricle. It is helpful to move the transducer approximately 1 cm laterally and angle the beam medially. the risk of aortic dissection is increased ninefold by the presence of a BAV. Significant regurgitation is usually due to prolapse of the larger of the two aortic cusps. Valve calcification usually involves the base of the cusps and the raphe. Subcostal short axis views of the base may also demonstrate aortic valvular anatomy and 88 are especially useful when parasternal views are suboptimal. The aortic valve appears to be trileaflet in the diastolic frame but is shown to be bicuspid with a raphe in systole. Approximately 50% of cases of coarctation of the aorta are associated with BAV.21). is elliptical (Figure 7. Aortic root dilatation and ascending aortic aneurysm are commonly associated with BAV and occur out of proportion to the hemodynamics of concomitant aortic stenosis or regurgitation suggesting an intrinsic defect of the aortic root tissue. left atrium). Stenosed BAVs often exhibit systolic doming (Figure 7. BAVs are prone to accelerated calcification and are the most frequent cause of AS in the fifth to sixth decades. the minimal orifice Figure 7. The morphology of the BAV can be defined echocardiographically in short axis images in greater than 90% of cases. Most bicuspid valves are at least mildly regurgitant and in younger patients with BAV significant AR is much more common than significant aortic stenosis (AS).21 Short axis of the aortic valve in zoom mode.22).THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. This bicuspid aortic valve exhibits systolic doming and mild stenosis (LV.22 Parasternal long axis view of the aortic valve in systole.

There are two raphes (arrows) seen in this systolic frame (RA. . Alternatively. left atrium. it may encircle the LVOT or more rarely arise from the anterior MV just proximal to the aortic valve. Fixed outflow tract obstruction at the subvalvular level is caused by a discrete outcropping of tissue in the form of a membrane or shelf that narrows the outflow tract (Figure 7. with congenitally abnormal valves by careful imaging and Doppler interrogation of the descending aorta from the suprasternal notch. Typically a ridge of tissue arises from the IVS a few millimeters proximal to the right coronary cusp. Imaging of the ascending aorta distal to the sinotubular junction is required in patients with BAV and is best accomplished from the right parasternal window with the patient in the right lateral decubitus position. calcification affects the bodies of the cusps beginning at the base with initial sparing of the commissures. male sex. pulmonary artery). The pressure gradient across the obstruction 89 Aortic stenosis Congenital AS Congenital AS is either acommissural or unicommissural. M-mode or short axis imaging at the base of the cusps may underestimate the degree of stenosis. The Doppler color flow jet of AR is often eccentric in BAVs when the two cusps are unequal in size. In the acommissural type the valve functions as a diaphragm with a small central orifice and there is marked systolic doming. LA. The extension of the membrane into the outflow tract is usually triangular in shape being broader at the base than at the tips. Rheumatic AS Rheumatic valvulitis causes thickening of the cusps. but is associated with the same risk factors as atherosclerosis: hypertension. Subvalvular AS Obstruction to LV outflow can occur proximal to the aortic valve and may be fixed or dynamic. Aortic valve sclerosis without hemodynamically important stenosis marks the early stage of the disease process.23). The rate of progression of calcification varies greatly. and advanced age.23 Parasternal short axis view in a patient with a unicommissural aortic valve.24). which may become significant prior to the development of calcification. usually between the right and left cusps and between the right and noncoronary cusps leaving only a small slitlike orifice between the left and noncoronary cusps (Figure 7. Senile calcific AS In senile AS. Severe subaortic obstruction usually presents in infancy. Subvalvular obstructions are best visualized echocardiographically in the parasternal or apical long axis planes or in the apical five-chamber view. A unicommissural valve has two raphes. and progressive stenosis. diabetes. Coarctation of the aorta should be excluded in all patients Figure 7. It is invariably associated with rheumatic MV disease. Dynamic LVOT obstruction associated with systolic anterior motion of the MV is a feature of hypertrophic obstructive cardiomyopathy (see Chapter 8). PA. It is the most common cause of AS in patients 70 years. The stenosis caused by either type is usually severe and patients present in infancy. commissural fusion. smoking. right atrium.VALVULAR HEART DISEASE area is at the tips of the leaflets. hypercholesterolemia.

Two-dimensional echo Two-dimensional echo imaging from the parasternal LV long axis (Figure 7. This type of obstruction is associated with stenoses of the pulmonary arteries. LVH can be defined as a relative wall thickness (enddiastolic wall thickness 2/end-diastolic LV cavity radius) 0. right ventricle. The presence of the normal box-shaped aortic valve pattern on M-mode echocardiography excludes the diagnosis of significant AS except when the valve is congenitally abnormal and exhibits systolic doming. LA. Symptoms of AS The prognosis in AS relates to development of symptoms. can be reliably assessed by CW Doppler. The prognosis of a patient with symptoms at rest is poor. When wall stress can no longer be normalized by further LVH. AO. Severe supravalvular obstruction exposes the coronary arteries to elevated pressures and accelerated atherosclerosis. pulmonic stenosis. which is characterized by mental retardation. Figure 7. The obstruction usually occurs just above the sinotubular junction and the narrowing may be focal or tubular.24 Parasternal long axis view in a patient with fixed left ventricular (LV) outflow tract obstruction from a subaortic ridge of tissue (arrow) (RV. Supravalvular aortic stenosis is a feature of William syndrome. from the subcostal short axis. Progression to heart failure caused by deteriorating systolic function occurs late in the course of the disease and is associated with myocyte degeneration and fibrosis. Concentric LV hypertrophy (LVH) is invariably present in hemodynamically significant AS and is best assessed from the parasternal long and short axis views (Figure 7. syncope or dyspnea attributable to the stenosis without surgical relief of obstruction. usually at the bifurcation or in branch vessels.27) or if these are inadequate.THE ECHOCARDIOGRAPHERS’ GUIDE elfin facies. Supravalvular AS Congenital supravalvular AS results from a narrowing of the ascending aorta. hypercalcemia. A jet of AR that is redirected upon striking the obstruction may first suggest subaortic stenosis. LV dilatation occurs. Subaortic stenosis may recur after successful surgery. Rarely. The aortic valve may be damaged by the high velocity jet from the obstruction causing the commonly associated aortic regurgitation. and 90 Doppler-echocardiography in AS M-mode Diminished leaflet excursion and leaflet calcification seen on M-mode does not predict the severity of aortic stenosis. systolic function is preserved and LV cavity size remains normal because the LVH normalizes systolic wall stress. left atrium. In ‘compensated’ AS.25) and short axis (Figure 7.26) show thickened and calcified leaflets with restricted leaflet motion. LVOT membranes are usually echo-bright but if thin may be difficult to recognize. aorta). supravalvular obstruction may also occur from deposition of large atherosclerotic plaques in the ascending aorta as occurs in familial homozygous hypercholesterolemia. 75% of patients die within 3–5 years of the onset of symptoms of chest pain. Coronary ostial lesions are common. systolic .42.

Doppler echo The pressure gradient (Figure 7. Figure 7. AO.26 Parasternal short axis views in a patient with aortic stenosis and regurgitation.29) or apical long axis. CW Doppler velocity signals should be obtained from the apical five-chamber (Figure 7. The non-imaging or CW transducer is important in obtaining the maximum velocity because its small footprint allows it to be manipulated in the intercostal spaces for optimum alignment with flow. left atrium. PA. Twodimensional imaging identifies the optimal location for placement of the non-imaging probe and color flow Doppler identifies the direction of transaortic flow.25 Parasternal long axis in a patient with aortic stenosis. The angle of the CW beam is adjusted incrementally using the audio signal and the spectral display until a complete spectral envelope is obtained from each window. LA.30) and suprasternal notch views in every patient with AS. The highest velocity obtained is used to estimate the Figure 7. The systolic frame shows moderate reduction in the aortic valve cross-sectional area. right atrium. The diastolic frame shows a small. central regurgitant orifice (RA.VALVULAR HEART DISEASE function deteriorates and ‘decompensated’ AS ensues. Aortic valve excursion is markedly reduced in this early systolic frame (LV.28) across the aortic valve in AS is measured with CW Doppler from the imaging windows that allow the beam to be aligned parallel to transaortic flow. left ventricle. aorta). left atrium. right parasternal (Figure 7. pulmonary artery). LA. 91 .

The transducer is at the apex and flow is away from the transducer. LV AO Figure 7.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. 92 .27 Parasternal short axis images of the left ventricle (LV) from a patient with severe aortic stenosis demonstrate severe concentric LV hypertrophy and normal systolic function. Figure 7.28 Aortic (red. AO) and left ventricular (LV) pressure tracings (black) in a patient with aortic stenosis. The pressure gradient measured by continuous wave Doppler is the peak instantaneous gradient (long vertical arrow) and not the peak to peak gradient (short vertical arrow) measured at cardiac catheterization.29 Continuous wave Doppler tracing of aortic stenosis. The peak velocity of the signal is approximately 4 m/s indicating a peak instantaneous transaortic gradient of 64 mmHg.

VALVULAR HEART DISEASE Figure 7. Conversely. The sample volume will be approximately 0.7 m/s to 1. the VelocityLVOT term in the pressure gradient equation can be ignored and the formula simplifies to Pressure gradient 4(VelocityAOV2) Omission of VelocityLVOT when it is high will overestimate the transaortic gradient. The Doppler peak instantaneous pressure gradient is determined from the transaortic flow velocity by the formula: Pressure gradient 4(VelocityAOV2 VelocityLVOT2) where VelocityAOV is the maximum recorded CW velocity through the aortic valve and VelocityLVOT is the maximum PW Doppler velocity recorded in the LVOT. There is also aortic regurgitation.0 cm proximal to the valve.5–1.31).30 Continuous wave Doppler tracing of aortic stenosis. Peak flow velocity in the LVOT normally ranges from 0.2 m/s indicating a peak instantaneous transaortic gradient of 108 mmHg. the transaortic gradient will be low when there is severe stenosis and poor LV pump function. The peak velocity of the signal is approximately 5. The equation is rearranged to estimate aortic valve area: AOVCSA LVOTFVI LVOTCSA/ AOVFVI The PW Doppler envelope of the LVOT flow and the CW envelope of transaortic flow must be clear and complete for accurate 93 .5 m/s and varies with stroke volume. The latter is best obtained by placing the PW sample volume in the region of flow acceleration immediately proximal to the aortic valve and gradually withdrawing it until a smooth thin envelope representing laminar flow with a well-defined peak velocity is achieved. The continuity equation assumes that all of the stroke volume passing through the LVOT passes through the aortic valve. LV stroke volume is calculated as the product of the LVOT FVI and the cross-sectional area of the LVOT. pressure gradient across the aortic valve and assess the severity of AS as Doppler velocities can be underestimated when the beam is not aligned with the flow but they cannot be overestimated. The aortic valve area calculated using the conservation of energy principle/continuity equation is independent of stroke volume and is therefore an integral part of the evaluation of AS severity (Figure 7. LVOT stroke volume (LVOTFVI LVOTCSA) is equal to aortic valve stroke volume (AOVFVI AOVCSA). The transducer is at the second right intercostal space and flow is toward from the transducer. The pressure gradient may be elevated out of proportion to the severity of AS when stroke volume is increased as in AR or bradycardia. Calculation of the aortic valve area is mandatory in these conditions. When peak velocity of LVOT flow is 1 m/s or less. The LVOT is circular and its crosssectional area is calculated from the LVOT diameter measured from the parasternal long axis view in early systole as the distance between the insertion points of the right and noncoronary cusps of the aortic valve.

Rheumatic AR results from commissural fusion. Prolapse of a trileaflet aortic valve may be caused by myxomatous degeneration of the leaflet tissue or annulus in association with mitral and tricuspid valve prolapse. The LVOT diameter measurement is critically important as erroneous measurements are squared in the LVOTCSA calculation. The yellow vertical arrows in the middle and right panels indicate the velocity calibration of 1 m/s. Critical AS is defined as an aortic valve area 0.2 cm is measured (left panel). The most common cause of AR is aortic root dilatation secondary to hypertension. If the transaortic gradient increases with increased stroke volume the AS is severe.7 cm2 indicating critical aortic stenosis. if so. In some patients with AS and poor LV function it may be difficult to determine the predominant condition and aortic valve area may increase with increased stroke volume. and prolapse of the MV and increased risk for aortic dissection. Congenital and acquired AS are usually associated with some degree of AR.8 cm2. Aortic root enlargement prevents normal leaflet coaption causing central AR.7 cm2. In contrast to MR where the LV discharges its regurgitant volume into the low pressure LA.0–1.0 cm2 and moderate AS as 1.6–3. The aortic valve area (3. Coexistant mitral regurgitation by Doppler color flow is frequent and the severity of MR decreases following aortic valve replacement in approximately 50% of patients. The flow velocity integral of the continuous wave signal of flow through the valve is measured at 104 cm. the LVOT cross-sectional area is therefore 3.7–1. Marfan syndrome is usually associated with progressive aortic enlargement limited to the aortic root and ascending aorta. AR causes LV volume overload so that LV cavity volume increases to accommodate forward and regurgitant stroke volumes (Figure 7.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. A left ventricular outflow tract (LVOT) diameter of 2. valve area determination. severe AS is not present.8 cm2 20 cm)/104 cm 0. The pulsed-wave Doppler sample volume is placed in the LVOT and the flow velocity integral is measured at 20 cm (middle panel). Patients who do not demonstrate an increase in stroke volume or transaortic gradient with dobutamine have mild AS.31 The measurements required for calculation of the aortic valve area by the continuity equation are displayed.32). The presence of coexistent AR and MR is easily 94 demonstrated using color Doppler in the parasternal long axis and apical views.6 cm2). which interferes with effective valve closure. Impaired relaxation with a decreased E wave and augmented A wave on transmitral Doppler and a prolonged isovolumic relaxation time are common in AS.5 cm2. Dobutamine stress echo may be used to establish whether aortic valve area increases significantly with dobutamine. which is not the cause of their LV dysfunction. The aortic valve area for adults is approximately 3. severe AS as 0. in AR the LV stroke . myxomatous degeneration. Aortic regurgitation AR results from congenital or acquired abnormalities of the valve cusps or from enlargement of the aortic root.0 cm2 (2.

VALVULAR HEART DISEASE NL AS AR Figure 7. AS causes pressure overload hypertrophy and AR causes volume overload hypertrophy. Symptom onset is related to LV size and LV cavity enlargement is a marker of incipient LV systolic dysfunction and increased mortality. when the LV end-diastolic dimension is greater than 75 mm or when the resting LV ejection fraction falls below 50%. the disease is generally progressive such that LV volumes continue to increase and the LV becomes more spherical. Diastolic aortic leaflet prolapse. Wall thickness is normal or increased and the septum exhibits a biphasic systolic excursion pattern. and a patient with severe aortic regurgitation (AR). neither of these findings correlate with the severity of AR. The AR jet often impinges upon the anterior MV leaflet limiting its diastolic excursion and causing high frequency fluttering of the anterior mitral leaflet or chordae. An equilibrium may be sustained for many years wherein the patient remains asymptomatic with little change in LV size. leaflet perforation. The left ventricle is enlarged. vegetative endocarditis and systolic doming are best visualized in parasternal long axis and when this view is Figure 7. Assessment of the severity of AR M-mode echo The M-mode echo of the left ventricle in a patient with chronic AR is characterized by LV cavity enlargement and LVH with preserved systolic function (Figure 7. Left ventricular muscle mass is increased in AS and AR. AR presents the LV with both a pressure and volume overload. a patient with severe aortic stenosis (AS). In severe AR concentric hypertrophy becomes inadequate to normalize systolic wall stress and systolic function deteriorates. surgery for asymptomatic patients is generally recommended when the LV end-systolic diameter exceeds 55 mm.32 Illustrates the relative muscle (blue) to cavity (red) ratios from a normal subject (NL).33 M-mode echocardiogram of a patient with chronic aortic regurgitation. however. To prevent irreversible damage to the LV. Patients usually first present with symptoms of dyspnea on exertion or effort intolerance and valve surgery is indicated at the onset of symptoms. The LV responds to increased diastolic load (wall stress) by cavity enlargement and eccentric hypertrophy that initially preserves stroke volume. systolic function preserved and the interventricular septum exhibits biphasic systolic excursion.33). and the increased systolic load (wall stress) induces concentric hypertrophy that normalizes the increased systolic wall stress. 95 . volume is ejected into the high-pressure systemic circuit. Two-dimensional echo Aortic valve morphology in chronic AR can be precisely characterized in the large majority of patients and the etiology determined by a thorough examination of the valve in the parasternal short and long axis views. The Mmode of the aortic valve in AR usually appears normal even when the AR is severe.

34 Apical long axis with color Doppler showing moderate aortic regurgitation (LV.5 m/s. As the LV enlarges it becomes more spherical.34). The severity of the AR can be semiquantified by the spatial extent of the color disturbance.THE ECHOCARDIOGRAPHERS’ GUIDE unavailable. and the apical five-chamber and long axis views (Figure 7.35). LV size.5–4. Regurgitant volume in AR is not the only determinant of the size of the Doppler color flow. and function can be assessed from the apical four-chamber and other apical views but care must be taken to image the full length of the ventricle without foreshortening. The severity of chronic AR is directly related to LV chamber size and the LV can become enormously dilated (cor bovinum). shape of the regurgitatant orifice and the compliance of the LV. the direction of the jet. left atrium).35 Parasternal long axis view showing moderately severe aortic regurgitation with an eccentric jet. 1 AR when the color signal is within 1 cm of the aortic valve. shape. The AR jet is driven by the pressure difference between the aorta and the LV in diastole. 3 AR when it extends to the papillary muscles and 4 AR when the color disturbance fills the LV. apical long axis or apical fivechamber images in zoom mode should be attempted. 2 AR when the color jet extends to the MV leaflet tips. The color jet of AR must therefore alias several times as this gradient equates to a CW Doppler velocity of 3. Figure 7. LA. Doppler AR from trivial to severe can be detected by color flow Doppler as a brightly colored mosaic jet in the LVOT in diastole that is easily seen in the parasternal long and short axis views. Regurgitant AR jets that run along the anterior MV or septum may not propagate due to loss of momentum and result in underestimation of the severity of AR (Figure 7. It is also determined by the pressure gradient between the aorta and the LV. Figure 7. 96 . left ventricle.

37 Pulsed-wave (PW) Doppler with the sample volume in the left ventricular outflow tract (LVOT) in a patient with aortic regurgitation. while a color jet 25% of the LVOT diameter indicates angiographic grade 1 (mild) AR. Measurement of jet width indexed to the LVOT diameter is used to assess the severity of AR (Figure 7. Stroke volumes quantified from PW Doppler FVI and crosssectional area measurements of the PA or mitral annulus do not include regurgitant volume.VALVULAR HEART DISEASE Figure 7.38). Aortic regurgitant volume and regurgitant fraction can be determined by comparing two measured stroke volumes. Stroke volume calculated from LVOT diameter and the flow velocity integral of the PW Doppler signal includes the regurgitant volume. Measurement of the area of the color signal in the LVOT in short axis immediately subjacent to the aortic valve plane indexed to the LVOT cross-sectional area at this level also correlates with angiographic severity of AR.37). the regurgitation is severe. Stroke volumes derived from diastolic and systolic volumes quantified from apical images or from the LVOT diameter and PW Doppler FVI include regurgitant volume (Figure 7.36). one that includes regurgitant volume. Stroke volume calculated from RVOT diameter and FVI does not. and one that does not. When the color jet cross-sectional area occupies 50% of the cross-sectional area of the LVOT in this plane. Color Doppler signals of AR are rarely adequate by TTE for the PISA method for regurgitant orifice area determination but this area can be estimated by the continuity principle. whereas if it is 25% the AR is mild or mild to moderate. Retrograde flow in the aorta can be detected by PW Doppler in moderate and severe AR (Figure 7. A color jet width 65% of the LVOT diameter corresponds to angiographic grade 4 (severe) AR. Comparison of the two stroke volumes yields the regurgitant volume. The PW sample volume is placed in the aorta approximately 2 cm distal to the aortic valve and aligned with transaortic flow from the Figure 7.36 Measurements of the width of the color jet of aortic regurgitation (arrow) and the ratio of jet width to left ventricular outflow tract diameter are facilitated by the use of color M-mode. 97 .

39) from the suprasternal notch. Retrograde flow in the aorta caused by aortic regurgitation is shown as flow toward the transducer. suprasternal or high right intercostal position. Retrograde flow in the aorta caused by aortic regurgitation is shown as flow toward the transducer. Holodiastolic retrograde flow in the descending aorta sampled from the suprasternal notch represents severe or moderate to severe regurgitation depending on the FVI of the diastolic signal. The slope of Figure 7. These volumes are obtained by placing the PW sample volume in the ascending or descending aorta (Figure 7. The forward stroke volume is the product of the systolic FVI and the cross-sectional area of the aorta and the regurgitant volume is the product of the diastolic FVI and aortic cross-sectional area. which is equal to the FVI of the CW signal of AR multiplied by the unknown regurgitant orifice area. The product of the FVI of aortic retrograde flow and the cross-sectional area (CSA) of the aorta at the same level is equal to the regurgitant volume. Holodiastolic retrograde flow sampled in the abdominal aorta (Figure 7. Regurgitant fraction can also be estimated as the ratio of forward stroke volume to regurgitant volume. The velocity of the CW Doppler signal of AR decelerates through diastole and the rate of deceleration reflects the rate of equilibration of aortic and LV pressures. FVIAO CSAAO FVIAOV FVIAO CSAAO/FVIAOV CSAAOV or CSAAOV The assumption that coronary blood flow contributes little to the diastolic FVI may cause the regurgitant orifice area to be slightly overestimated.38 Pulsed-wave Doppler with the transducer at the apex and the sample volume in the aorta approximately 2 cm distal to the aortic valve. The magnitude of retrograde aortic blood flow is proportional to the severity of the aortic incompetence. Systolic and diastolic aortic diameters cannot be assumed to be equal and should be measured individually as the large forward stroke volume causes a significant increase in the size of the aorta.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7.39 Pulsed-wave Doppler with the transducer in the suprasternal notch and the sample volume in the proximal descending thoracic aorta. .40) from the subcostal window 98 represents severe AR provided that there is no patent ductus arteriosus.

However. Acute AR can be difficult to assess echocardiographically. The steeper the slope the more severe the AR. the CW signal of AR is a marker of the severity of the regurgitation. Holodiastolic retrograde blood flow indicates severe aortic regurgitation. The LV cannot adapt acutely to the regurgitant volume by cavity enlargement. 99 . High LV diastolic pressure tends to minimize the findings of retrograde flow in the aorta and tachycardia can make the color jet small and difficult to visualize.43). A deceleration slope of less than 200 cm/s indicates mild regurgitation and a slope of greater than 400 cm/s indicates severe regurgitation.40 Pulsed-wave Doppler with the transducer in the subcostal region and the sample volume in the abdominal aorta. Acute severe AR Severe AR may develop acutely when there is destruction of the leaflets from infection or from loss of commissural support and prolapse of the aortic valve into the LVOT with aortic dissection.42).41 The slope of the continuous wave Doppler signal of aortic regurgitation (AR) describes the rate of equilibration of aortic and left ventricular diastolic pressures. An intimal flap may be seen in the lumen of the proximal ascending aorta from type A aortic dissection. LV systolic function is acutely reduced rather than being hyperdynamic as in chronic compensated AR due to the sudden hemodynamic burden. Figure 7. LV diastolic pressure and pulmonary venous pressure rise dramatically causing pulmonary edema. Aortic and LV pressures equilibrate rapidly in diastole so that LV diastolic pressure rapidly exceeds LA pressure causing premature MV closure and diastolic MR. The cause of the regurgitation may also be recognized on twodimensional imaging. acute severe AR can be diagnosed from the slope of the CW signal of AR (Figure 7. which is very steep and reaches the baseline before the QRS complex of the ECG indicating equilibration of aortic and ventricular pressure in diastole and by premature MV closure detectable on M-mode in the absence of first degree A-V block (Figure 7. More severe AR causes a faster rate of equilibration and a steeper deceleration slope (Figure 7. Moderate AR is indicated by the slope of the AR signal in (A) and severe AR indicated in (B).VALVULAR HEART DISEASE Figure 7.41). or there may be avulsion of the aortic valve leaflets due to vegetative endocarditis.

named for the leaflets to which Tricuspid stenosis The etiology of tricuspid stenosis (TS) is almost always rheumatic heart disease (RHD) that is associated with rheumatic disease of the mitral and aortic valves. Calcification of the TV annulus is much less common than MAC. 100 . TV annular calcification (TAC) occurs more commonly in elderly people and in patients with altered RV hemodynamics. and the septal. also has direct chordal connections to the septum. which dictates the clinical course. MV closure occurs before the next QRS complex (upward pointing arrows). The posterior and anterior leaflets are seen in the RV inflow tract (RVIT) view.44). The posterior is the smallest of the three leaflets and opens along the diaphragmatic surface of the RV. The anterior and septal leaflets are seen in the apical four-chamber view where the TV is distinguished from the MV by the more apical insertion of the septal leaflet of the TV. the posterior. The RA and inferior vena cava (IVC) Figure 7.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. There is rapid equilibration of aortic and left ventricular diastolic pressure and they are nearly equal at end-diastole. There are three principal papillary muscles. which is attached at its base to the membranous and muscular interventricular septum. Pure TS is rare and is more commonly combined with TR. THE TRICUSPID VALVE Anatomy The TV annulus is larger than the mitral annulus. The septal leaflet. but accessory papillary muscles are common for the TV. commissural fusion. The chronic inflammation occurring in RHD causes TV leaflet thickening.43 Premature mitral valve (MV) closure (downward pointing arrows) caused by acute severe aortic regurgitation. It is usually seen as an echo-dense reflection from the annulus adjacent to the anterior tricuspid leaflet in the apical four-chamber view.42 The continuous wave Doppler signal in a patient with acute severe aortic regurgitation. and there are three leaflets of unequal size: the anterior. they attach. chordal thickening. its leaflets are thinner. The PW signal of trans-tricuspid flow is biphasic but varies more with the respiratory cycle than does transmitral flow. and retraction that results in restricted leaflet motion and decreased TV orifice area (Figure 7.

left atrium). M-mode echo The E–F slope of the TV by M-mode echo is reduced. RA. Doppler The Doppler velocity waveform of transtricuspid flow in TS is similar to that of MS. right ventricle. There is severe mitral stenosis and moderately severe tricuspid stenosis (arrow) (RV. LV. damage to the valve leaflets. A mean gradient of 4 mmHg is consistent with severe TS. The TV orifice can rarely be seen from the subcostal short axis view but usually cannot be planimetered. Mild TR occurs commonly in normal individuals. the leaflets are thickened and their mobility is restricted. Annular dilatation results Figure 7. Diastolic doming will be evident on twodimensional imaging in TS (Figure 7. papillary muscles or RV myocardium.45 RA/RV view in diastole showing diastolic doming of the tricuspid valve and moderate tricuspid stenosis. but the peak and mean velocities and gradients are lower (Figure 7. It is present in 90% of patients with a PA systolic pressure 40 mmHg. The slope of trans-tricuspid flow reflects the rate of equilibration of RA and RV diastolic pressures and the orifice area can be calculated from the pressure half-time as TVA 220/P 1/2. Tricuspid regurgitation are enlarged.44 Apical four-chamber view in a patient with rheumatic heart disease. right atrium. This empiric equation is less well validated for TS than MS. LA. and is nearly universal in patients with severe pulmonary hypertension (Figure 7. 101 . A careful examination of the TV is mandatory for all patients with RHD.46). RV size will be determined by the degree of pulmonary hypertension secondary to mitral valve disease and the degree of TR. Pathological TR can result from dilatation of the tricuspid annulus. the apical or subcostal four-chamber views. Figure 7.47).45). left ventricle.VALVULAR HEART DISEASE Two-dimensional echo The M-mode echo features described above are corroborated by two-dimensional imaging of the TV which is optimally visualized either in the parasternal RVIT view.

with RV volume overload.47 Apical four-chamber view with color Doppler showing severe tricuspid regurgitation (TR) (RV. LV. Annular dilatation interferes with normal coaptation of the leaflets resulting in incomplete closure and central regurgitation. right ventricle. radiation therapy. ruptured chords and flail leaflet segments is usually seen in association with MV prolapse. The CW Doppler waveform of TR loses its characteristic bell-shaped appearance and becomes dagger shaped when the tricuspid . Cardiac output is reduced in severe TR and often associated with symptoms of fatigue and effort intolerance. the RV becomes more globular and forms the cardiac apex. Assessment of severity of TR Two-dimensional echo In severe TR the RA and RV are enlarged. The peak diastolic gradient is 16 mmHg. or left-to-right shunting. The peak velocity of the CW Doppler signal of TR in conjunction with an estimate of RA pressure is used to assess PA pressures. LA. Paradoxical septal motion is frequently seen 102 Figure 7. Doppler The severity of TR is graded by the spatial extent of the color disturbance. The MHV and SVC are ideal for PW Doppler interrogation because they are parallel to the ultrasound beam. Severe TR allows RV systolic pressure to be transmitted back into the systemic veins resulting in systemic venous hypertension. Venous hypertension can cause liver and renal dysfunction. or RV biopsy. from RV cavity enlargement. It is 1 if the TR color signal is seen only within 1 cm of the valve and 4 if the color signal is seen throughout the RA. The tricuspid leaflets can be damaged by blunt chest trauma. left atrium). infection. RHD.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. jugular venous distension. left heart failure. Sodium and fluid retention contribute to lower extremity edema. left ventricle.46 Continuous wave Doppler signal of flow velocities through the tricuspid valve in a patient with tricuspid stenosis and regurgitation. Systolic flow reversal in the middle hepatic vein (MHV) and superior vena cava (SVC) are markers of severe TR. ascites. and anasarca in severe TR. and flow reversal causing a pulsatile liver. Myxomatous degeneration of the TV causing prolapse. Severe TR causes the IVC to become engorged and expand in systole. that can be secondary to cor pulmonale.

103 . RA. LV. of the TV and PV and the absence of left heart valve involvement allows carcinoid heart disease to be distinguished from RHD (Figure 7.50 Long axis of the pulmonary artery (PA) in systole showing moderate pulmonic stenosis in a patient with carcinoid heart disease (LV. malignant tumor that secretes a serotoninlike amine and other vasoactive substances that damage the tricuspid and pulmonic valves.50). right ventricle. left ventricle. left atrium). right atrium. Most (90%) carcinoid tumors are located in the gastrointestinal tract but only metastatic carcinoid tumors to the liver cause carcinoid heart disease. Figure 7.49). This characteristic appearance Figure 7.48 Apical four-chamber view showing diastolic doming of the tricuspid valve in a patient with carcinoid heart disease.48) such that TR usually predominates but TS is also present (Figure 7. right ventricular outflow tract). The reason that right heart valves are predominantly affected is because the secreted vasoactive substances are inactivated in the liver and lungs. LA. The peak velocity occurs earlier and the velocity returns to baseline more quickly in severe TR indicating a more rapid equilibration of RV and RA pressures. RVOT. The TV and PV leaflets become thick and ridged and ultimately fixed in a partially opened position (Figure 7.VALVULAR HEART DISEASE regurgitation is severe. Carcinoid heart disease Carcinoid heart disease is caused by a rare.49 Continuous wave Doppler signal of tricuspid stenosis and regurgitation in a patient with carcinoid heart disease. left ventricle. Figure 7. The mitral valve opens normally (RV.

Pulmonic stenosis The PV may rarely become stenosed in RHD but almost all cases of pulmonary stenosis (PS) are congenital in origin (Figure 7. Congenital PS results from fusion of the leaflet tips leaving a central orifice or when the valve is dysplastic. 104 . normal systolic flow across the PV is laminar and less than 0. The right coronary artery is also seen (arrow left panel) (RA. which is aligned with the commissure between the left and right aortic valve cusps. In dysplastic PS the valve is thick and immobile and often associated with annular hypoplasia. right ventricle. The infundibulum has prominent trabeculations. A limb of the septal band extends to the left posterior sinus and trabeculations running parallel to the parietal band extend to the right posterior sinus.9 m/s. aorta). and right posterior. Two leaflets of the PV can be seen bridging the PA in diastole but in systole the leaflets are difficult to distinguish from the walls of the PA. while the aortic valve is pointed to the right shoulder. Color flow Doppler is very sensitive for detecting pulmonary insufficiency (PI) and a minor amount of PI is present in most normal individuals. The PV and PA are ideally situated for Doppler interrogation of blood flow velocity because the PA is parallel to the ultrasound beam in the parasternal short axis of the aortic valve. which extend to the valve sinuses. left posterior.THE ECHOCARDIOGRAPHERS’ GUIDE THE PULMONIC VALVE Anatomy The PV annulus occupies a plane that is offset by 60–90 from the plane of the aortic annulus so that the PV annulus points to the left mid-scapular line facing almost directly posteriorly with a slight leftward and superior tilt.51). The infundibular septum is subjacent to the commissure between the left and right PV cusps. The patient has mild to moderate pulmonary stenosis (arrow right panel). The normal PV has three cusps of approximately equal size: the anterior. This severe Figure 7. AO. The free wall of the infundibulum subtends the remainder of the PV annulus. In this view. The PV is the least well visualized echocardiographically of all the valves in normal patients and the PV cannot usually be visualized in short axis.51 The pulmonary artery (PA) bifurcation is seen in this short axis view.

Two-dimensional echo Two-dimensional echo enables complete assessment of RV size. The peak velocity is approximately 3. semi-quantification of systolic function and direct visualization of the PV leaflets and their excursion. Assessment of severity of PS M-mode echo M-mode echo of PS shows a deep. In carcinoid heart disease. wall thickness.52 Continuous wave Doppler signal of pulmonic stenosis.53). Over time this type of valve becomes fibrosed and thickened and is associated with post-stenotic dilatation of the PA. moderate PS is 50–75 mmHg.VALVULAR HEART DISEASE type of stenosis usually requires relief of the obstruction in infancy. Supravalvular PS may be caused by tubular or shelf-like narrowings. They sometimes occur at the bifurcation causing left or right pulmonary artery stenosis. exaggerated A wave if the leaflet is pliable because with atrial contraction. Mild supravalvular PS sometimes occurs at the site of anastomosis in orthotopic heart transplant recipients (Figure 7. cavity architecture. RVH with abnormal septal thickness and motion are present in proportion to the severity of PS. 105 . The continuity equation is not applied for the determination of PV cross-sectional area because the PW Doppler sample of blood flow obtained in the RVOT is not representative of flow across the lumen and the true diameter of the RVOT is difficult to obtain. The subcostal short axis view of the base of the heart is best for the Doppler evaluation of infundibular stenosis as the ultrasound beam can be aligned parallel to flow. the PV thickens. RVOT obstruction can also occur at the subvalvular level from hypertrophy of the infundibulum muscle bands. which yields a peak gradient of 58 mmHg. A peak systolic gradient greater than 75 mmHg is considered severe. the PV leaflets scar and shrivel and the annulus constricts resulting in PS of mild-to-moderate severity. Pulmonic insufficiency Hemodynamically significant PI is usually secondary to dilatation of the pulmonary Figure 7. Branch stenoses distal to the bifurcation cannot be reliably evaluated with TTE. which can be multiple. This hypertrophy is often associated with valvular PS but may occur in isolation. and mild PS is a gradient of less than 50 mmHg and is generally well tolerated.52). In the nondysplastic type of valvular PS the leaflets are initially mobile with systolic doming.8 m/s. Mild pulmonary insufficiency is also seen. The right pulmonary artery can be seen in long axis from the suprasternal notch projection but the distal left pulmonary artery is rarely seen. Doppler The peak systolic gradient is easily determined by CW Doppler (Figure 7. right ventricular diastolic pressure approaches PA diastolic pressure.

This commonly occurs in pulmonary hypertension and following surgery for tetralogy of Fallot or after a balloon valvuloplasty for PS. Endocarditis of the TV is often associated with intravenous drug use or prolonged use of indwelling catheters. but congenital abnormalities such as PS and tetralogy of Fallot are associated with infective endocarditis of the PV. The TV is usually intrinsically normal when the infection is the result of IV drug use. artery. The severity of PI is assessed from the spatial extent of the Doppler color flow disturbance but this may be misleading as it is often difficult to completely visualize the jet in one plane (Figure 7.54).53 Parasternal short axis view showing the bifurcation of the pulmonary artery (PA). aorta). aorta).54 Parasternal short axis view showing the bifurcation of the pulmonary artery (PA). Figure 7. Color Doppler shows moderately severe pulmonary insufficiency. such as in RV infarction. Ventricular septal defects and patent ductus arteriosus and complex congenital heart disease predispose to endovascular infection. A suture line (arrow) is present in the PA approximately 2 cm distal to the pulmonic valve in this patient with a heart transplant (AO. The PV is the least affected. PI is usually clinically silent. The PA is mildly dilated (AO. 106 ENDOCARDITIS Infective endocarditis is defined as a focal infection of the endocardial lining of the heart usually involving a valve that is damaged or congenitally abnormal. If diastolic retrograde flow in the main branches of the PA is present the PI is at least moderately severe. but severe PI may cause RV volume overload.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. Measurements of the jet width at the annulus and the ratio of jet to annular diameter are the preferred methods. Aortic and mitral valve endocarditis is associated more with incompetent than stenotic valves (Figure 7. The endocardium may . Color Doppler shows moderate pulmonary insufficiency.55). The deceleration slope of PI can be helpful and severe PI will have a rapid slope indicating a rapid equilibration of PA and RV pressures but a rapid PI slope also occurs with decreased RV compliance.

and fibrin. hypermobile masses and Figure 7.56 Parasternal long axis view. Two-dimensional echo A vegetation is a mass of microorganisms. attached to one leaflet or two adjacent leaflets. left atrium.55 M-mode echocardiogram of the mitral valve in a patient with mitral valve (MV) endocarditis. Shaggy echoes on the posterior MV leaflet are consistent with a valvular vegetation. Aortic valve vegetations are usually focal. perforation. The clinical course of infectious endocarditis may be insidious with fever. LA. chordal rupture and flail leaflets and when vegetations mechanically interfere with valve coaptation. A murmur may develop or change in character and initiate an echocardiographic examination for evidence of vegetative endocarditis. The overall mortality for endocarditis is approximately 10%. malaise and weight loss. chills. globular. Vegetative endocarditis can cause acute. Echocardiographically they appear as lowdensity. LV. left ventricle. inflammatory cells. Direct extension of infection to the annulus and surrounding structures is more be damaged by high velocity jets across a VSD or by jets of AR and become the site of infection. There is a large vegetation attached to the aortic valve that prolapses into the LV outflow tract in diastole (RV. AO. and shock culminating in irreversible heart failure. right ventricle. aorta). They are associated with AR of varying severity and appear as shaggy masses attached to the cusps that often prolapse into the LVOT in diastole (Figure 7. Endocarditis causes valve dysfunction through leaflet destruction. Patients with hypertrophic cardiomyopathy are prone to endocarditis due to abrasion of the mitral valve from systolic contact with the septum and damage to the aortic valve from the high velocity systolic jet.VALVULAR HEART DISEASE Figure 7. severe valvular regurgitation from destruction of the valve leaflets. They are usually attached to the undersurface of a valve (i. platelets.56).e. septicemia. exhibit chaotic high-frequency oscillations. the atrial aspect of the mitral valve or the ventricular side of the aortic valve) but can also be attached to the endocardial surface of a cardiac chamber or to the chordal apparatus. Aortic valve vegetations may involve the anterior MV leaflet or chordal structures from the AR jet or spread directly through the intervalvular fibrosa. 107 . Aortic valve vegetations and flail aortic valve leaflets are best seen in the parasternal long-axis view.

There is a large. left ventricle. They are focal and attach to the atrial side of the valve leaflets. septated abscess (AB) is seen adjacent to the aortic valve annulus. Thickening of the aortic root. New AV block or bundle branch block suggests abscess formation. AO. which are indications for emergency surgery. common in the aortic than other valves and may result in the formation of abscess (Figure 7. mobile vegetation attached to the anterior mitral valve leaflet (arrow) (LV. pericardium or other cardiac chamber.57 Parasternal short axis view.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. fistula. Figure 7. LA. Vegetations most commonly affect the mitral valve (Figure 7. left atrium. A large. This patient had acute severe aortic regurgitation and required emergent surgery (LA.57) or fistulous communication to the myocardium. near the membranous septum and AV node. compression of the coronary ostia or pseudoaneurysm. left atrium. aorta).58).58 Parasternal long axis view. Vegetations may occasionally be large enough to cause LVIT obstruction. 108 . aorta). AO. There is a large mobile aortic valve vegetation (arrow). vegetations attached to the annulus or echolucent pockets adjacent to the annulus suggest perivalvular spread of the infection and abscess formation that requires emergent TEE. TEE is superior to TTE for assessing perivalvular abscess. Periannular extension of aortic valve infection often occurs at the weakest portion of the annulus.

Pericardial effusion in the setting of mitral or aortic endocarditis suggests a communication between an abscess and the pericardium or concomitant purulent pericarditis. Vegetations 10 mm in diameter Figure 7. LA. The mitral valve is densely calcified (RV. Isolated endocarditis of the PV (Figure 7. pulmonary artery. TV endocarditis is rarely associated with intracardiac abscess formation.60) is extremely rare even in intravenous drug users but PV vegetations may rarely coexist with vegetations on the other valves. Right heart endocarditis accounts for 10% of all cases of endocarditis and has a 10% in-hospital mortality. right ventricle. Mechanical destruction of the MV. 109 . and location. mobility. or avulsion. such as chordal rupture. Vegetations in fungal endocarditis tend to be large. acutely increases MR severity and can cause LV dysfunction and heart failure.60 Parasternal short axis view.61). aorta). calcification and myxomatous degeneration of the MV. Early use of antibiotics reduces the risk of embolization. A vegetation (arrow) is identified on the pulmonic valve (RV. LA. TV vegetations tend to be large and are seen on the atrial side of the valve where they may be confused with RA thrombus. and those that are mobile or pedunculated are at increased risk of embolization. AO. left atrium. There is a vegetation (arrow) attached to the tricuspid valve causing severe tricuspid regurgitation. Serial echocardiograms are clinically useful for monitoring response to therapy.59 Apical four-chamber view. leaflet perforation.VALVULAR HEART DISEASE Endocarditis most commonly occurs on damaged valves and it may be difficult to distinguish small vegetations from focal leaflet thickening. Figure 7. LV. PA.59). Most cases involve the TV alone (Figure 7. The risk of embolization of vegetations is determined by their size. right atrium. mobile and echo-dense with a heterogeneous echo texture (Figure 7. RA. right ventricle. Periannular extension of MV infection occurs more commonly with prosthetic valves but may affect native valves. although myxomatous degeneration is usually nonfocal. left ventricle. left atrium). MV vegetations embolize more frequently than aortic vegetations particularly if the vegetation involves the anterior MV leaflet.

are prone to embolization and are associated with minor valvular regurgitation. LA. when the TTE is negative but clinical suspicion is high and when prosthetic valve endocarditis or perivalvular infection/abscess are suspected. multiple vegetations. embolization is rare and this form of endocarditis is usually clinically silent. left atrium. and embolization are common features of NBTE. but multiple valve involvement. They are prone to perivalvular spread and embolization. The left heart valves are more commonly affected. Infective endocarditis cannot be definitively excluded by TTE alone on native or prosthetic valves particularly when image quality is technically limited. They may be multiple. 3–4 mm in size. prolonged use of indwelling catheters. Lambl’s excrescences are filamentous structures that project linearly from the tips of the valve cusps that are seen usually in elderly people by TEE or rarely by TTE and should not be mistaken for vegetations. Libman–Sacks verrucous endocarditis is a NBTE occurring in systemic lupus erythematosus. disseminated intravascular coagulation and other hypercoagulable states. appear on the valvular or mural endocardial surface of the heart associated with mild MR or AR. Fibroelastomas are rare benign tumors composed of connective tissue that can attach to any of the heart valves and can be difficult to distinguish from vegetations. AO. LV. immunosuppression. TEE VERSUS TTE IN ENDOCARDITIS The specificity of TTE for detecting vegetations in patients with proven endocarditis is approximately 98% but its sensitivity is only 60–70%. prolonged use of antibiotics. Fungal endocarditis is associated with negative blood cultures. right ventricle. TTE cannot usually detect vegetations less than 3 mm in diameter. The posterior MV leaflet is most commonly affected. When TTE clearly visualizes valvular anatomy there is no indication for TEE NONBACTERIAL THROMBOTIC ENDOCARDITIS Nonbacterial thrombotic endocarditis (NBTE) or marantic endocarditis is not caused by an infecting organism but is associated with malignancies. Loffler’s endocarditis is a manifestation of the hypereosinophilic syndrome. and the implantation of cardiac devices.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. The mortality for fungal endocarditis is greater than for bacterial endocarditis and valve surgery is almost always necessary.61 Large vegetations are present on the aortic and mitral valves of this patient with fungal endocarditis (RV. which is discussed in Chapter 8. typically have multiple frond-like excrescences that exhibit chaotic motion. aorta). 110 . They occur most frequently on the aortic valve. Friable vegetations composed largely of platelets and fibrin form on but do not destroy the valve leaflets. left ventricle. Wart-like vegetations composed of fibrin. TEE is as specific as TTE and its sensitivity is 90–95%. In most cases TEE is not indicated as the initial exam for endocarditis but becomes necessary when TTE is nondiagnostic.

Similarly. surgery that spares and realigns the aortic valve leaflets while repairing or replacing the aortic root is often applicable in aortic root dissection or dilatation. However. (C) Carpentier–Edwards bovine pericardial valve.62 Prosthetic heart valves. an autograft is a valve that is translocated from one position in the heart to another. Similarly. If replacement is necessary. Neither TTE nor TEE can distinguish between healed or active vegetations. The biologic tissue in valves like the Carpentier–Edwards porcine valve (Figure 7. A homograft is a valve from a human donor. (A) Starr–Edwards ball and cage valve. TTE can guide and focus the TEE and should be done prior to TEE except in MV prostheses where TTE is unable to visualize the atrial surface of the valve due to shadowing and reverberation artifact. the biologic leaflets are prone to progressive calcification and rigidity that can result in 111 . homografts. Biologic prostheses contain some biologic tissue. (D) St Jude bileaflet mechanical valve. porcine valve cusps or bovine pericardium shaped for use as valve leaflets.62): biologic heterografts. (B) Bjork–Shiley tilting disk valve. SURGICAL TREATMENT OF VALVULAR HEART DISEASE Valve repair is preferred to replacement for mitral and tricuspid valve disease and a variety of surgical techniques are used including chordal lengthening or shortening procedures. regurgitation through a prosthetic MV can be difficult to detect with TTE but can be reliably assessed by TEE. and mechanical valves. and they are usually mounted onto a clothcovered sewing ring or stent. Figure 7.63) and the Ionescu–Shiley bovine pericardial valve are resistant to thrombosis compared to mechanical valves and anticoagulation is not required after the immediate postoperative period. surgery that retains chordal integrity is preferred as cutting the chordae prevents the muscle fibers that attach to the cardiac skeleton by way of the papillary muscles from contributing effectively to contraction and maintaining LV shape. which usually involves the implantation of an annular ring. such as in the Ross procedure where the PV is used to replace the aortic valve and the PV is replaced with a homograft. quadrangular or triangular leaflet resection and often reduction in the annular circumference. chordal translocation and insertion of artificial chords. which can distinguish the normal central regurgitation of some prostheses from pathological regurgitation. There are three types of valve prosthesis in general use (Figure 7. Valve replacement surgery has proved to be vastly superior to medical management for patients with advanced valve disease and about 80 different models of valve prostheses have been developed and approved for use for valve replacement. A negative TEE does not always exclude the diagnosis of early or nonvegetative endocarditis and should be repeated within 7–10 days if clinical suspicion persists.VALVULAR HEART DISEASE unless periannular abscess or fistulae are suspected. Mechanical prostheses are composed primarily of metal or pyrolytic carbon and like biologic valves are generally sutured to the valve annulus using a fabric-covered sewing ring after the diseased valve has been removed.

Evidence of valvular obstruction can be determined by Doppler interrogation. mobile. There are three types of occluder: central occluders. Tilting disk valves such as the Bjork–Shiley and the Omniscience valve have a single wafer-thin disk that pivots on a hinge or strut with an opening angle of 60–70 and provide good central flow. Homografts are aortic valves within their proximal aortas that are harvested from human cadavers. masses attached to the prosthesis establishes the diagnosis of thrombus. An M112 mode directed from the apex is ideal for the timing of valve opening and closure in this type of valve.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. It has no record of structural failure but it offers significant obstruction to central flow. Bileaflet mechanical prosthetic valves have two occluding leaflets made of pyrolytic carbon. When anticoagulated. and bileaflet valves. They are the most commonly used valves for the aortic position. but thrombus must be differentiated from pannus on an obstructed mechanical valve. Thrombosis of a prosthetic valve may cause acute hemodynamic deterioration or it may present with gradually worsening symptoms of heart failure.63 M-mode echocardiogram through a normally functioning porcine valve in the mitral position. monoleaflet tilting disk valves.64). Mechanical valves are thrombogenic and require anticoagulation (Figure 7. with a life expectancy of 20–30 years. TEE is required for adequate visualization of a mechanical mitral prosthesis and usually required for prostheses in other positions. Mechanical heart valves are rarely used in the right heart because low velocity flow is prothrombotic. and an occluder within the housing. They have low risk of thrombosis and infection and because they have no sewing ring they have larger effective orifice areas than stented bioprostheses. The visualization of multiple. a housing. Their resistance to infection makes them . The motion of the central occluders in the left heart valves is toward and away from the apex. As with most mechanical valves. The Starr–Edwards valve with a ball and cage central occluder was first implanted in 1968 and is still being used today. All mechanical prostheses consist of a sewing ring. approximately 1% per year. trivial regurgitation in bileaflet valves is built-in to minimize thrombosis. Mechanical prostheses are more durable than biologic valves. the risk of an embolic event in a patient with a mechanical valve is similar to that of a patient with a biologic valve. Structural failure is usually due to progressive aortic root dilatation with aortic regurgitation. Their supply is limited but they are used in aneurysms or dissections of the proximal aorta when aortic repair and valve resuspension cannot be performed and in patients with small aortic roots. Pannus formation is the gradual ingrowth of fibrous tissue over the sewing ring seen in both biologic and mechanical valves that can cause obstruction to flow and serve as a nidus for thrombus. which tilt open in parallel and offer trivial resistance to forward flow. in which a ball or a disk moves forward within the housing to permit forward flow and is pressed back toward the sewing ring to prevent regurgitant flow. prosthetic stenosis. tearing of the leaflets and valvular regurgitation or more rarely.

Prosthetic valvular endocarditis Endocarditis affects approximately 1–1. This usually occurs in valve replacement for AS.66). especially useful in active endocarditis complicated by abscess or dehiscence of a prosthetic valve. and perivalvular regurgitation result 113 . has a low risk of infection and provides excellent hemodynamic results with no LVOT gradient. there is less clinical improvement and incomplete regression of LVH. which is often associ- ated with annular calcification and LVH and results in a prosthesis–patient mismatch. The infection usually begins at the sewing ring where the valve is anchored to the annulus. Bileaflet mechanical valves have larger effective orifice areas (EOA) than stented biologic prostheses and ball and cage valves. The prosthesis is encased in thrombus and cannot open fully (RV. is a PV autograft to the aortic position with a homograft to the pulmonic position.65) and annulus is much lower than for mechanical valves.64 Parasternal long axis view. Apart from the cloth-covered sewing ring the material in mechanical prostheses does not allow adherance of microorganisms when it is free of thrombus. All aortic valve replacements with the exception of homografts and stentless heterografts are inherently stenotic. which exists when the valve is too small for the patient. left atrium). In biologic valves the infection is generally confined to the leaflets and the risk of spread to the sewing ring (Figure 7. (A) Bjork–Shiley tilting disk valve is in the mitral position. It is particularly beneficial for children requiring aortic valve surgery because the PV graft retains the ability to grow. left ventricle. The risk of endocarditis is lowest in homografts. LV. Valve gradients vary with EOA and can be high despite normal prosthetic function depending on the valve type and size. In prosthesis–patient mismatch the gradients are higher. When the annular size is reduced it may be necessary to insert a smaller than optimal replacement. LA.VALVULAR HEART DISEASE Figure 7.5% of prosthetic valves per year. first performed in 1967. Vegetations may intrude on the valve cusps or occluders and interfere with valve closure or more rarely valve opening. Abscess (Figure 7. right ventricle. It does not require anticoagulation. The procedure is technically demanding and late complications include progressive aortic dilatation with AR and PS.67). The Ross procedure. fistula formation (Figure 7.

THE ECHOCARDIOGRAPHERS’ GUIDE Figure 7. A periannular abscess (*) has developed from infection of the sewing ring of the bioprosthesis (RA. pulmonary artery). AO.67 Parasternal short axis view. Figure 7. aorta). LA. LV. PA. Doppler/echocardiography is used to evaluate prosthetic valves in the same way that it is used to evaluate native valves but technical factors can make the evaluation of prosthetic valves more difficult. PA. right atrium. left atrium. left atrium. Partial dehiscence of the prosthesis secondary to annular necrosis can cause rocking of the sewing ring when 40% of annulus is dehisced. Mitral prostheses are occasionally sewn to a small rim of leaflet tissue rather than the annulus when the annulus is calcified and this increases the mobility of the sewing ring but it should not be confused with the rocking of a dehisced valve. AO. 114 . Color flow Doppler reveals a fistulous communication (arrow) between the left ventricular (LV) outflow tract just proximal to the biologic aortic prosthesis and the right atrium (RA) (RV. pulmonary artery. LA. right ventricle. left atrium. from annular necrosis and can cause prosthetic valve dehiscence. left ventricle. LA.66 Parasternal long axis view of a periannular abscess (arrow) adjacent to the sewing ring of a biologic aortic valve prosthesis (RV. right ventricle. Subclinical hemolysis can be detected in the majority of patients with a normally functioning mechanical valve but severe hemolytic anemia is rare and is usually associated with perivalvular regurgitation and the need for reoperation. Figure 7.65 Parasternal short axis view. aorta). Mechanical valves make imaging difficult because of shadowing and reverberation artifacts.

Echocardiographic assessment in the early postoperative period before discharge is invaluable as a baseline for future comparison. Doppler examination of eccentric jets from valves with central occluders may underestimate true pressure gradients.VALVULAR HEART DISEASE whereas biologic leaflet tissue may be obscured by echoes from the sewing ring. Despite these limitations a combination of TTE and TEE is almost invariably successful in evaluating prosthetic valve function. hemodynamics and the complications of replacement. In patients with aortic valve replacements the posterior aortic root is not well seen by TTE and the anterior aortic root is not well seen by TEE. 115 . Scarring from the surgery often hampers TTE and post-operative images from the right parasternal window are usually limited. whereas elevated gradients due to pressure recovery distal to the minimal valve orifice are seen in some valves.

.

and diastolic and systolic dysfunction but there is some overlap between the groups.1). parasitic infections or infiltrative processes. 117 . and restrictive (RCM) and these are defined by characteristic abnormalities of ventricular architecture. A pleural effusion (PL) is seen posterior to the LV (LA.1 Parasternal long axis view in a patient with left ventricular (LV) systolic dysfunction secondary to X-radiation therapy. The three types of CM are dilated (DCM). hypertrophic (HCM). such as ischemic CM or left ventricular dysfunction attributable to cardiotoxic agents (Figure 8.8 CARDIOMYOPATHIES CONTENTS q Dilated Cardiomyopathy Cardiomyopathy q Hypertrophic Cardiomyopathy q Restrictive The term cardiomyopathy (CM) should be reserved for primary diseases of the myocardium of unknown etiology but it is often applied to conditions whose cause is known. Figure 8. left atrium).

Approximately 20% of patients with DCM have a first-degree relative with evidence of DCM.8 cm) and the percent fractional shortening is decreased. Myocarditis from a viral infection is an important cause of DCM. aorta). progressive LV enlargement is followed by left atrial (LA) enlargement. Typically. Regardless of the etiology. About 15% of patients with myocarditis progress to DCM. The left ventricular cavity is enlarged (left ventricular internal dimension at enddiastole 7. Its exact etiology is unknown in most cases. Figure 8. ventricular arrhythmias and sudden death or there may be a long latent period. Ejection fraction falls and LV volumes rise as wall stress increases. but there is an important genetic component. right ventricle. 118 .3 Parasternal long axis view in a patient with dilated cardiomyopathy. Patients with myocarditis may present with severe biventricular congestive heart failure (CHF).THE ECHOCARDIOGRAPHERS’ GUIDE DILATED CARDIOMYOPATHY DCM affects 40–50 people per 100 000 population. As the LV enlarges it becomes more spherical and orientation of the papillary muscles to the annulus is changed. left atrium.2 M-mode echocardiogram in a patient with dilated cardiomyopathy. Stroke volume is preserved at the expense of ejection fraction. which is secondary to Figure 8. There is myocardial involvement in 5% of all viral illnesses. the heart responds to damage with cavity enlargement. LV. elevated filling pressures and mitral regurgitation (MR). LA. which is a stimulus for LV hypertrophy but the increased wall thickness is often inadequate to normalize wall stress. AO. The LV is markedly enlarged and LV global systolic function is severely impaired (RV. Left ventricular (LV) cavity enlargement causes increased wall stress. left ventricle.

hypocontractile LV is predisposed to thrombus formation and thromboembolism may occur at any stage of the disease. 8.2.CARDIOMYOPATHIES Figure 8. 119 . right ventricle. which are progressive. In short axis at the level of the aorta and LA. The relative wall thickness is greatly decreased. RA. Enlargement of the right heart chambers may be due to the myopathic process but it is usually secondary to elevated pulmonary pressures. left ventricle. resulting in mal-coaptation of the leaflets with central MR. but arrhythmias and sudden death may be the first symptoms. LV diastolic volume is 1 L (RV.4 M-mode echocardiogram of the mitral valve in a patient with dilated cardiomyopathy. Interventricular septal motion is often abnormal because of left bundle branch block (LBBB) or nonspecific intraventricular conduction delay. the M-mode demonstrates LA enlargement.4) and there may be an A–C shoulder indicating an increased LV end-diastolic pressure (LVEDP). Systolic dysfunction is almost always global (Figure 8.5). reduced anterior motion of the aorta during systole and there may be truncation of the aortic valve motion pattern in systole indicating reduced forward flow. Patients usually present with symptoms of CHF. There is four-chamber enlargement but left heart chamber enlargement predominates. Echocardiographically. An M-mode of the mitral valve displays an increased E-point–septal separation (Figure 8. The E point septal separation is increased and the fractional shortening is greatly diminished.5 Apical four-chamber view in a patient with dilated cardiomyopathy. left atrium). Two-dimensional echocardiography demonstrates variable degrees of fourchamber enlargement. Figure 8. LV enlargement and decreased systolic function are the major findings in DCM. right atrium. LV. LA.3). An M-mode echocardiogram at the ventricular level demonstrates cavity enlargement and decreased fractional shortening (Figures 8. The dilated.

5. The apical short axis is especially useful for this. Figure 8. The diagnosis of apical mural thrombus should only be made when the thrombus is seen in two different and preferably orthogonal echocardiographic planes. which become prominent when the LV dilates. Alcohol depresses myocardial contractility acutely even in non-alcoholic normal volunteers.7). LV. dyspnea on exertion.6). Thrombus typically forms at the apex and apical mural thrombus must be distinguished from apical trabeculations. 120 . Biventricular enlargement. the progression of alcoholic DCM can be slowed and sometimes reversed with total abstinence in the early stages. right ventricle.7 The restrictive pattern of transmitral flow is often seen in dilated cardiomyopathy and reflects increased left ventricular enddiastolic pressure and the effects of the mitral regurgitant volume. edema. decreased LV systolic function and symptoms of heart failure. some distinct etiologies deserve emphasis.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 8.8). There is moderately severe mitral regurgitation (MR) (RV. The right ventricle (RV) is dilated to a variable degree and the angle of the moderator band to the Alcoholic cardiomyopathy accounts for approximately a third of all cases of DCM. orthopnea. Unlike other forms of DCM. and fatigue can progress gradually or rapidly. The restrictive pattern of transmitral flow with an augmented E wave and rapid deceleration is often present and reflects increased LVEDP and the effects of the mitral regurgitant volume (Figure 8. Cardiac enlargement and subclinical myocardial depression can be appreciated in alcoholics without cardiac symptoms. Tricuspid regurgitation (TR) is also very common and pulmonary artery pressure should be estimated from the peak TR jet velocity (Figure 8. left ventricle). Alcoholic cardiomyopathy Spontaneous echo-contrast is often seen when LV enlargement and systolic dysfunction are severe and are associated with increased risk of thrombus formation.6 Same patient as in Figure 8. A central jet of MR is almost invariably present in DCM and may be severe (Figure 8. interventricular septum may approach 90 in marked RV enlargement but LV enlargement predominates and the RV does not become apex forming. It can be difficult to distinguish primary DCM with MR from chronic severe MR with secondary LV dysfunction. Despite the nearly identical cardiac morphology and common clinical path in different forms of DCM.

8 Moderately severe tricuspid regurgitation is seen with color Doppler in this apical four-chamber view in a patient with dilated cardiomyopathy (RV. Figure 8. and progress to death or cardiac transplantation (Figure 8. right atrium. HIV/AIDS cardiomyopathy Human immunodeficiency virus (HIV) DCM accounts for 3–4% of all cases of DCM and is the cause of a third of HIV-related deaths. left atrium). left ventricle. Most women have a full clinical recovery with return to normal of LV size and function usually within 6 months of delivery. LV.9). LA. some patients continue to deteriorate. 121 . HIV DCM occurs late in the course of the disease.CARDIOMYOPATHIES Peripartum cardiomyopathy DCM that presents in the last trimester of pregnancy or within the first few months post-partum is termed peripartum cardiomyopathy and is indistinguishable from idiopathic forms of DCM.9 Apical four-chamber view in a patient with peripartum cardiomyopathy (RV. Anthracycline cardiomyopathy Doxorubicin and daunarubicin are anthracyline chemotherapeutic drugs that have a Figure 8. left ventricle. right atrium. left atrium). right ventricle. RA. LA. right ventricle. LV. However. RA.10). is associated with a greatly decreased CD4 count and has a higher mortality than other forms of DCM (Figure 8.

left ventricle. It is caused by the hemoflagellate protozoan. The LV myocardium in anthracycline cardiomyopathy is highly echo-reflective (Figure 8. The RV apex may also be aneurysmal and apical thrombus and . Figure 8. sudden death. systolic volume is increased with little increase in diastolic volume and there is further cavity enlargement over time. Trypanosoma cruzi. that enters the body with the bite of a blood-sucking insect.10 A long axis view from a low transducer position demonstrates very poor global systolic function in this patient with HIV/AIDS.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 8. similar to those caused by apical myocardial infarction. left ventricle. or with biventricular failure. left atrium). Initially. A left pleural effusion (PL) is seen posterior to the LV (DAO. may also be present.11 Parasternal long axis view in a patient with dilated cardiomyopathy from adriamycin cardiotoxicity (LV. LV. There may be four-chamber dilatation indistinguishable from other types of DCM. dose-related cardiotoxicity. Chagas’ disease Chagas’ disease is a major health problem in Central and South America affecting as 122 many as 20 million people. the reduviid bug. LA. irreversible LV systolic dysfunction. They can cause global. but apical aneurysms. LA. left atrium). descending aorta. Chagasic myocarditis can present with incessant ventricular tachycardia or other arrhythmia.11).

left atrium. It is linked to the X chromosome. The LV lateral and posterobasal walls and posterobasal papillary muscle are progressively replaced with fibrous tissue resulting in segmental dysfunction. aorta). Prolonged tachyarrhythmias Prolonged rapid atrial pacing ( 180 bpm) can produce models of DCM in experimental animals and DCM can be caused by prolonged tachyarrhythmias in humans. particularly in children.12).12 Parasternal long axis view in a patient with global left ventricular (LV) systolic dysfunction (A) associated with prolonged bouts of SVT. AO. 123 . affecting young males and typically affects the heart at the onset of puberty. or even atrial fibrillation can cause DCM. Incessant or repetitive episodic ventricular tachycardia. which may become global as the LV enlarges and systolic function deteriorates. Figure 8.CARDIOMYOPATHIES systemic and pulmonary thromboemboli are common. supraventricular tachycardia. which is often reversible with the restoration of normal heart rate and rhythm (Figure 8. Muscular dystrophies Duchenne muscular dystrophy and the less severe Becker muscular dystrophy cause pseudohypertrophy and atrophy of the skeletal muscle as muscle fibers are surrounded by fat and fibrous tissue. Systolic function returned to normal (B) with resolution of the arrhythmia (LA.

arrhythmias. and thromboembolism. Systolic function is normal or supernormal but diastolic dysfunction is common. which communicate with the coronary circulation. Intratrabecular recesses are prone to thrombus formation. posterior septum. The hypertrophied interventricular septum budges into and narrows the LVOT. 124 . whereby the myocardium is not uniformly compacted and large intertrabecular sinusoids persist (Figure 8. The sinusoids are distinct from those of the ‘spongy myocardium’ seen in severe congenital aortic stenosis. The noncompaction predominates at the apex and at the mid-lateral and mid-inferior walls but systolic dysfunction is global and not limited to those regions. The papillary muscles are often hypertrophied Figure 8. LV hypertrophy (LVH) is genetically determined and occurs in the absence of any hemodynamic stimulus. a thin compacted epicardial layer and an endocardial layer that is not compacted but composed of a loose network of hypertrophied trabeculations and endomyocardial recesses that communicate with the LV cavity. In some cases hypertrophy is limited to the upper anterior septum resulting in disproportionate upper septal thickness (DUST) or the hypertrophy may extend to the LV free wall. This variant. In hypertensive hypertrophic disease of the elderly the upper septum is disproportionately thickened and angled into the LV outflow tract (LVOT).14).THE ECHOCARDIOGRAPHERS’ GUIDE LV noncompaction LV noncompaction is a rare congenital abnormality. Half of all referrals for cardiac transplantation are for DCM and while heart transplantation offers an 85% 1-year and 68. and CHF are common in this condition. only about 2000 heart transplants are performed annually in the United States due to the shortage of donors. The endocardial layer is generally at least twice the thickness of the epicardial layer. known as ‘spade heart’ because of the characteristic shape of the LV cavity is associated with giant inverted T waves in the lateral precordium on the electrocardiogram (EKG). inferior wall. Typically.5% 5-year survival rate.15). HYPERTROPHIC CARDIOMYOPATHY In HCM. Left ventricular remodeling and not contractile dysfunction is now recognized as the principal lesion in DCM and in other etiologies of systolic failure and this view has led to the development of surgical and device-based therapies that can return the failing heart to a more normal size and geometry. right ventricle. the anterior interventricular septum is predominantly affected and asymmetric septal hypertrophy (ASH) is present (Figure 8. LA. This condition is more common in women and associated with concentric LVH and aortic root dilatation secondary to hypertension. The noncompacted layer is composed of a dense network of trabeculations and endocardial recesses in communication with the LV cavity (RV. Hypertrophy confined to the apex accounts for approximately 2% of HCM cases in the United States but up to 25% of HCM cases in Japan (Figure 8. left atrium).13 Apical four-chamber view in a patient with left ventricular (LV) noncompaction cardiomyopathy. The LV myocardium is divided into two layers. or RV free wall while the posterior wall is usually spared.13).

CARDIOMYOPATHIES Figure 8. 125 . left atrium). The interventricular septum (black arrow) is massively thickened at 3. LA. LV. The apex is hypertrophied and there is a systolic disturbance in the color Doppler signal near the apex caused by systolic entrapment of blood between the hypertrophied apical walls (RV. LA.14 Parasternal long axis view in a patient with hypertrophic cardiomyopathy.5 cm in diastole (LV. right atrium. Figure 8. RA.15 Apical four-chamber view in a patient with apical hypertrophic cardiomyopathy or spade heart. left atrium). left ventricle. right ventricle. left ventricle.

Neither ASH nor dynamic LVOT obstruction with SAM is completely sensitive and specific for HCM. left atrium). and displaced anteriorly and superiorly. There is massive septal hypertrophy but no systolic anterior motion of the mitral valve and no left ventricular outflow tract obstruction (LV. Freidreich ataxia. A proportion (10–15%) of patients with Figure 8.17 Parasternal long axis view in a patient with nonobstructive hypertrophic cardiomyopathy. These factors cause dynamic subaortic LVOT obstruction that varies through systole in some patients with HCM. left ventricle.16 Parasternal long axis view in a patient with obstructive hypertrophic cardiomyopathy. Patients with HCM are often characterized as having obstructive (HOCM) or nonobstructive (HNOCM) types (Figure 8. The mitral leaflets and chords are elongated in half of all patients with HCM and the point of coaptation is abnormal. Systolic anterior motion of the mitral valve blocks the left ventricular outflow tract (LV. occurring at the body of the leaflets rather than at their tips. left ventricle. This displacement of the mitral valve is referred to as systolic anterior motion (SAM) (Figure 8. LA.17) but the presence and severity of a LVOT obstruction is dynamic and can be altered by changes in LV loading conditions.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 8. left atrium). Factors that decrease preload or afterload or increase contractility or heart rate reduce end-systolic volume and increase the gradient in patients with obstruction or may provoke an obstruction in a patient who has HNOCM.16) which causes obstruction to outflow and a posteriorly directed MR jet. glycogen and lipid storage diseases. ASH is also seen in amyloid. 126 . The increased systolic flow velocity through the narrow LVOT pulls the portion of the mitral valve apical to the coaptation point into contact with septum by the Venturi effect. LA. and pheochromocytoma.

SAM is absent in the majority of patients with HCM but can be provoked in many patients without HCM by dobutamine. Dyspnea is common in patients with HCM and is usually attributable to increased LA pressures secondary to poor diastolic function and/or MR. particularly in endurance athletes with physiologic hypertrophy.CARDIOMYOPATHIES systemic or renovascular hypertension have ASH rather than concentric hypertrophy. HCM in children will sometimes present with RVOT obstruction mimicking congenital infundibular stenosis. Arrhythmias are common in HCM. Ischemia can cause angina in HCM in the absence of epicardial coronary disease.5 cm) but systolic thickening is decreased. In approximately 5% of patients with HCM. particularly VF and VT. Figure 8.18 Mid-systolic notching on the aortic valve Mmode in a patient with hypertrophic cardiomyopathy and dynamic left ventricular outflow tract obstruction. Syncope is usually associated with arrhythmias or may be caused by transient increases in LVOT obstruction. The interventricular septum is usually thick (greater than 1.18). Regions of myofibrillar disarray and fibrosis are substrates for arrhythmias. The MV Mmode shows SAM (Figure 8. Atrial fibrillation can cause severe clinical deterioration and heart failure and increases the risk of thromboembolism. The symptoms of HCM are similar to those of aortic stenosis: syncope. and HCM is the most common cause of sudden cardiac death in the young. and angina. Severe symptomatic CHF is rare except in atrial fibrillation and in a subset of patients with end-stage disease. dyspnea. 127 .19 M-mode echocardiogram at the mitral valve (MV) level demonstrating systolic anterior motion of the MV and systolic anterior motion septal contact (arrows). ASH also occurs in RV pressure overload and in normal subjects. Sudden cardiac death is common in HCM especially with exertion. M-mode echocardiographic examination demonstrates LA enlargement secondary to MR or decreased LV compliance and the aortic valve often closes in mid-systole reflecting the time course of the dynamic LVOT obstruction (Figure 8. progressive LV systolic dysfunction develops with wall thinning and cavity enlargement resembling DCM.19) and the duration of mitral–septal contact in HOCM. SAM is absent in hypertrophic HNOCM. Septal hypomobility permits Figure 8. LVH can compress intramuscular coronaries and there is a mismatch between coronary blood flow and increased LV mass.

5 cm. The parasternal long axis view reveals the base to apex extent of the hypertrophy. propagation Figure 8. Septal thickness greater than 3. left atrium). LA. and therefore it is relatively unloaded.3:1. The myocardium has an abnormal acoustic signature that is echobright and has a speckled or granular appearance. 128 .0 cm at end-diastole is associated with increased risk of sudden death. Left ventricular (LV) systolic function is supernormal (RV. Diastolic dysfunction is the hallmark of HCM and should be carefully assessed with pulsed-wave (PW) Doppler of transmitral and pulmonary vein flow. LV internal diameter in diastole is almost always less than 4. ASH is defined as a ratio of septal to posterior wall thickness of 1. This type of brightly reflecting myocardium is also seen in patients with cardiac amyloid and in some patients with chronic renal failure. its systolic excursion is relatively unopposed. Figure 8.20 Parasternal short axis view in a patient with hypertrophic cardiomyopathy and marked asymmetric septal hypertrophy. The point of SAM–septal contact can be precisely identified in the parasternal or apical long axis view (Figure 8.21 Apical long axis view in zoom mode showing SAM–septal contact (LV.20). Anterior displacement of the mitral valve and subvalvular apparatus will be seen. left ventricle. right ventricle). allowing ASH to be distinguished from DUST and serial short axis images demonstrate its circumferential involvement (Figure 8.THE ECHOCARDIOGRAPHERS’ GUIDE hyperdynamic posterior wall motion.21) and a small echo-bright friction lesion or callous on the septum or rarely on the MV can sometimes be seen at this point of contact.

the right parasternal and especially suprasternal approaches are generally not helpful. Combined subaortic and valvular aortic stenosis can coexist and the late peaking flow from the subaortic stenosis can be superimposed on the more symmetrical envelope of the valvular stenosis. inhalation of amyl nitrate. 129 . AO. The subaortic gradient can be assessed with continuous wave Doppler from the apical window. abnormalities in TDI strain and strain rate imaging are present in carriers of the HCM genotype prior to the development of hypertrophy when other echo/Doppler findings are normal. Figure 8. In the apical variant of HCM a small turbulent jet may be appreciated in the LV cavity near the apex. Color Doppler interrogation of the LVOT is performed in long axis views from the apical and parasternal windows and turbulent blood flow is seen in systole beginning at the point of SAM–septal contact. left atrium.23 Continuous wave Doppler of the left ventricular outflow tract in a patient with hypertrophic cardiomyopathy. The gradient peaks in late systole and the LVOT spectral envelope has a dagger shape (Figure 8. aorta). and tissue Doppler imaging (TDI) in patients suspected of having this disease. TDI may be especially useful in evaluating patients with HCM. Both longitudinal TDI diastolic velocities from the apical window and transmural TDI velocity gradients across the posterior wall from the parasternal window can differentiate the pathologic hypertrophy of HCM from the physiologic LVH of athletes. The peak pressure gradient is 88 mmHg. Mitral regurgitation is invariably present when there is obstruction and the severity of MR is related to the degree of obstruction. A gradient may be provoked with maneuvers that decrease LV systolic volume.22 Parasternal long axis view in systole with color Dopper in a patient with obstructive hypertrophic cardiomyopathy showing turbulent flow in the left ventricular outflow tract (white arrow) and a posteriorly directed jet of mitral regurgitation (black arrow) (LV. The velocity reaches a maximum in late systole. The MR jet in HOCM is posteriorly directed (Figure 8. In addition. which decreases both pre. left ventricle.and Figure 8. If the jet is more complex.CARDIOMYOPATHIES velocity.22). Mild aortic regurgitation (AR) is present in a quarter to a third of patients with HOCM and probably reflects damage to the aortic valve caused by the high velocity systolic jet. such as. Patients with no gradient at rest may demonstrate a gradient with a change in loading conditions. LA.23). there may be another etiology for the MR.

RCMs can be divided into two principal categories. RA. The left panel is the baseline prior to the procedure. Gradient reduction and symptomatic improvement with this technique is similar to that with surgical myotomy-myectomy but neither technique alters the natural history of the disease. The LV systolic function may be normal or decreased and if decreased it may be globally or regionally affected. right atrium. Between 40% and 50% of patients with HCM have no LVOT obstruction at rest or with provocation. LVOT gradients can also be abolished by the selective destruction of the obstructive part of the left upper septum by the injection of alcohol into the first or first and second septal perforating arteries (Figure 8. A trough of septal muscle is surgically removed through the aortic valve often under epicardial echocardiographic guidance. In the right panel. which decreases preload during the ‘strain’ phase. primary (as in endomyocardial fibrosis) and secondary (as in the infiltrative myocardial diseases). RESTRICTIVE CARDIOMYOPATHY The RCMs are rare and consist of a relatively heterogeneous group of diseases. LA. Diastolic dysfunction and the propensity for ventricular arrhythmias.24 Off-axis apical four-chamber views in a patient with obstructive hypertrophic cardiomyopathy in the cardiac catheterization lab for a percutaneous transluminal septal myocardial ablation (PTSMA). angina or DOE can be accomplished with MV replacement using a low-profile prosthesis and chordal preservation or more commonly by septal myotomy-myectomy. 130 . Symptoms of CHF are caused by elevated filling and the inability to increase cardiac output on exertion. Primary RCMs Endomyocardial fibrosis Endomyocardial fibrosis (EMF) causes 25% of all cardiovascular deaths in east Africa and South America and is thought to be the result of hypereosinophilia. left ventricle. The unifying factor in RCM is increased resistance to diastolic filling. Surgical relief of LVOT obstruction resulting in exercise-limiting symptoms of syncope.24). Right heart failure with peripheral edema and ascites may predominate. In the middle panel contrast has been injected into the first septal perforator to assess the location and extent of myocardium supplied by that vessel. LV size is usually normal but LV wall thickness is normal or increased. 2 mL of 99% alcohol (ETOH) has been injected into the septal perforator to selectively destroy a portion of the upper septum (LV. left atrium). often requiring an automatic implantable cardiovertor defibrillator. Eosinophils infiltrate the endocardium causing necrosis Figure 8. persist. or the Valsalva maneuver.THE ECHOCARDIOGRAPHERS’ GUIDE afterload.

Secondary RCMs (infiltrative diseases) Infiltration of the heart with toxic. There is extensive thrombus. MR and TR are present and may be severe. thickwalled LV that contracts poorly and fills slowly (Figure 8. Two-dimensional echocardiography reveals a normal-sized. left atrium). RA. heart block. Small pericardial effusions without hemodynamic significance are common.25). Right and left ventricular walls are thick and hypokinetic and the endocardium is highly echo-reflective.28). if LV wall thickness is 1. Progressive biventricular failure marked by restrictive filling ensues. but thromboembolic events are uncommon (Figure 8.25 Apical four-chamber view in a patient with Loffler’s endocarditis. The myocardium in cardiac amyloid is highly echo-reflective and has a sparkling. coronary arteries. systolic function (Figure 8. is similar to tropical EMF and is associated with idiopathic hypereosinophilia. There are several types of amyloidosis. LV. The posterior mitral leaflet may become entrapped in thrombus resulting in severe MR. The outflow tracts are spared. Amyloid also accumulates in the atrial walls.5 cm mean survival is 0. Amyloid heart disease In amyloid heart disease intracellular amyloid is deposited in the left and right ventricular myocardium where it disrupts diastolic function and later in the course of the disease. Mild AR and moderate AV valve regurgitation is common. In idiopathic RCM there is restriction to ventricular filling without endocardial thickening. bright.26). Patients with amyloid and an LV wall thickness 1. LV and RV walls are usually thick.5 years. right ventricle. Dense sheets of pearly white fibrous tissue replace the endocardium of both ventricles beginning at the apices with gradual spread to the atrioventricular (AV) valves.5 cm have a mean survival of 1. interatrial septum. ASH occurs in approximately a third of patients with amyloid heart disease (Figure 8.CARDIOMYOPATHIES of the endocardium and subendocardial muscle fibers. LA. There is extensive endocardial scarring and thrombus formation with cavity obliteration in advanced cases. and atrial fibrillation are common. . the amyloid proteins are morphologically distinct for each type. insoluble amyloid protein fibrils is the most common cause of RCM. Transmitral Doppler velocities show a restrictive pattern of diastolic filling pattern. and conduction system. and hypocontractile. Familial forms exist and are sometimes associated with distal skeletal muscle disease (Figure 8. Diastolic dysfunction progresses inexorably 131 Figure 8.29). right atrium. and all indices of diastolic function are severely depressed. left ventricle. Sinu-atrial disease.4 years. valves. Loffler’s endocarditis Loffler’s endocarditis. Mural thrombus forms over the fibrous tissue and may obliterate the apices. Echocardiographic findings included biatrial enlargement and small to normal ventricular cavity sizes. fibrosis or infiltrative process. ground glass appearance. also known as fibroplastic endocarditis or eosinophilic endomyocardial disease.27). which has obliterated the RV and LV apices (RV.

Figure 8.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 8. left atrium). left ventricle. RA.26 Apical four-chamber view in a patient with idiopathic restrictive cardiomyopathy. LV. LA. RA. right atrium. The ventricular walls are thick and highly echo-reflective. LV. The ventricles are small and there is marked biatrial enlargement (RV. right atrium.27 Apical four-chamber view in a patient with amyloid heart disease. LA. left atrium). right ventricle. 132 . left ventricle. There is biatrial enlargement and a small pericardial effusion (*) is noted adjacent to the RA free wall (RV. right ventricle.

pancreas. Initially wall thickness is normal and systolic function is preserved but with time the heart enlarges (Figure 8. and heart. Hemochromatosis Hemochromatosis results in excessive iron deposits in the liver. Excess iron accumulates due to a hereditary defect leading to the absorption of excessive iron from the intestines.CARDIOMYOPATHIES Figure 8. One-year survival is reduced to 50% in patients with a deceleration time of 150 ms. There is a spectrum of diastolic dysfunction with restrictive disease being the most severe. A deceleration time of the transmitral Doppler E wave of 150 ms predicts a 90% 1-year survival rate.28 Parasternal short axis in a patient with amyloid heart disease. Sarcoidosis Sarcoidosis is a multisystem disease of unknown etiology wherein noncaseating epitheloid granulomas (epitheloid cell 133 Figure 8. from abnormal relaxation to pseudonormal to restrictive patterns of filling. A small pericardial effusion is seen posterior to the LV (*). The walls do not become thickened with iron infiltration as with amyloid infiltration. Iron is deposited in the muscle cells of the epicardial third of the myocardium and this is associated with destruction of myocytes and replacement fibrosis. skin. There is asymmetric septal hypertrophy and systolic contraction and diastolic filling are impaired. . Similar iron deposition occurs in hemosiderosis from multiple ( 100 units) blood transfusions over many years.30) and patients usually present with left and/or right heart failure and echocardiographic features of DCM. The left ventricular (LV) walls are thick and highly echo-reflective.29 M-mode echocardiogram in a patient with amyloid heart disease.

ARVD is associated with arrhythmias including VT and sudden death. RA. tubercles) are formed in the skin. right ventricle. Diffuse infiltration of the lung parenchyma with pulmonary hypertension and cor pulmonale is common.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 8. lateral. The RV is enlarged and there is an RV apical aneurysm (A) (LV. LA. 134 . right atrium. RV apical aneurysms are most common and these may involve the RV inferior. left ventricle. Uhl’s anomaly Uhl’s anomaly or arrhythmogenic RV dysplasia (ARVD) is characterized by genetically determined progressive atrophy and fibrofatty replacement of the RV myocardium extending from epicardium to endocardium. There is moderate four-chamber enlargement and reduced global systolic function (RV. LA. Cardiac involvement is rare but granulomas can form in the heart and have a predilection for the basal septum and LV free wall causing regional contractile dysfunction and less often diastolic dysfunction. Figure 8. or free wall (Figure 8. or eyes.31). right atrium. The RV dilates and systolic function progressively deteriorates. LV. left atrium). RA. lungs.30 Apical four-chamber view in a patient with hemochromatosis.31 Apical four-chamber view in a patient with Uhl’s anomaly or arrhythmogenic right ventricular (RV) dysplasia. Granulomas cause interstitial inflammation and fibrosis and may affect the conduction system and papillary muscles. left ventricle. left atrium). There is a spectrum of RV involvement ranging from segmental RV thinning and akinesis to severe global RV and occasionally LV dysfunction.

and the terminal portions of the superior vena cava (SVC) and pulmonary veins and reflects back on itself as the parietal pericardium which lines the fibrous pericardium. It covers the outer surface of the heart including the proximal great arteries. the junctions of visceral and parietal layers. The reflections of the serous pericardium. but its most important function is to limit acute diastolic distension of the cardiac chambers.9 DISEASES OF THE PERICARDIUM CONTENTS q Anatomy q Pericarditis q Pericardial Effusion q Constrictive Pericarditis q Specific Etiologies q Tamponade ANATOMY The pericardium envelops the heart and is composed of serous and fibrous layers. It is about 2 mm thick and receives oxygenated blood from the internal mammary arteries. and descending thoracic aorta (DAO). Patients with pericarditis are typically febrile and have positional chest pain. The outer surface of the fibrous pericardium is firmly attached to the central tendinous and left muscular portions of the diaphragm. aggravated by cough and respiration 135 . However. The space between the visceral and parietal layers of the pericardium normally contains 15–30 mL of fluid secreted by microvilli on the pericardial surface. The thin inner serous visceral pericardium is the epicardium. the pericardium will stretch to accommodate it. inflammation. and malignancy from contiguous organs. which act as a lubricant allowing the two layers to slide over each other with minimum friction.e. The inferior vena cava (IVC) enters the pericardium directly through the central diaphragm and is therefore not covered by the fibrous pericardium. esophagus. when the increase in intrapericardial volume is gradual. These attachments limit displacement of the heart. Pericardial fluid is normally drained by the lymphatic system of the parietal pericardium into the thoracic duct or by way of the right pleural space into the right lymphatic duct. where it melds with their adventitia. beyond this point it is inelastic with a nearly vertical relation between pressure and volume. The fibrous pericardium allows only minor increases in intrapericardial volume. costal cartilages. This fluid contains phospholipids. PERICARDITIS Pericarditis may be idiopathic or due to viral infection with or without accompanying myocarditis. The pericardium acts as a barrier to the spread of infection. i. form two prominent sinuses. The transverse sinus is a tunnel-like projection of the pericardium anterior to the SVC and atria and posterior to the great arteries. and more loosely to the sternum. parietal pleurae. The oblique sinus is an inverted U-shaped cul-de-sac located behind the left atrium between the right and left pulmonary veins. vertebral bodies.

malignancy. 136 . right ventricle. A normal echocardiogram does not exclude the diagnosis of pericarditis. The pericardium can accommodate a large amount of fluid ( 2 L) without sudden hemodynamic collapse if it develops slowly. A small amount of pericardial fluid ( 20 mL) is often visible as Figure 9. PERICARDIAL EFFUSION Pericardial effusions can accompany pericarditis from any etiology. quantifying. can raise intrapericardial pressure dramatically and cause fatal tamponade. LV. serosanguineous.1 M-mode echocardiogram shows a small posterior pericardial effusion as a separation between the visceral and parietal layers of the pericardium (arrow) that persists throughout the cardiac cycle. A small effusion ( 150 mL) that accumulates rapidly. The pericardium may react to inflammation with exudation of fluid and fibrin but in most cases of pericarditis there is no significant accumulation of fluid. They can be due to trauma. however. circumferential pericardial effusion (PE). Pericardial fluid may be serous. heart failure. and assessing the hemodynamic impact of pericardial effusions and can often provide additional information about the pericardial contents.2 Parasternal short axis view in a patient with a moderate sized. Echocardiography is the diagnostic modality of choice for detecting. The Figure 9. failure of lymphatic drainage or may be of iatrogenic origin. and relieved by sitting with the trunk bent forward. or purulent depending on the etiology.THE ECHOCARDIOGRAPHERS’ GUIDE pericardial surfaces become thickened and rough. left ventricle). A small left pleural effusion (PL) is also seen (RV.

left ventricle. it extends apically. a slight separation between the visceral and parietal layers of the pericardium by Mmode echo in normal patients. It is generally necessary to reduce the gain so that only the pericardial reflectors remain. A separation that persists through diastole as well as systole represents a small effusion (Figure 9.DISEASES OF THE PERICARDIUM Figure 9. Occasionally. left ventricle. aorta).2) and superior to the right atrum (RA) from the apical four-chamber view but small or even moderate-sized effusions may be obscured if excessive gain is employed.4). The vast majority of pericardial effusions terminate at the level of the posterior atrioventricular (AV) groove regardless of their size and unlike pleural effusions they are not visible posterior to the left atrium (LA). 137 . AO.1). RA. Moderate-sized effusions are visible circumferentially as echo-free regions anterior to the right ventricular (RV) free wall and posterior to the left ventricle from the parasternal imaging window (Figure 9. right ventricle. Dao. Most but not all pericardial effusions terminate at the level of the atrioventricular groove (RV. Pericardial effusions can be distinguished from pleural effusions by localizing the effusion relative to the DAO in the parasternal long axis view (Figure 9. Figure 9. right atrium.3 Subcostal four-chamber view in a patient with a loculated pericardial effusion (PE) (RV.3).5). left atrium. In this case fluid is walled off by adhesions between the visceral and parietal layers (Figure 9. LV. Small effusions tend to pool at the base of the heart. LA. laterally and then anteriorly becoming circumferential.4 Apical four-chamber view in a patient with a small pericardial effusion (PE) and a larger pleural effusion (PL). LV. right ventricle. It is essential to distinguish pericardial effusions from pleural effusions (Figure 9. large pericardial effusions extend into the oblique pericardial sinus. Effusions may be loculated and seen adjacent to only one or two cardiac chambers. As an effusion enlarges. An isolated anterior hypoechoic zone probably represents a fat pad rather than fluid. descending thoracic aorta).

138 . LV. Regions of increased echo density within Figure 9.6). left ventricle).5 Parasternal long axis view of a patient with a pericardial effusion (PE) and a pleural effusion (PL). Nodular thickening of the pericardial surface may represent tumor. left ventricle).6 Subcostal short axis view in a patient with a large. The pericardial contents can be qualitatively evaluated by assessing its density and heterogeneity. dense. hemorrhagic pericardial effusion (PE) (LV. right ventricle.THE ECHOCARDIOGRAPHERS’ GUIDE Pericardial effusions are anterior to the DAO and pleural effusions are posterior and lateral to the DAO. An effusion with an echo density greater than that of fluid may represent hematoma or infection (Figure 9. Figure 9. PEs are anterior to the descending thoracic aorta (Dao) and PLs are posterior and lateral to the Dao in this view (RV. The heart may swing freely within a large pericardial effusion and this motion corresponds to the phasic variation in QRS amplitude termed electrical alternans.

the inspiratory fall in intrathoracic pressure is not transmitted to the pericardial space. diastolic pressures are elevated but true filling pressure is equal to the transmural pressure. left ventricle). Fibrin strands are seen. TAMPONADE Tamponade occurs when the heart is compressed by the pericardial contents to the extent that cardiac filling is impaired. In tamponade.7) or hematoma. Fibrin strands attached to both pericardial surfaces are often seen as pericardial effusions begin to organize and form fibrous adhesions (Figure 9. an effusion may represent fibrin (Figure 9. one of which (arrow) is attached to both the visceral and parietal pericardial surfaces (RV. When intrapericardial pressure is equal to ventricular diastolic pressure. The interventricular septum shifts to the left and further impedes LV filling.8 Parasternal short axis view in a patient with a moderate-sized pericardial effusion (PE). right ventricle. filling pressure is zero and continued cardiac output becomes dependent on respirophasic variations in ventricular filling and ventricular interdependence. LV. .8).DISEASES OF THE PERICARDIUM Figure 9. left ventricle). In tamponade.7 The echodense region adjacent to the right ventricular free wall (arrow) within the pericardial effusion (PE) in this parasternal short axis view may represent fibrin deposits or hematoma (LV. which is diastolic pressure minus intrapericardial pressure. RV filling and output are augmented in inspiration. Systolic blood pressure (BP) rises and falls with the respiratory cycle in tamponade. LV filling and output are accentuated at the expense of RV filling and output. In expiration the situation is reversed. pulmonary capillary wedge pressure falls and with it left ventricular (LV) filling. The difference between the inspiratory and expiratory systolic BP is the pulsus paradoxus and in tamponade it is usually greater than 139 Figure 9.

pericardial effusion. . The RV free wall indents when RV filling pressure is exceeded by intrapericardial pressure (LV. RV.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 9. In addition. LA. RV infarction.9 Parasternal short axis view in a patient with a large pericardial effusion (PE) and cardiac tamponade showing right ventricular (RV) diastolic indentation in early diastole that reverses by end-diastole.10 Diastolic indentation of the right ventricular outflow tract (arrow) is evident in this diastolic frame (PE. and pulmonary embolism in the absence of a pericardial effusion. AO. left ventricle. LV. pulsus paradoxus occurs in patients with chronic obstructive pulmonary disease (COPD). asthma. 10 mmHg. left atrium. However. right ventricle. as occurs when preexisting heart failure has caused chronic elevation in LV filling pressure or when pulmonary hypertension has caused chronic elevation in RV filling pressure. and it is absent when elevated pericardial pressure impacts on the RV and LV unequally. left ventricle). aorta). Pulsus paradoxus is also absent when the inspiratory increase in RV filling is matched by an inspiratory increase in shunt flow through an atrial septal defect (ASD) or when there is significant retrograde filling of the LV from aortic regurgitation that is independent of respiration. Tamponade is a clinical diagnosis and not a diagnosis that can be made echocardiographically. Doppler/echocardiography is sensitive to the exaggerated respiratory variation and ventricular interdependence that is driven by increased 140 Figure 9. Pulsus paradoxus is not pathognomonic of tamponade.

M-mode echocardiography facilitates recognition of the timing of RV indentation (LA.9). the walls of the chamber are forced inward or indented. and it can assess the hemodynamic impact of a pericardial effusion.12 M-mode echocardiogram of a patient with a loculated posterior pericardial effusion (PE) and cardiac tamponade. RV diastolic indentation can be clearly demonstrated in the subcostal views and in the parasternal long axis view (Figure 9.11). Timing of the indentation is facilitated by M-mode interrogation from either projection using a fast sweep speed (Figure 9. Conversely. posterior wall. Abnormal posterior motion of the RV free wall in early to mid-diastole indicates that pericardial pressure exceeds RV filling pressure (Figure 9. 141 . interventricular septum). The IVC is enlarged and does not collapse with inspiration when RA pressure is greater than 15 mmHg (Figure 9. When pericardial pressure exceeds the pressure in a cardiac chamber. Collapse of the RA wall is an early and sensitive sign of increased intrapericardial pressure.10) as the RV outflow tract is the most distensible part of the RV free wall. left atrium). Figure 9.12). RA and RV indentation will occur early at a relatively low pericardial pressure.13).11 M-mode echocardiogram at the level of the aorta (AO) and left atrium (LA). intrapericardial pressure.DISEASES OF THE PERICARDIUM Figure 9. When RV filling pressure is low as in the hypovolemic patient. this sign may be absent in a patient with RVH and pulmonary artery hypertension when RV filling pressure is high and LV free wall indentation may precede RV indentation (Figure 9. Respirophasic variation in ventricular filling can be identified by reciprocal changes in ventricular dimensions as the interventricular septum shifts leftward with inspiration and back during expira- tion. There is diastolic indentation of the right ventricular (RV) outflow tract (RVOT) (arrows). There is diastolic indentation of the left ventricular posterior wall (PW. IVS.

Respirophasic variations in Doppler flow velocities mirror the hemodynamics in tamponade. Systemic venous flow velocity profiles can be obtained from the SVC when the transducer is positioned in the left supraclavicular fossa and the beam is angled caudad and parallel to the spine and from the middle hepatic vein from the subcostal position where the beam can be aligned with blood flow. An inspiratory fall in the transmitral E wave is normally less than 10%. absent or reversed. Pericardiocentesis is performed emergently in patients with tamponade and may be life Figure 9.16). reflecting the decreased gradient between the extracardiac pulmonary veins and the LA. total intrapericardial volume is constant and filling occurs predominantly in systole when blood is ejected during which pericardial pressure falls. LV isovolumic relaxation time (IVRT) is prolonged with inspiration and the MV may open only with atrial contraction. The E wave velocity increases phasically with expiration and decreases with inspiration. A normal expiratory decrease in the transtricuspid E wave can be as high as 25%. There are normally two negative peaks representing forward flow in systole and diastole. 142 . Systemic venous flow is predominantly systolic and diastolic flow is reduced. The systolic wave is normally higher than the diastolic and both increase with inspiration. There may also be a small retrograde deflection caused by atrial contraction. When greater than 25% it is suggestive of tamponade and this finding is associated with RV diastolic indentation (Figure 9. There is marked respirophasic variation in transmitral flow velocities. In tamponade. LVOT flows are similarly affected (Figure 9. On the first beat of inspiration. transmitral E wave velocity falls. A variation of 50% is consistent with tamponade (Figure 9.14). diastolic and often systolic velocities fall or reverse.15). Inspiratory augmentation may be normal or reduced in tamponade but on the first beat after expiration and coincident with minimum transtricuspid velocity.13 The inferior vena cava (IVC) and hepatic veins are markedly enlarged and the IVC diameter does not vary with respiration in this patient with a pericardial effusion and cardiac tamponade.14 Pulsed-wave Doppler with the sample volume at the tips of the mitral valve leaflets in a patient with cardiac tamponade.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 9.

DISEASES OF THE PERICARDIUM

Figure 9.15 Pulsed-wave Doppler with the sample volume in the left ventricular outflow tract (LVOT) in a patient with cardiac tamponade. There is marked respirophasic variation in the peak LVOT flow velocity. The peak velocity increases phasically with expiration and decreases with inspiration.

saving. Needle aspiration of pericardial fluid is also performed to obtain a sample for analysis especially when there is a suspicion of a malignant or infectious etiology. The patient’s head is elevated to facilitate inferior and anterior pooling of fluid. The subcostal route is preferred as it avoids the pleural space and internal mammary and major coronary arteries. Blind pericardiocentesis carries a risk of damage to the liver,

lung, or heart. Pericardiocentesis is generally performed in the cardiac catheterization laboratory with hemodynamic monitoring and fluoroscopic guidance or increasingly with echocardiographic guidance.

CONSTRICTIVE PERICARDITIS
In constrictive pericarditis the pericardium is stiff and fibrotic and restricts diastolic filling. The pericardial layers are usually fused by dense adhesions and the pericardial space obliterated. In late stages of the disease the pericardium may calcify. Constriction begins with a pericarditis that is usually accompanied by an effusion. The effusion is reabsorbed but the pericardium remains inflamed. In patients with endstage pericardial constriction, symptoms of ascites, peripheral edema, and hepatic insufficiency predominate and can mimic RV failure. Diastolic compliance is normal in patients with constriction and early diastolic filling is unimpaired but terminated abruptly when the limits of the pericardium are reached. This is seen as a rapid early posterior deflection of the posterior LV wall on M-mode that abruptly plateaus. An interventricular septal notch or bounce is seen on the M-mode echo (Figure 9.17). The septum moves sharply to the left in early diastole and then quickly back to the right. This finding is independent of cycle length and
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Figure 9.16 Pulsed-wave Doppler with the sample volume at the tips of the tricuspid valve leaflets in a patient with cardiac tamponade. There is marked respirophasic variation in transtricuspid flow velocities. The E wave velocity increases phasically with inspiration and decreases with expiration.

THE ECHOCARDIOGRAPHERS’ GUIDE

Figure 9.17 M-mode echocardiogram in a patient with constrictive pericarditis. The interventricular septum moves sharply to the left and then quickly back to the right in early diastole (downward pointing arrows). This septal bounce or notch is a common finding in constrictive pericardial disease. There is rapid posterior motion of the posterior wall in early diastole but this motion is terminated abruptly when the limit of the constricting pericardium is reached and there is little further motion through the rest of diastole. It is sometimes possible to distinguish the visceral and parietal pericardial layers (upward pointing arrow) and in constrictive pericardial disease they are usually fused together – the separation between them is constant throughout the cardiac cycle (LV, left ventricle).

seen even in patients with atrial fibrillation. It is more prominent with inspiration and reflects a transient inequality in the nearly equal left and right filling pressures. The IVC is dilated and does not decrease in size with inspiration reflecting elevated RA pressure. The pericardium may be thick and if it is very thick or calcified, echo images may be very difficult to obtain. The Doppler transmitral E wave velocity is high, the E–F slope rapid, and the IVRT is characteristically short. The respirophasic variations in ventricular output and LV filling are similar to those seen in pericardial tamponade because the constricting shell does not permit the inspiratory fall in intrathoracic pressures to be transmitted to the cardiac chambers. Pulsus paradoxus and reciprocal changes in ventricular size are common. Early transmitral flow velocity falls with the first beat of inspiration and early transtricuspid flow velocity falls with expiration. The S2 and D peak velocities in the pulmonary venous waveform are enhanced with expiration and fall with inspiration. These changes are more
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conspicuous than the variation in transmitral velocities and occur independently of cardiac cycle length. Early diastolic RA filling is rapid and systolic filling is preserved, so that the middle hepatic venous waveform is biphasic with a ‘W’ pattern. Forward flow is accentuated with inspiration and diastolic flow is reversed in expiration. This respirophasic pattern is also seen in patients with COPD or asthma when strong respiratory effort exaggerates changes in intrathoracic pressure. Respirophasic SVC flow reflects changes caused by pulmonary disease more than changes in cardiac disease. A variation in SVC flow of 20 cm/s favors the diagnosis of pulmonary disease and 20 cm/s indicates constriction. The minimum transmitral E wave is coincident with the second or third beat of inspiration when the variation is due to COPD but coincides with the first beat of inspiration when caused by constriction. Constrictive pericardial disease can be difficult to distinguish from noninfiltrative restrictive cardiomyopathy and this

DISEASES OF THE PERICARDIUM

Table 9.1 Restrictive cardiomyopathy (RCM) versus constrictive pericarditis (CP) RCM Septal shift Tissue Doppler Indices 8 Atria enlarged Respiratory variation Shortened deceleration time MHV expiratory diastolic flow reversal E/E No No No Yes No 15 CP Yes Yes Yes Yes Yes 8 Normal

Purulent effusions result in extensive adhesions with loculations and localized fusion of the pericardial space. Pus cannot be aspirated and suspected purulent effusions require surgical exploration, drainage with pericardial lavage, intrapericardial installation of antibiotics, and usually extensive pericardiectomy. The mortality for purulent pericarditis is greater than 50%.

Post-infarction pericarditis
This occurs within four days of infarction and is exudative. Pericarditis occurs in approximately 6% of patients with an infarction and 20% of patients with large anterior wall infarcts. It is often patchy, adjacent to the infarcted myocardium. Dressler syndrome or post-infarction syndrome occurs in approximately 5% of patients from weeks to months after an infarction and consists of recurrent fevers, pleuritis, and pericarditis. It affects the pericardium diffusely and is probably immunologically mediated. Post-pericardiotomy syndrome is seen late after cardiac surgery, catheter perforation or cardiac trauma. It is similar to Dressler syndrome and is thought to be an immune response to bleeding into the pericardial sac and mediastinum.

distinction is important because pericardial stripping can be curative. The distinction between the two conditions is based upon the finding that blood flow velocities are respirophasic in constrictive disease but not in restrictive disease and because myocardial relaxation is normal in constriction but not in restriction. Respirophasic variation in transmitral E wave ((E expiration E insiration)/E inspiration) is 10% in RCM but 25% in constrictive pericarditis. A small minority of patients with constriction may not demonstrate respirophasic variations in flow velocities initially, but these findings can be provoked by pharmacologic interventions that reduce preload. Color Mmode propagation velocities (Vp) and tissue Doppler indices of early filling (E ) are normal ( 50 cm/s and 8 cm/s, respectively) in constrictive pericarditis and significantly reduced in RCM. Equivocal findings will be present in cases of mixed pericardial/muscle disease (Table 9.1).

Post-cardiac surgery
Pericardial effusions and tamponade can develop following cardiac surgery from bleeding at suture sites and from epicardial pacemaker leads (Figure 9.18). The pericardium is generally left open after surgery and the usual signs of increased intrapericardial pressure will be absent. Alternatively, the cut edges of the pericardium may adhere to the sternum. Effusions that develop in this setting will be loculated posteriorly. Postoperative hematomas often exert a local hemodynamic effect on one or two cardiac chambers and may need to be surgically evacuated.

SPECIFIC ETIOLOGIES Bacterial or purulent pericarditis
This was usually secondary to pneumonia or empyema before the introduction of antibiotics. Today it is usually due to extension of endocarditis, early postoperative infection or hematogenous spread during bacteremia.

Congenital pericardial cysts
These are circumscribed pouches or diverticula that form in utero. Ninety percent
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left ventricle. The LA or left atrial appendage can herniate through a defect in the pericardium and sudden death from strangulated hernias has been reported. Figure 9. Congenital complete absence of the parietal pericardium This is rare and usually asymptomatic. There is paradoxical septal motion and the right heart appears to be enlarged when viewed from the parasternal transducer position but not from the apical window. LA. 146 . They are benign and asymptomatic and usually present as an incidental finding on a chest X-ray or computed tomography. They are usually anechoic having the acoustic signature of clear fluid.18 Apical four-chamber view in a patient with pericardial effusion (PE)/hematoma in cardiac tamponade resulting from postoperative bleeding following coronary bypass surgery (RV. but may be filled with a proteinaceous slurry that can be seen to move in real-time imaging.THE ECHOCARDIOGRAPHERS’ GUIDE form at the right costophrenic angle and are seen along the superomedial margin of the right atrium in the apical four-chamber view. RA. left atrium). right atrium. LV. It is usually the left parietal pericardium that is deficient and this causes the heart to shift to the left. right ventricle.

10
CONTENTS
q

DISEASES OF THE AORTA

Anatomy

q

Atherosclerotic Disease

q

Aortic Dissection

ANATOMY
The ascending aorta curves anteriorly, superiorly, and to the right from the aortic annulus. It is approximately 5 cm long and 3 cm in diameter and terminates at the origin of the innominate artery. The aorta continues as the aortic arch or transverse aorta, which travels leftward and posteriorly, arching over the right pulmonary artery. This segment is about 4 cm long and extends from the innominate artery to the ligamentum arteriosum directly opposite the left subclavian artery (Figure 10.1). The descending aorta (DAO) extends from the ligamentum arteriosum and is divided into thoracic and abdominal segments at the diaphragm. The abdominal DAO is adjacent to the left margin of the vertebral column, parallel, posterior, and leftward to

the inferior vena cava (IVC) and bifurcates into right and left iliac arteries at the level of the umbilicus. The thin inner layer of the aorta, the intima, is comprised of the endothelium and surrounding elastic fibers and connective
RCC RSC In TAO LCC LSC

AAO

PA

Figure 10.1 Drawing of the aorta. The ascending aorta (AAO) crosses over the right pulmonary artery (PA) and continues as the transverse aorta (TAO) or aortic arch. Three arteries arise from the superior aspect of the aortic arch. They are from proximal to distal the inomminate, which branches into the right subclavian (RSC) and right common carotid (RCC) arteries, the left common carotid (LCC) and the left subclavian (LSC). The descending aorta (DAO) begins at the ligamentum arteriosum (arrow) and is divided into thoracic and abdominal sections at the diaphragm.

DAO

Diaphragm

147

THE ECHOCARDIOGRAPHERS’ GUIDE

tissue. The medial layer is approximately 1 mm thick and contains smooth muscle cells, collagen, and elastin. The outer adventitial layer is composed of tough connective tissue. The aorta can be damaged by trauma, inflammation, infection, atherosclerosis, degenerative changes and hereditary connective tissue disease. Elastic elements in the intima and media stretch with systole and store energy, which is released in diastole helping to propel blood to the periphery. These elements are attenuated with aging and the aorta becomes less distensible, enlarges, and elongates. Atherosclerosis can cause focal fibrosis and calcification of the aortic wall, which can lead to aneurysm formation, embolic events, and

dissection. Hypertension accelerates both atherosclerotic and degenerative changes.

ATHEROSCLEROTIC DISEASE
The spectrum of atherosclerotic disease of the aorta extends from mild focal thickening of the aortic wall to large, raised, calcified plaques that protrude into the lumen and may be associated with thrombus (Table 10.1). Alternatively, ulcerated plaques can penetrate into the aortic wall and produce an intramural hematoma or a pseudoaneurysm (contained rupture) of the aorta (Figure 10.2). Atherosclerotic aortic aneurysms result from weakening of the

Table 10.1

Aortic atherosclerosis classification Normal Mild 3.0 mm None Moderate 5.0 mm Raised plaques Severe 5.0 mm Protruding plaques and/or debris

Intimal thickening Luminal irregularities

2.0 mm None

Figure 10.2 Parasternal long axis in a patient with a pseudoaneurysm or contained rupture of the descending thoracic aorta (Dao), which has been walled off by thrombus. A pleural effusion (PL) is also seen (RV, right ventricle; LV, left ventricle; LA, left atrium; AO, aorta).

148

DISEASES OF THE AORTA

Figure 10.3 Subcostal four-chamber view in a patient with a giant (9.7 cm) aneurysm of the descending thoracic aorta (Dao) (RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium).

aortic wall from extension of atheroma into the medial layer with destruction of the muscular and elastic tissues. Aneurysms are a localized dilatation of the aorta of greater than 50% of the normal diameter (Figure 10.3). Fusiform aneurysms involve the entire circumference of the aorta. Saccular aneurysms affect only a part of the circumference. Surgery is generally indicated for aneurysm 5 cm as the risk of rupture is proportional to size. The abdominal aorta is more commonly affected than the thoracic aorta with both occlusive and aneurysmal atherosclerotic disease (Figure 10.4). In addition to atherosclerosis, aneurysms can result from inflammation, as in Takayasu or giant cell arteritis; infection, as in syphlitic aortitis; or mycotic aneurysm from embolization of infected material or from medial necrosis associated with hereditary conditions including Marfan and Ehlers–Danlos syndrome. Congenital aneurysms of the sinus of Valsalva can rupture into the right atrium (RA), right ventricle (RV), or pulmonary artery (PA) or may compress one of the coronary arteries (Figure 10.5).

Figure 10.4 Subcostal views of the abdominal aorta in long axis (left panel) and short axis (right panel) in a patient with a giant aneurysm of the abdominal aorta, which is partially filled with thrombus (Dao, descending aorta; LA, left atrium; AO, aorta).

149

left atrium. Echocardiography The diagnosis of an aortic dissection rests on the visualization of an intimal flap dividing true and false lumens (Figure 10. The primary cause of death is aortic rupture into the pericardium causing tamponade.6). propagates at least to the aortic arch and usually for a variable distance beyond the arch DeBakey type 2 Originates in and is confined to the ascending aorta DeBakey type 3 Originates in the descending aorta Type 3A stops above the diaphragm Type 3B extends below the diaphragm Stanford classification Type A Involves the ascending aorta Type B Doesn’t involve the ascending aorta The tear commonly originates at the right anterior aortic wall just superior to the right coronary artery.2). The inner layer forms a flap within the aortic lumen that separates it into true and false channels. AO.2 Aortic dissection classification DeBakey classification DeBakey type 1 Originates in the ascending aorta. or at the ligamentum arteriosum near the innominate artery.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 10. Acute severe aortic regurgitation (AR) results from retrograde extension of the dissection with disruption of the commissures or interference with aortic valve closure by the dissection flap (Figure 10. aorta). Table 10. The true 150 .7).5 Parasternal long axis view in a patient with a sinus of Valsalva aneurysm (arrow) of the noncoronary sinus (LV. Aortic rupture into the left pleural space is a common terminal event in distal dissection. or both directions (Table 10. Absent pulses or neurological deficits can result when the dissection extends into the walls of branch arteries and compromises blood flow. AORTIC DISSECTION In aortic dissection a tear in the intimal layer allows pulsatile blood flow to tear through the medial layer and divide the aortic wall into intimal-medial and medialadventitial components. and can propagate longitudinally in antegrade. LA. Acute type A aortic dissection has a mortality rate of approximately 1–2% per hour without surgical repair whereas type B aortic dissections may be managed medically with blood pressure reduction. retrograde. left ventricle.

Color Doppler is also used to assess the presence and severity of AR. lumen expands in systole and may collapse in diastole. left ventricle).6 Parasternal long axis view in a patient with a proximal aortic dissection.8) and short axis views demonstrate the aortic valve. left atrium).DISEASES OF THE AORTA Figure 10. absent or retrograde flow in the false lumen. Transesophageal echocardiography (TEE) alone or in combination with TTE is the preferred diagnostic modality for aortic dissections. transverse aorta). The false lumen may contain thrombus or spontaneous echo contrast (smoke). LA. The left parasternal long axis (Figure 10.8 A parasternal long axis view from a high intercostal space shows aneurysmal dilatation of the ascending aorta (Aao) in a patient with Marfan syndrome (LV. The diagnosis of an aortic dissection cannot therefore be excluded by TTE alone.7 Suprasternal notch view of the descending aorta (Dao) in a patient with a type B aortic dissection. A pericardial effusion (*) is also seen and is an ominous sign in this setting as the primary cause of death in aortic dissection is tamponade from rupture of the aorta into the pericardial space (LV. The dissection flap is indicated by arrows. sinuses of Valsalva Figure 10. The dissection flap is indicated by an arrow (TAO. Figure 10. and is often able to identify the site of origin of a dissection and fenestrations between true and false lumens. 151 . The aorta can be assessed almost completely from the aortic valve to its bifurcation using a combination of imaging windows. Transthoracic echocardiography (TTE) has sensitivity for detecting aortic dissection of only 40%. left ventricle. Color Doppler demonstrates forward systolic flow in the true lumen and reduced.

Figure 10. right ventricle). left atrium). left ventricle. LA. 152 . Figure 10. LV. LA. Figure 10. LVOT.10 A dissection flap is seen in the long axis of the ascending aorta (Aao. If the Dao is seen in the parasternal long axis view then the scan plane can be rotated 90 while holding the Dao in view (PE. LA. A dissection flap is seen in the descending thoracic aorta (Dao) in this patient with a type B aortic (AO) dissection. left atrium). left ventricle. pericardial effusion.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 10.11 Parasternal long axis view. left atrium. left ventricular outflow tract. A large pleural effusion (PL) is also present (RV.9 The apical five-chamber view demonstrates marked aortic (AO) root enlargement in this patient with severe aortic regurgitation (LV. right ventricle.12 The descending thoracic aorta (Dao) can often be visualized in its long axis from the parasternal window. arrow) from the second right intercostal space in a patient with a type A aortic dissection. RV.

13 The abdominal aorta is visualized in its long axis in this patient with an aortic atheroma (arrow) (DAO. descending thoracic aorta. right atrium).DISEASES OF THE AORTA Figure 10. RA. The suprasternal notch transducer position is used to assess the transverse and proximal descending aorta although the proximal transverse aorta is usually less well seen. The DAO is seen in cross-section in the parasternal long axis view just superior to the atrioventricular groove (Figure 10.12).10) when the patient is positioned in the right lateral decubitus position.13).9) and apical long axis views.11) and it can be seen in its long axis when the plane is rotated 90 clockwise while keeping it in view (Figure 10. 153 . The DAO can usually be seen in a variation of the apical two-chamber view in which the scan plane is angled medially and inferiorly. Short axis imaging of the abdominal aorta is optimal with the patient supine and the transducer placed on the abdomen and angled directly posteriorly. The distal thoracic and abdominal aorta are seen from the subcostal window when from a short axis of the ventricles. and proximal ascending aorta and these structures are also seen from the apical fivechamber (Figure 10. The ascending aorta is best seen from the upper right sternal border (Figure 10. the plane is angled medially and inferiorly (Figure 10.

.

The systolic frame demonstrated that the fossa ovalis is not thickened and that ‘mass’ is lipomatous hypertrophy of the interatrial septum. points of attachment. right atrium. size. left ventricle. LV. and distinguished from ultrasound artifacts and implanted devices (Figure 11. vegetations (see Chapter 7). and tumors. acoustic signature. left atrium). LA. which is a benign condition (RV. 155 . right ventricle. location. and hemodynamic significance. RA.11 CARDIAC MASSES CONTENTS q Secondary Cardiac Tumors Malignant Cardiac Tumors q Primary Benign Cardiac Tumors q Primary Cardiac masses include thrombus (see Chapters 4 and 6).2) by careful assessment of mass.1 Apical four-chamber view in a patient with an apparent mass on the interatrial septum. shape. Figure 11.1). Masses can be reliably detected echocardiographically (Figure 11. mobility.

THE ECHOCARDIOGRAPHERS’ GUIDE

and location, tumors can cause obstruction to left or right ventricular inflow or outflow tracts; arrhythmias and conduction defects; coronary compression; pericardial effusions; pericardial tamponade; and cardiac encasement with symptoms of constriction. However, most metastases are small and do not interfere with cardiac function. Cardiac involvement is clinically silent in 90% of cases but a pericardial effusion or tamponade may be the initial sign of metastatic disease. Tumors invade the heart by:
q

q q

q

Figure 11.2 Apical four-chamber view with an apparent mass in the left ventricular (LV) apex and another attached to the tricuspid valve. Both masses are thrombus. The former was associated with apical akinesis and the latter was covering a right ventricular (RV) pacing wire (RA, right atrium; LA, left atrium).

direct extension from contiguous structures (i.e. mediastinal lymphomas, esophageal carcinoma) hematogenous spread (i.e. melanomas) retrograde lymphatic spread (i.e. bronchogenic and breast cancer) transvenous extension via the cavae or pulmonary veins (i.e. renal cell and hepatocellular carcinoma) (Figure 11.3).

SECONDARY CARDIAC TUMORS
At least 95% of all cardiac tumors are metastases (Table 11.1). Cardiac metastases are present at autopsy in 10–12% of patients with malignancies. Depending on their size

Table 11.1

Cardiac tumors 5% of all cardiac tumors 75% of primary tumors 50% of benign tumors 75% of myxomas 23% of myxomas 25% of primary tumors 95% of malignant tumors 95% of all cardiac tumors 36% of secondary tumors 20% of secondary tumors 7% of secondary tumors 6% of secondary tumors

Primary Benign Myxomas Left atrial Right atrial Malignant Sarcomas Secondary Lung Nonsolid Breast Esophagus

Lung cancer is the most common source of cardiac metastases, being the primary tumor in approximately 36% of cases. It may invade the pulmonary veins and cause obstruction and pulmonary venous hypertension (Figure 11.4) but it more commonly involves the pericardium and epicardium indicating retrograde lymphatic spread, as most of the lymphatics that drain the pericardial cavity are located on the visceral pericardium. Secondary cardiac tumors can affect any region of the heart but the great majority of them are pericardial. Malignant pericardial effusions are usually due to metastatic spread to the pericardium (Figure 11.5). The epicardium can also be involved with tumor extension into the myocardium but this is rare. Breast cancer, lung cancer, lymphomas, and leukemias account for 80% of all malignant effusions and malignancy accounts for 50% of all effusions that require intervention. Pleural effusions coexist in a third of cases. Malignant effusions are usually bloody and tamponade can develop rapidly from erosion of a pericardial blood vessel or cardiac chamber. The pericardium is often diffusely or focally thickened and effusive– constrictive disease is common. Malignant

156

CARDIAC MASSES

Figure 11.3 Subcostal view of the inferior vena cava (IVC) (left panel) and apical four-chamber view (right panel) in a patient with renal cell carcinoma. The tumor has extended along the IVC and into the right atrium (RA) and now obstructs the tricuspid valve (RV, right ventricle; LV, left ventricle; LA, left atrium).

Figure 11.4 Subcostal four-chamber view in a patient with a massive tumor (*) that has invaded the atria from the pulmonary veins. A large right pleural effusion (PL) is also present (RV, right ventricle; LV, left ventricle; LA, left atrium).

Figure 11.5 Parasternal short axis view in a patient with a metastatic tumor on the right ventricular (RV) epicardium (*) that has extended into the RV cavity (arrow) (LV, left ventricle).

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THE ECHOCARDIOGRAPHERS’ GUIDE

effusions usually indicate advanced disease and poor long-term prognosis.

PRIMARY BENIGN CARDIAC TUMORS
Only 5% of cardiac tumors are primary and 75% of these are benign.

Myxomas
Half of all benign cardiac tumors are myxomas, 75% of these are located in the left atrium (LA) (Figure 11.6), 23% in the right atrium (RA) (Figure 11.7) and the remainder arise from the ventricles or mitral valve (MV) apparatus. Myxomas are more common in females and 90% of myxomas are found in patients between the ages of 30 and 60 years. Atrial myxomas are usually attached to the fossa ovalis either by a broad base or by a narrow stalk or pedicle.

When large and mobile they can prolapse through the MV in diastole producing symptoms that mimic mitral stenosis. Atrial myxomas may also present with a nonspecific systemic illness with fever, weight loss, joint pain, and fatigue. Portions of the tumor or thrombus on the tumor surface may embolize suggesting endocarditis or vasculitis. Echocardiographically, myxomas have a bright, speckled, gelatinous, heterogeneous appearance often with cystic echolucencies due to hemorrhage or liquefaction necrosis and may be 5 cm in diameter. Most myxomas are solitary and sporadic, but there is a familial form, Carney complex, in which multiple myxomas occur in atypical locations.

Rhabdomyomas
The most common tumors in children are rhabdomyomas, which are almost invariably multiple, pedunculated, mural masses in the ventricles. They are slow growing and spontaneous regression is common. They are associated with tuberous sclerosis, a congenital familial disorder marked by tumors and sclerotic patches of the brain, tumors of the eye and kidneys, epilepsy, and progressive mental deterioration.

Fibromas
Fibromas are usually solitary, wellcircumscribed, benign connective tissue tumors that are often located within the interventricular septum (Figure 11.8). They typically affect children and range from 1 cm to 10 cm in diameter. They are echodense with a homogeneous consistency and often have a central calcified core.

Papillary fibroelastomas
Papillary fibroelastomas generally arise from the ventricular aspect of semilunar valves, the atrial sides of atrioventricular valves and rarely from the chordae or right or left ventricular endocardium. The left heart valves account for 80% in adults but the tricuspid valve is most commonly

Figure 11.6 A low parasternal long axis view in a patient with a left atrial myxoma (*) (RV, right ventricle; LV, left ventricle; AO, aorta).

158

8 Parasternal long axis view in a patient with a fibroma (*) within the interventricular septum. mobile masses attached to the valve by a short stalk. superior vena cava). left ventricle. which partially obscures distal structures (RV. Morphologically they resemble a sea anemone. and can embolize or obstruct a coronary artery but do not obstruct forward flow. aorta. They are 2–4 cm in diameter. homogeneous tumors that are usually small. Hemangiomas Hemangiomas are vascular tumors that arise from the epicardium or endocardium but are usually intramural and usually seen in the walls of the right heart. and asymptomatic. S. affected in children. right ventricle. LV. sessile. Lipomas Lipomas are bright.CARDIAC MASSES Figure 11. Twenty-five percent of lipomas are intramyocardial and most are subepicardial. subendocardial. right ventricle. echodense acoustic signature. having multiple villous fronds attached to a central core of dense connective tissue. The tumor is echodense and casts an acoustic shadow. AO. aorta). shimmering. usually 1. 159 . Figure 11. AO. Fibroelastomas are small. Echocardiographically. LA.5 cm in diameter. pulmonary artery. PA.7 Off-axis subcostal short axis at the base in a patient with a small right atrial myxoma (*) (RV. left atrium. and have a spongy. they are very bright.

large tumor masses with irregular margins. They present as broad-based masses at the cavo-atrial junction that invade the RA endocardium and extend into the pericardium. pleura. right atrium). LA.9 Parasternal short axis view in a patient with an angiosarcoma. 160 . right ventricle. heterogeneous. and tricuspid valve and may metastasize to the lungs. They are invasive but they do not Figure 11. Echocardiographically.9).10 Apical four-chamber view in a patient with a rhabdomyosarcoma that has a broad base of attachment to the lateral wall of the left atrium (LA) and has spread into the left ventricular (LV) lateral wall myocardium (RV. The tumor has invaded the mediastinum and distorted the anatomy of the great vessels so that the aortic (AOV) and pulmonic (PV) valves almost occupy the same plane (RA.THE ECHOCARDIOGRAPHERS’ GUIDE PRIMARY MALIGNANT CARDIAC TUMORS Ninety-five percent of malignant primary cardiac tumors are sarcomas. left atrium). RA. right atrium. Figure 11. angiosarcomas are echo bright. inferior vena cava. Mean survival from diagnosis is rarely greater than six months. Angiosarcomas Angiosarcomas occur almost exclusively in the RA in the third to sixth decades of life and affect males twice as often as females. Rhabdomyosarcomas Rhabdomyosarcomas can affect any cardiac chamber. These tumors are aggressive and directly invade the mediastium (Figure 11.

Infiltration of the myocardium can cause regional wall motion abnormalities and a heterogeneous echocardiographic texture of the walls involved. pericardial effusions are often the only echocardiographic finding in cardiac lymphoma.CARDIAC MASSES usually extend beyond the parietal pericardium.10). However. such as patients with acquired immune deficiency syndrome (AIDS) or organ transplant. There is occasionally diffuse infiltration of the right atrial and right ventricular walls in which focal nodules may be appreciated. Primary cardiac lymphomas Primary cardiac lymphomas are rare and most often encountered in patients with a compromised immune system. 161 . They generally have a broad base of attachment and a heterogeneous tissue texture (Figure 11.

.

Oxygenated blood in the IVC is preferentially directed across the interatrial septum (IAS). when evaluating complex congenital malformations it is essential to follow a disciplined. segmental approach to identify atrial situs and document veno–atrial.12 CONGENITAL CARDIAC MALFORMATIONS CONTENTS q Fetal Cardiac Anatomy q Echocardiography Lesions q Complex Congenital Cardiac Malformations q Shunt Lesions q Obstructive One percent of all children are born with a congenital heart defect and the number of adults with congenital heart disease (CHD) is increasing as a result of effective therapy in infancy and childhood. 163 . the direction of which is dependent on the relative atrial pressures. Knowledge of the normal fetal circulation is necessary because some congenital abnormalities are the result of the persistence of elements of the fetal circulation after birth. atrio–ventricular. through the foramen ovale. The retrosternal cardiac position that often accompanies congenital cardiac malformations and scar tissue from prior corrective or palliative surgeries often makes imaging difficult in the adult patient with congenital heart disease. Flow through the PDA decreases and the duct ultimately closes and becomes the ligamentum arteriosum. Relatively deoxygenated blood from the superior vena cava (SVC) is preferentially directed through the tricuspid valve (TV). which is guarded by a flap valve. Additionally. PFOs can stretch in the presence of atrial enlargement and permit significant shunt flow. The eustachian valve and Chiari network help direct and separate the two streams of blood. a patent foramen ovale (PFO) is present in approximately 20% of the normal adult population. Pressure in the left atrium (LA) becomes greater than pressure in the right atrium (RA) and the flap valve of the foramen ovale closes and usually seals shut becoming the fossa ovalis in the first months of infancy. At birth. and chamber and great vessel morphology.1). PFOs permit paradoxical emboli and have been increasingly recognized as a source of stroke. Furthermore. sequential. Careful attention to patient positioning and the use of off-axis imaging windows is frequently necessary. However. and ventriculo–arterial connections. oxygen is provided to the fetus by the maternal placental circulation via the umbilical veins and inferior vena cava (IVC). pulmonic valve (PV) and the ductus arteriosus (PDA) to the descending aorta (Figure 12. the lungs expand and resistance to blood flow into the lungs greatly decreases. FETAL CARDIAC ANATOMY In utero. to the left side of the heart to facilitate the rapid growth of the head. The fetal lungs require only enough blood flow to support development and the pulmonary circulation is largely bypassed.

coronary sinus in the apical four-chambered view with the scan plane angled posteriorly (dorsally) (Figure 12.3). left ventricle. When the left SVC persists. Oxygenated blood from the inferior vena cava (IVC) passes through the flap of the foramen ovale (arrow in right atrium (RA)) and relatively deoxygenated blood from the superior vena cava (SVC) passes through the tricuspid and pulmonic valves and then through the ductus arteriosus (arrow in PA) (RV. right ventricle. Mirror image reversal of the abdominal aorta and IVC (situs inversus) indicates mirror image reversal of atrial situs (Figure 12. Atrial . LV. descending thoracic aorta.2 This parasternal long axis view shows a grossly enlarged coronary sinus (CS) (RV. LA. RA. left atrium. LV. In early embryonic life there are paired left and right SVCs. This can be confirmed with an injection of contrast medium into a vein in the left arm. When the abdominal aorta is anterior to and slightly to the left of the spine and the IVC is to the right of the spine then the atrial situs is normal (situs solitus) with the right atrium on the right and left atrium on the left. DAO. With subsequent development venous return from the left arm and left side of the head is diverted to the right SVC via the brachiocephalic vein and the distal left SVC becomes incorporated into the coronary sinus and the rest withers to become the ligament of Marshall. LPA. left ventricle. left pulmonary artery). AO.4). aorta).1 Diagram of the fetal circulation.THE ECHOCARDIOGRAPHERS’ GUIDE S V C AO RPA LPA LA D A O PA RA LV I V C RV Figure 12. Contrast enters the RA from the 164 ECHOCARDIOGRAPHY The segmental approach to echocardiographic diagnosis of complex congenital abnormalities begins with the establishment of the atrial situs.2). A greatly enlarged coronary sinus seen in the parasternal long axis usually indicates a persistent left SVC (Figure 12. LA. right ventricle. Figure 12. left atrium. right atrium. which can be imaged directly from the left supraclavicular fossa. which can be ascertained by examining the spatial relationship of the IVC and abdominal aorta. blood from the left upper body returns to the RA via the coronary sinus.

which is also right sided.37 (B) (Dao. which is situated on the superior right atrium wall and the elevated rim of tissue surrounding the fossa ovalis. 165 . The IVC is on the patient’s right and the aorta is on the patient’s left. The AV valves are always concordant with the ventricles. The TV inserts into the interventricular septum (IVS) at a more apical position than the mitral valve (MV) but this relationship is lost in complete endocardial cushion defect (ECD). Situs solitus is shown in Figure 2. The contrast material enters the right atrium and ventricle (RV) via the coronary sinus demonstrating a persistent left superior vena cava (LV.CONGENITAL CARDIAC MALFORMATIONS Figure 12. The systemic veins usually enter the RA and the pulmonary veins usually enter the LA but this is insufficiently reliable for identifying the atrial type. The body of the LA has a smoother contour than that of the RA and lacks pectinate muscles except in its appendage and the LA appendage has a narrow base while the base of the right atrial appendage is broad.3 The cause of the enlarged coronary sinus (CS) in Figure 12. There is a mirror image reversal of the normal relationship or situs inversus. Figure 12. The atrioventricular (AV) connections are then established. isomerism with bilateral right-sidedness (asplenia) is detected when the IVC is anterior to the abdominal aorta and both vessels are on the same side of the spine. left ventricle). descending thoracic aorta).4 The transducer is positioned in the subcostal region and angled caudad to visualize the spatial relationship of the abdominal aorta and the inferior vena cava (IVC).2 is revealed by an injection of agitated saline into a left arm vein. Atrial morphology is confirmed directly by identifying the flap of the fossa ovalis opening into the LA and by visualizing the limbus. Bilateral left-sidedness (polysplenia) is associated with interruption of the IVC in 70% of cases.

Near equalization of systemic and pulmonary pressures causes the shunt to become bidirectional (right to left during Figure 12. The MV has two predominant papillary muscles. or from the apical imaging window and permits identification of ventriculo–arterial connections as concordant or discordant. This feature of ventricular morphology is usually decisive. the aorta is seen to ascend anteriorly and from it will arise the coronary and brachiocephalic arteries. When a PDA is small it can be well tolerated for many decades but when large it can cause pulmonary hypertension or heart failure from LV volume overload. smaller papillary muscles. Atrioventricular connections are assessed to be either concordant (RA to RV).THE ECHOCARDIOGRAPHERS’ GUIDE Identification of the AV valve aids in recognition of the ventricular type. The incidence of PDA is higher in premature infants and up to 30 times higher in people living at high altitudes ( 5000 m). To establish the ventriculo–arterial connections it is necessary to recognize that the aorta arches and the pulmonary artery (PA) bifurcates. SHUNT LESIONS Patent ductus arteriosus When the ductus arteriosus remains patent (PDA) after birth. the magnitude of the flow is determined by the size of the ductus and by the aortic–pulmonary pressure gradient. From the left and right parasternal and suprasternal notch transducer positions.5 The pulmonary artery (PA) is enlarged in the parasternal short axis image on the left. The bifurcation of the PA must be visualized to unequivocally identify the great vessels. 166 . subcostal short axis views. The congenital abnormalities described below may be complex but can be resolved by the application of the segmental chamber analysis. This can be accomplished from off-axis high parasternal views. the right ventricle (RV) is more heavily trabeculated at the apex than the left ventricle (LV) and contains the moderator band. Importantly. the TV has multiple. Color Doppler demonstrates a continuous jet entering the right PA just distal to the bifurcation from a persistent ductus arteriosus (AO. aorta). The TV has chordal insertions directly to the IVS but the MV does not. discordant (RA to LV). ambiguous or unilaterally absent regardless of the position of each chamber within the chest. blood flows continuously from the aorta to the PA.

RA. LV. These are a type of an ECD commonly associated with a cleft MV and mitral regurgitation of varying severity (Figure 12. PDAs are best visualized from the parasternal view of the bifurcation of the PA on the inferior aspect of the proximal right PA. Once identified.CONGENITAL CARDIAC MALFORMATIONS systole and left to right during diastole). Atrial septal defects These occur in the midportion of the IAS in the region of the fossa ovalis in 65–80% of cases and are termed ostium secundum atrial septal defects (ASDs) (Figure 12.8) and are frequently associated with trisomy 21 (Down syndrome). Figure 12.6).5).9). PDAs may be the site of endovascular infection. and occur at an earlier age.5 m/s.6 Continuous wave Doppler directed through the color jet in Figure 12. right atrium.7). Color flow Doppler (right panel) shows left to right flow across the defect (RV.7 Apical four-chamber view in a patient with a large secundum atrial septal defect (*).5 demonstrates a diastolic velocity of 3 m/s and a systolic velocity of 4. 167 . Color Doppler of the PA reveals a bright continuous flow that extends several centimeters into the PA (Figure 12. most often with a direct connection of the Figure 12. right ventricle. the site of the PDA can be interrogated by continuous wave (CW) Doppler and systolic and diastolic aortic/PA pressure gradients assessed (Figure 12. Ostium primum ASDs are anterior and inferior to the fossa ovalis and in continuity with mitral and tricuspid valve tissue inferiorly (Figure 12. left atrium). which usually overrides the defect but a minority are adjacent to the IVC. left ventricle. Sinus venosus ASDs are usually located at the roof of the atria close to the insertion of the SVC. LA. Symptoms are generally more severe in primum than secundum ASDs. Sinus venosus ASDs are associated with partial anomalous pulmonary venous drainage.

RA. left atrium).8 Apical four-chamber view in a patient with a primum atrial septal defect (ASD). subcostal short axis and the upper right sternal transducer position the IAS is perpendicular to the beam while shunt flow is parallel to it facilitating pulsed-wave and color Doppler interrogation. Figure 12. left ventricle. A coronary sinus ASD or unroofed coronary sinus is a rare type of ASD that results from a defect in the vessel wall separating the coronary sinus from the LA. The goal of echocardiography in the evaluation of a patient with an ASD is to identify the location and size of the defect.10). as from the apical fourchambered view. LV. Flow across the ASD is continuous and 168 .8. LA. the pulmonary and systemic blood flows (Qp/Qs). and PA systolic pressure. right atrium. The mitral and tricuspid valves are coplanar (RV. From the subcostal fourchamber. the relationship of the defect to the AV valves. right upper and middle pulmonary veins to the SVC (Figure 12. There is a cleft in the anterior mitral valve leaflet.9 A short axis view in the same patient as Figure 12.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 12. The IAS is normally thin and difficult to visualize adequately when parallel to the ultrasound plane. right ventricle.

An injection of agitated saline into a peripheral vein causes opacification of the right heart chambers and the appearance of contrast (bubbles) in the left atrium in the presence of an ASD either at rest or with a Valsalva maneuver. primum atrial septum. Muscular VSDs are entirely surrounded by ventricular myocardium and are subclassified by their location. as defects in the inlet (between the RV and LV inflow tracts (RVIT and LVIT)). trabecular (usually in the vicinity of the moderator band) or outlet (between the infundibulum and LVOT) portions of the IVS. ASDs are also associated with atrial arrhythmias and paradoxical emboli. the PA and right heart chambers may be dilated. left inferior pulmonary vein. Depending on the magnitude of the shunt. RIPV Figure 12. By carefully aligning the ultrasound beam 169 low velocity. Subarterial or doubly committed VSDs result from a deficiency of the infundibular septum and are bound superiorly by the semilunar valves. Reducing the velocity scale facilitates the recognition of shunt flow by color Doppler. The magnitude of the shunt flow is expressed as the ratio of pulmonary to systemic flows (Qp:Qs) and can be estimated as the ratio of the Doppler derived RV outflow tract (RVOT) and LVOT stroke volumes. right inferior pulmonary vein. The arrow points to the flap of the fossa ovalis (P. L. Defects less than 2 cm in diameter which are surrounded by atrial septal tissue are usually amenable to transcatheter device closure.11). Transthoracic echocardiography (TTE) can accurately diagnose the presence of an ASD but transesophageal echocardiography (TEE) is necessary to assess the pulmonary venous connections.10 A diagram of normal atrial and atrial septal anatomy in apical four-chamber orientation. determine whether defects are single or multiple and whether they are suitable for device closure. solitary and restrictive. Perimembranous VSDs often close spontaneously during early childhood by incorporation of TV tissue into the defect. Surgical patch closure is one of the safest and most effective cardiac surgical procedures and is generally recommended. right ventricle. limbus. left atrium). the IVS may show paradoxical motion and the LV may be small and under-filled. right atrium. LA. Perimembranous ventricular septal defects (VSDs) are usually small. PA pressure may be estimated from the peak velocity CW signal of the tri- . RV. Bubbles must appear in the left atrium within five cardiac cycles of their appearance in the RA to confirm the presence of an ASD as the late arrival of contrast may occur through pulmonary AV malformations. ASDs are often clinically silent but significant shunting (Qp:Qs 2. pulmonary hypertension and/or right heart failure. are located beneath the posterior right and noncoronary cusps of the aortic valve in the region of the interventricular portion of the membranous septum (Figure 12. LIPV. LV. Muscular VSDs may be multiple and located in different parts of the muscular septum. left ventricle.CONGENITAL CARDIAC MALFORMATIONS RV IVS LV P RA LA LIPV L cuspid regurgitation (TR) jet. Ventricular septal defects Most defects of the IVS (approximately 70%). Flow across a restrictive VSD can be readily appreciated by color Doppler imaging.0) ultimately causes symptoms of dyspnea. The high velocity jet across this type of defect can cause a Venturi effect that sucks the right or noncoronary cusp into the defect causing aortic regurgitation. RA. RIPV.

LVOT. often with a bicuspid or unicuspid morphology. Restricting bands used to be placed around the PA to protect the pulmonary vasculature in infants with nonrestrictive VSDs who were not candidates for definitive surgical repair. RA. 170 Tetralogy of Fallot Embryologic malalignment of the infundibular septum with the rest of the muscular septum causing a large. nonrestrictive.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 12.14). with the jet. LV. Qp:Qs and pulmonary artery pressures must be carefully evaluated in all cases of left-to-right shunt. right atrium. right ventricle. The pulmonary valve annulus is small and the pulmonic valve is usually stenotic. perimembranous VSD is the cardinal feature of tetralogy of Fallot (TOF). RVH and muscle bundles in the infundibular wall may contribute to the RVOT obstruction. LA.1). Patients with TOF and severe PS or TOF with pulmonary atresia present in early infancy with cyanosis and hypoxemia . Subtracting the trans-septal gradient from the cuff systolic blood pressure yields an estimate of the RV systolic pressure. which is the most common cause of cyanotic heart disease (Table 12. left atrium. Anterior deviation of the infundibulur septum narrows the RVOT (Figure 12. which is sufficient to prevent pulmonary hypertension in TOF. which often requires off-axis. AO.11 Color flow Doppler in the parasternal long axis (left panel) and parasternal short axis (right panel) showing systolic flow through a perimembranous interventricular septum (RV. which should be in agreement with estimate obtained from the maximum TR velocity and RA pressure. Nonrestrictive VSDs are large and the pulmonary circulation is exposed to systemic pressure in the absence of pulmonic stenosis (Figure 12. left ventricle. CW Doppler will yield the velocity of the interventricular flow from which the trans-septal pressure gradient can be calculated by the modified Bournoulli equation.12) and these patients usually require surgery in infancy.13) and causes the aorta to override the muscular IVS (Figure 12. LV outflow tract). Symptoms and exercise tolerance vary with the degree of pulmonary stenosis (PS). non-standard transducer positions. aorta.

CONGENITAL CARDIAC MALFORMATIONS Figure 12. right ventricle. Essential elements of the echocardiographic evaluation of a patient with TOF include determination of the site and severity of RVOT obstruction. This is better achieved from the apical view when the transducer is angled anteriorly past the LVOT and from the subcostal short axis at the base of the heart.1 Tetrology of Fallot Figure 12. right ventricle. left atrium). Transseptal flow will usually be low velocity reflecting nearly equal RV and LV systolic pressure. left atrium). Right ventricular hypertrophy Pulmonic stenosis Ventricular septal defect Overriding aorta 171 . The RV systolic pressure can be estimated by the CW signal of TR as usual. left ventricle. right atrium.12 Apical four-chamber view from a patient with a nonrestrictive ventricular septal defect (VSD) (RV. estimation of RV and PA pressures and assessment of pulmonary regurgitation.13 In tetralogy of Fallot anterior deviation of the infundibular septum (arrow) narrows the RV outflow tract and causes the ventricular septal defect (*) with an overriding aorta (RV. LA. right atrium. The RVOT is visualized from the parasternal short axis and parasternal long axis views of the RVOT but these views do not always permit alignment of the CW Doppler beam with flow when the obstruction is at the infundibular level. LA. the magnitude and direction of trans-septal flow. RA. LV. PA systolic pressure is obtained by subtracting the RVOT gradient from the RV systolic Table 12. upon closure of the PDA as the pulmonary circulation is largely supplied by retrograde flow from the aorta through the duct. RA.

PA is on the left and the aorta on the right. although some authors insist that for the diagnosis of DORV.14 This parasternal long axis view demonstrates the ventricular septal defect (*) and overriding aorta in tetralogy of Fallot (RV. left ventricle. without PS the symptoms will be those of a nonrestrictive VSD. This type of DORV mimics complete transposition of the great arteries and cyanosis is predominant. Surgical scars in the vicinity of the RVOT are a substrate for arrhythmias. The RVOT may be enlarged with a patch across the PV annulus. which must therefore be large and this exposes the pulmonary vasculature to systemic pressure unless there is also subpulmonic obstruction. With PS. the aorta and mitral valves must not be in continuity but separated by an infundibulum. TOF is often associated with a right aortic arch. The aorta sits adjacent to the VSD and preferentially receives oxygenated blood. It is often an incidental finding without hemodynamic significance but if the opening in the membrane is small. aorta). LV. pressure. LA. In DORV all oxygenated blood must pass through the VSD. to the RA via subdiaphragmatic connection of a vertical vein to the IVC (scimitar syndrome) or the pulmonary . Double outlet right ventricle Double outlet RV (DORV) may be considered to be an exaggerated form of TOF in which the aorta is to the right of the IVS. left atrium. the 172 Cor triatriatum In cor triatriatum the pulmonary veins enter an accessory chamber that is separated from the LA by a membrane (Figure 12. An imperforate cor triatriatum membrane will be associated with total anomalous pulmonary venous return (TAPVR). symptoms will mimic those seen in mitral stenosis. AO. Pulmonary venous return to the heart will be to the RA by way of an ascending vertical vein to the brachiocephalic vein and SVC. OBSTRUCTIVE LESIONS Congenital valvular abnormalities are discussed in Chapter 8. symptoms will resemble TOF. Surgical repair of TOF consists of a patch closure of the VSD and alleviation of the RVOT obstruction. and this is often associated with significant pulmonary insufficiency. In the Taussig–Bing type of DORV the great vessels are transposed.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 12.15). right ventricle.

173 . which if high. Coarctation of the aorta Coarctation of the aorta is a narrowing or complete interruption of the aorta in the region of the ligamentum arteriosum that is usually discrete but may be a tubular narrowing affecting a variable length of the aorta (Figure 12. tral cyanosis will be present.16 Suprasternal notch view in a patient with coarctation of the aorta (Tao. In severe cases presenting in infancy.15 A non-obstructing membrane is seen in the left atrium (LA) (arrow) in this apical four-chamber view in this patient with cor triatriatum (RV. The pressure gradient persists through diastole. descending aorta). flow to the distal aorta may be predominately through a PDA and peripheral but not cen- Figure 12.17).16. Coarctation is four times more common in males and often associated with a bicuspid aortic valve.CONGENITAL CARDIAC MALFORMATIONS Figure 12. left ventricle). veins will remain at the level of the heart and drain into the RA.16).17 Continuous wave Doppler through the coarctation shown in Figure 12. Coarctation of the aorta is usually only visualized from the suprasternal notch (SSN). transverse aorta. Figure 12. or coronary sinus individually or in combinations. LV. Dao. which also enables CW Doppler assessment of the pressure gradient across the obstruction. The distal thoracic and abdominal aorta are diminished in size in proportion to the degree of obstruction. right ventricle. persists through diastole (Figure 12. TAPVR is to the RA so that an ASD is obligatory. SVC. Generally.

Right-to-left shunting at the atrial Figure 12. Figure 12. The TR signal originates from the point of coaptation of the tricuspid leaflets. 174 . A large portion of the right ventricle (RV) is ‘atrialized’ (LV. left ventricle. right atrium. The following examples are chosen because. The point of tricuspid valve closure is displaced toward the apex. RA.18). the anterior leaflet is elongated and sail-like and may cause RVOT obstruction. they are encountered in the adult population. left atrium). which is displaced toward the apex. forming a common chamber with the RA and not contributing to RV systolic contraction (Figure 12. TR is almost universally present and often severe but the velocity is low. The TR originates at the coaptation point and the extent of its displacement can be readily recognized with color Doppler (Figure 12.19). The coaptation point is apically displaced and the portion of the RV proximal to the coaptation point is ‘atrialized’. The TV tissue is markedly redundant and dysplastic. LA. although rare.19 This patient has moderate tricuspid regurgitation (TR) by color flow Doppler. Ebstein anomaly In Ebstein anomaly the TV leaflets do not separate adequately from the RV endocardium but remain attached at variable points.THE ECHOCARDIOGRAPHERS’ GUIDE COMPLEX CONGENITAL CARDIAC MALFORMATIONS An exhaustive treatment of the subject of complex congenital cardiac abnormalities is beyond the scope of this text.18 Apical four-chamber view in a patient with Ebstein anomaly.

There is a primum atrial septal defect (*) and a ventricular septal defect (arrow) (RV. Echocardiographic findings in partial ECD consist of a primum ASD. 175 . right ventricle. left ventricle). RA.20).20 Parasternal short axis view in a patient with an endocardial cushion defect. from which is derived the tissue that divides the embryologic common AV canal into separate tricuspid and mitral orifices (Figure 12. which may have chordal attachments to the contralateral ventricle through the VSD or to the superior IVS. LV. degree of RV atrialization. the degree of TR. complete defects more commonly than partial. A defect on the upper ventricular septum is almost invariably present in complete ECD and there is one common AV annulus with five leaflets (Figure 12. cleft anterior MV leaflet and coplanar attachments of the anterior MV and septal TV leaflets. There is a common atrioventricular valve with five leaflets (RV. AV septal defect.21 Subcostal short axis view in a patient with complete endocardial cushion defect. right ventricle.21). Endocardial cushion defects ECD or atrioventricular canal defects result from failure in the development of the endocardial cushions. Doppler/ echocardiography is used to evaluate the extent and location of valve tethering and Figure 12. level from ASDs or stretched PFOs is common and can cause cyanosis. LA. A transitional type of ECD consists of a primum ASD with a common AV valve but in this Figure 12. left atrium).CONGENITAL CARDIAC MALFORMATIONS dysplasia. right atrium. Surgery is generally required before the age of 2 years for complete ECD. and the magnitude of atrial shunting. These may be partial or complete and commonly affect patients with trisomy 21 (Down syndrome).

ASD.THE ECHOCARDIOGRAPHERS’ GUIDE Figure 12.22 Parasternal long axis in a patient with Dloop transposition of the great vessels. The baffle is made of prosthetic material or pericardium in the Mustard procedure and flaps of atrial tissue in the Senning procedure For D-transposition with a malalignment VSD. superior vena cava. pulmonary artery. SVC. ventricular septal defect.2 Surgery for congenital heart defects To increase pulmonary artery blood flow as in tetralogy of Fallot Blalock–Taussig Subclavian artery to PA anastomosis Glenn shunt SVC to RPA anastomosis Waterston shunt Ascending AO to RPA anastomosis Potts shunt Descending AO to PA anastomosis For D-looped transposition Rashkind Blalock–Hanlon Mustard or Senning procedure Rastelli Jatene Balloon atrial septostomy to increase the mixing of systemic and pulmonary venous return in D-looped transposition of the great vessels Operative atrial septostomy to increase the mixing of systemic and pulmonary venous return in D-looped transposition of the great vessels Creates an intra-atrial baffle to direct pulmonary venous return to the RV and systemic venous return to the LV. The proximal PA is anastomosed to the AO and the RA connected to the distal PA PA. LV. aorta. RV right ventricle. The PV is sewn shut and a valved conduit used to connect the RV to the PA Arterial switch with reimplantation of the coronaries for complete transposition of the great vessels For univentricular atrioventricular connection Fontan procedure The RA is connected to the RPA either directly or with the interposition of a valved conduit and the ASD and VSD are closed Damas–Kaye–Stansel Modification of the Fontan procedure for univentricular AV connection to a morphologic LV with transposition and subaortic stenosis or restrictive VSD. PV. right PA. pulmonic valve. right atrium 176 . left ventricle. VSD. The PA is severed. The semilunar valves are coplanar. The aorta is connected to the LV through the VSD. RPA. RA. Table 12. AO. atrial septal defect. The aorta (AO) arises from the right ventricle (RV) and the pulmonary artery (PA) from the left ventricle (LV).

Echocardiographic evaluation of patients with Mustard or Senning procedures must include examination of the baffle for leaks and obstruction and a careful assessment of the size and function of the RV and the presence of TR. The PA does not curve around the aorta.CONGENITAL CARDIAC MALFORMATIONS type. Systemic venous return is to the aorta and pulmonary venous return is to the PA and this is incompatible with life without a large intracardiac shunt. right atrium. left atrium). In complete TGV (D-loop transposition) there is AV concordance and ventriculoarterial (VA) discordance. The right panel shows the communication between the systemic venous return and the left ventricle (LV) (RA. The LV is usually hyperdynamic. The left panel shows the communication between the pulmonary veins and the right ventricle (RV). In congenitally corrected or L-looped transposition both the AV and VA connections are discordant such that the ventricles Figure 12.2) was performed for complete transposition and a large number of patients have survived to adulthood because of these procedures (Figure 12. VSDs coexist in a third of cases but a balloon atrial septostomy (Rashkind procedure) is often required to create or enlarge an ASD as a palliative procedure in early infancy.23). LA. The aorta arises from a normally positioned RV anterior and to the right of the PA. The Jatene procedure or arterial switch with reimplantation of the coronary arteries completely corrects the defect.22). which reflects systemic pressure and is the reason for the RV hypertrophy. the VSD is closed by abnormal AV valve tissue. 177 . the great vessels are parallel and the semilunar valves are usually coplanar (Figure 12. Transposition of the great vessels Transposition of the great vessels (TGV) is the most common form of cyanotic heart disease presenting in infancy. The RV is the systemic ventricle and late RV failure and TR are common. Prior to the development of the arterial switch technique an atrial switch (Mustard or Senning) procedure (Table 12.23 Apical four-chamber view in a patient with D-loop transposition of the great vessels with an intra-atrial switch repair (Mustard procedure). An intra-atrial baffle is created to route systemic venous return to the LV and pulmonary venous return to the right ventricle.

The ventricles are inverted. RA. LA. 178 . Both atrioventricular valves are seen entering a common chamber.24 Apical four-chamber view in a patient with L-loop transposition of the great vessels. right atrium. The right ventricle (RV) is identified by the moderator band (arrow) and by the more apical insertion of the septal leaflet of the tricuspid valve (LV. This patient had dextrocardia and this image was recorded with the transducer at the right mid-clavicular line in the seventh intercostal space. Figure 12. The left ventricle (LV) was hypoplastic and posterior to the RV. left atrium).25 Off-axis apical ‘four-chamber’ view in a patient with univentricular atrioventricular connection to a morphologic right ventricle (RV).THE ECHOCARDIOGRAPHERS’ GUIDE Figure 12. left atrium). left ventricle. which is identified as a morphologic RV by the prominent apical trabeculations. Both great vessels came off the RV and the pulmonary vasculature was shielded by a stenosed pulmonic valve (LA.

Alternatively. bicaval to PA or RA to RV infundibular connections are made. while the other ventricle is hypoplastic. When combined venous return is to a morphological LV. the LV is a hypoplastic slit on the diaphragmatic aspect of the heart posterior to the RV and usually has neither inflow nor outflow.24). the RV consists of a small outflow chamber anterior and superior to the LV connected to it by a VSD. which is referred to as the dominant ventricle. Both great vessels arise either from the RV (DORV) or there may be PA atresia. The Fontan procedure was originally used for patients with tricuspid atresia. Patients with TV atresia usually have diminished pulmonary blood flow either from pulmonary valvular stenosis or a flow limiting VSD. Univentricular AV connection results from tricuspid atresia or mitral atresia in which ASDs are obligatory and from double inlet right or left ventricles (Figure 12. When the combined venous return is to a morphologic RV. Patients may remain asymptomatic for decades but as in patients with intra-atrial baffles. the latter with the hope that the hypoplastic RV can contribute to systolic flow.CONGENITAL CARDIAC MALFORMATIONS are inverted (Figure 12. late RV failure is common. The hypoplastic RV gives off at least one great vessel. 179 .25). The RA is connected to the right PA either directly or with the interposition of a valved conduit and the ASD and VSD are closed. Univentricular atrioventricular connection In univentricular AV connection both systemic and pulmonary venous drainage is to one ventricle.

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cardiac masses 160 anthracycline cardiomyopathy 121–2 aorta 147–53 anatomy 147–8 aortic dissection 150–3 atherosclerotic disease 148–50 aortic dissection 150–3 classification 150 echocardiography 150–3 Marfan syndrome 151 aortic regurgitation (AR) 94–100 acute severe 99–100 assessment 95 Doppler 96–9 M-mode 95 two-dimensional echo 95–6 aortic stenosis (AS) 89–94 congenital 89 Doppler echo 91–4 Doppler-echocardiography 90–4 M-mode 90 rheumatic 89 senile calcific 89 subvalvular 89–90 supravalvular 90 symptoms 90 two-dimensional echo 90–1 aortic valve anatomy 87 AS 89–94 bicuspid aortic valve (BAV) 87–9 valvular heart disease 87–100 apical four-chamber view. 70. congenital cardiac malformations 175–7 attenuation 1. 69. 169 atrioventricular canal defects. 71 apical window 22–8 apical long axis view 26 apical short axis view 27–8 apical two-chamber view 27. 28 coronary artery disease 68. aorta 148–50 atrial septal defects (ASDs) congenital cardiac malformations 167–9 ostium primum ASDs 167–8 ostium secundum ASDs 167 sinus venosus ASDs 167–8. congenital cardiac malformations 176 181 . 2 axial resolution 2 B-mode 3 bacterial pericarditis 145 BAV see bicuspid aortic valve Becker muscular dystrophy. where separate from text reference acoustic impedance 1 acoustic matching layer 3 acute chest pain. congenital cardiac malformations 176 Blalock–Taussig surgical technique.Index Note: bold denotes figures. cardiomyopathies 123 bicuspid aortic valve (BAV) 87–9 Blalock–Hanlon surgical technique. echocardiographic evaluation 66–7 acute infarction complications. coronary artery disease 67–74 acute pulmonary embolism 48–50 afterload 35 alcoholic cardiomyopathy 120 aliasing 6–7 amyloid heart disease 131–3 anatomy 13 aneurysms aortic atherosclerotic disease 148–50 coronary artery disease 67–9 angiosarcomas. 72. coronary artery disease 62–4. 66. 73 apical long axis view 26 apical short axis view 27–8 coronary artery disease 70 apical three-chamber view. 68. 28 MR 22–6 AR see aortic regurgitation arrhythmogenic RV dysplasia (ARVD) 134 AS see aortic stenosis ASDs see atrial septal defects atherosclerotic disease. coronary artery disease 65 apical two-chamber view 27.

68. 171 congenital complete absence of the parietal pericardium 146 congenital pericardial cysts 145–6 constrictive pericarditis (CP) 143–5 vs. 66. 169 surgery 176 transposition of the great vessels (TGV) 177–9 tetrology of Fallot (TOF) 170–2 182 univentricular atrioventricular connection 178. echocardiographic evaluation 66–7 CM see cardiomyopathies coarctation of the aorta. MR 84–5 complex congenital cardiac malformations 174–9 compression algorithms 4. 69. acute infarction 67–74 coronary anatomy 61–5 echocardiographic evaluation 66–7 long axis view 63. 72. 5 congenital cardiac malformations 163–79 ASDs 167–9 atrioventricular canal defects 175–7 coarctation of the aorta 173 complex congenital cardiac malformations 174–9 cor triatriatum 172–3 double outlet RV (DORV) 172 Ebstein anomaly 174–5 endocardial cushion defect (ECD) 175–7 echocardiography 164–6 fetal cardiac anatomy 163–4 obstructive lesions 172–3 ostium primum ASDs 167–8 ostium secundum ASDs 167 patent ductus arteriosus (PDA) 166–7 shunt lesions 166–72 sinus venosus ASDs 167–8. 6. restrictive cardiomyopathies 145 continuous wave (CW) Doppler 5. 71 papillary muscle rupture 74 parasternal short axis view 72. 73 thrombus 69. 73 pseudoaneurysm 71–2 right ventricular infarction 74 short axis view 64. congenital cardiac malformations 173 color Doppler flow mapping.INDEX carcinoid heart disease 103 cardiac masses 155–61 angiosarcomas 160 fibromas 158 hemangiomas 159 lipomas 159 myxomas 158 papillary fibroelastomas 158–9 primary benign cardiac tumors 158–9 primary cardiac lymphomas 161 rhabdomyomas 158 rhabdomyosarcomas 160–1 secondary cardiac tumors 156–8 cardiac rupture. 71 cardiac rupture 69–71 complications. 72. 70. 60 spectral Doppler 54–60 stiffness and relaxation 51–3 tissue Doppler imaging (TDI) 59–60 transmitral Doppler 54–6 two-dimensional imaging 53–4 digital scan converter (DSC) 4 dilated cardiomyopathy (DCM) 118–24 Doppler 5–11 AR 96–9 CW Doppler 5. 71 ventricular septal rupture 72–4 wall motion abnormalities (WMAs) 62–6 CP see constrictive pericarditis CW Doppler see continuous wave Doppler damping 2 DCM see dilated cardiomyopathy diastolic function 51–60 M-mode 53–4 propagation velocity 58–9 pulmonary vein Doppler 56–8. 70. 48 cor triatriatum. coronary artery disease 69–71 cardiomyopathies (CM) 117–34 alcoholic cardiomyopathy 120 anthracycline cardiomyopathy 121–2 Chagas’ disease 122–3 dilated cardiomyopathy (DCM) 118–24 hypertrophic cardiomyopathy (HCM) 124–30 HIV/AIDS cardiomyopathy 121 muscular dystrophies 123 noncompaction 124 peripartum cardiomyopathy 121 prolonged tachyarrhythmias 123 restrictive cardiomyopathies (RCM) 130–4 Chagas’ disease 122–3 chest pain. 6. 7 Doppler color flow 8–9 high-PRF Doppler 7–8 left ventricular (LV) systolic function 39–42 power Doppler 9 . 70. 7 contrast echocardiography 10–11 ‘cor pulmonale’ 45. 179 VSDs 169–70. 73 apical short axis view 70 apical three-chamber view 65 apical two-chamber view 68. congenital cardiac malformations 172–3 coronary artery disease 61–74 acute infarction complications 67–74 aneurysms 67–9 apical four-chamber view 62–4.

AS 91–4 Doppler-echocardiography. left ventricular (LV) systolic function 39–40 frame rate 4 Frank–Starling relationship 35–6 fungal endocarditis 109–10 Glenn shunt surgical technique. 71 parasternal window 14. AS 90–4 Doppler findings. cardiac masses 159 hemochromatosis 133. congenital cardiac malformations 176 lateral resolution 2–3 left ventricular (LV) noncompaction 124 left ventricular (LV) systolic function 35–42 apical area/length formula 37 Doppler 39–42 force and acceleration 39–40 LV cavity volume 36–7 LV mass/hypertrophy 38 M-mode 36–9 MR 40 shape 37 Simpson rule method 37. cardiac masses 159 Loffler’s endocarditis 131 long axis view coronary artery disease 63. aortic dissection 151 mitral regurgitation (MR) 22–6. congenital cardiac malformations 174–5 ECD see endocardial cushion defects echocardiographic evaluation chest pain 66–7 coronary artery disease 66–7 EMF see endomyocardial fibrosis endocardial cushion defects (ECD). 15. 82–7 causes 82–4 chronic 82 color Doppler flow mapping 84–5 ischemic 82–3 left ventricular (LV) systolic function 40 183 . mitral stenosis 78–82 double outlet RV (DORV). TTE 110 two-dimensional echo 107–10 valvular heart disease 106–10 vegetation 107–10 endomyocardial fibrosis (EMF) 130–1 eosinophilic endomyocardial disease 131 fast Fourier transformation (FFT) 6 fetal cardiac anatomy 163–4 FFT see fast Fourier transformation fibroelastomas 110 fibromas.INDEX PS 105 PW Doppler 5–7 spectral Doppler 6 Tei index 39 TR 102–3 TS 101 Doppler color flow 8–9 Doppler echo. congenital cardiac malformations 176 force and acceleration. congenital cardiac malformations 175–7 endocarditis fungal 109–10 nonbacterial thrombotic endocarditis (NBTE) 110 TEE vs. 16 pulmonary embolism (PE) 141 pulmonic stenosis (PS) 105 tricuspid stenosis (TS) 101 marantic endocarditis 110 Marfan syndrome. MR 25–6 Libman–Sacks verrucous endocarditis 110 lipomas. congenital cardiac malformations 176 HCM see hypertrophic cardiomyopathy hemangiomas. congenital cardiac malformations 172 DSC see digital scan converter Duchenne muscular dystrophy. 134 high-PRF Doppler 7–8 HIV/AIDS cardiomyopathy 121 hypertrophic cardiomyopathy (HCM) 124–30 symptoms 127 interpolation 4 Jatene surgical technique. 71 LVOT see left ventricular outflow M-mode 3 AR 95 AS 90 diastolic function 53–4 left ventricular (LV) systolic function 36–9 mitral stenosis 77 MR 84 parasternal window 14–15. 38 strain and strain rate 42 tissue Doppler imaging (TDI) 40–1 Tei index 39 three-dimensional echocardiography 39 two-dimensional echo 36–7 left ventricular outflow (LVOT). congenital cardiac malformations 176 Ebstein anomaly. cardiac masses 158 fibroplastic endocarditis 131 focal zone 2 Fontan procedure surgical technique. cardiomyopathies 123 Damas–Kaye–Stansel surgical technique.

63. 140. 71 M-mode 14–15. 146 pericarditis 135–6 post-cardiac surgery 145 post-infarction pericarditis 145 purulent pericarditis 145 specific etiologies 145–6 tamponade 139–43. 142. 146 pericardium 135–46 anatomy 135 bacterial pericarditis 145 congenital complete absence of the parietal pericardium 146 184 congenital pericardial cysts 145–6 constrictive pericarditis 143–5 pulmonary embolism (PE) 136–9. congenital cardiac malformations 176 power Doppler 9 preload 35 PRF see pulse repetition frequency primary benign cardiac tumors. 141. cardiac masses 158–9 primary cardiac lymphomas. cardiac masses 161 prolonged tachyarrhythmias 123 propagation velocity 1 diastolic function 58–9 prosthetic heart valves. congenital cardiac malformations 176 MVP see mitral valve prolapse myxomas. 146 peripartum cardiomyopathy 121 phased array 4 PI see pulmonic insufficiency piezoelectric crystal 2 PISA see proximal isovelocity surface area post-cardiac surgery 145 post-infarction pericarditis 145 Potts shunt surgical technique. 72. parasternal window 15–18 . congenital cardiac malformations 167 papillary fibroelastomas. 15.INDEX mitral regurgitation (MR) (cont. congenital cardiac malformations 167–8 ostium secundum ASDs. valvular heart disease 111–15 proximal isovelocity surface area (PISA) mitral stenosis 80–2 MR 86–7 PS see pulmonary stenosis pseudoaneurysm. coronary artery disease 74 ‘paraspinal’ imaging 34 parasternal window 13–22 long axis view 14. congenital cardiac malformations 166–7 pericardial effusion (PE) 136–9.) LVOT 25–6 M-mode imaging 84 mechanisms 82 mitral valve prolapse (MVP) 83–4 proximal isovelocity surface area (PISA) 86–7 pulmonary vein Doppler 85–7 spectral Doppler 85 two-dimensional imaging 84 mitral stenosis 76–82 Doppler findings 78–82 etiology 76–7 M-mode echo findings 77 proximal isovelocity surface area 80–2 two-dimensional echo findings 77–8 mitral valve anatomy 75–6 mitral stenosis 76–82 valvular heart disease 75–87 mitral valve prolapse (MVP) 83–4 MR see mitral regurgitation muscular dystrophies 123 Mustard procedure surgical technique. coronary artery disease 71–2 pulmonary embolism. 16 RA/RV view 15–18 RV inflow tract view 15–18 short axis view 18–22. 60 mitral regurgitation (MR) 85–7 pulmonic insufficiency (PI) 105–6 pulmonic valve anatomy 104 pulmonic insufficiency (PI) 105–6 pulmonic stenosis (PS) 104–5 valvular heart disease 104–6 pulse length 2 pulse repetition frequency (PRF) 4 pulsed-wave (PW) Doppler 5–7 purulent pericarditis 145 PW Doppler see pulsed-wave Doppler RA/RV view. acute 48–50 pulmonary stenosis (PS) 104–5 assessment 105 Doppler 105 M-mode 105 two-dimensional echo 105 pulmonary vein Doppler diastolic function 56–8. cardiac masses 158 nonbacterial thrombotic endocarditis (NBTE). 140. congenital cardiac malformations 172–3 ostium primum ASDs. 141. 142. cardiac masses 158–9 papillary muscle rupture. valvular heart disease 110 Nyquist limit 6 obstructive lesions. 73 patent ductus arteriosus (PDA).

INDEX Rashkind surgical technique. 48 RV pressure overload 44–8. 72. 71 time gain compensation (TGC) 3 tissue characterization 9–10 tissue Doppler imaging (TDI) diastolic function 59–60 left ventricular (LV) systolic function 40–1 TOF see tetralogy of Fallot TR see tricuspid regurgitation transducers 2–3. 32 suprasternal notch views 31–3 surgery. congenital cardiac malformations 176 surgical treatment. congenital cardiac malformations 167–8. 73 parasternal window 18–22. cardiac masses 156–8 Senning procedure surgical technique. 73 shunt lesions. left ventricular (LV) systolic function 42 subcostal window 28–31. congenital cardiac malformations 176 RCM see restrictive cardiomyopathies reject control 3 restrictive cardiomyopathies (RCMs) 130–4 amyloid heart disease 131–3 arrhythmogenic RV dysplasia (ARVD) 134. congenital cardiac malformations 166–72 Simpson rule method. 134 infiltrative diseases 131–4 Loffler’s endocarditis 131 primary 130–1 sarcoidosis 133–4 secondary 131–4 Uhl’s anomaly 134. cardiac masses 160–1 right parasternal transducer position 33 right ventricular infarction. 10 left ventricular (LV) systolic function 39 thrombus. congenital cardiac malformations 176 Rastelli surgical technique. coronary artery disease 74 right ventricular (RV) function 43–50 acute pulmonary embolism 48–50 ‘cor pulmonale’ 45. 49 RV volume overload 44. coronary artery disease 69. valvular heart disease 111–15 tamponade 139–43. 4 transmitral Doppler. endocarditis 110 two-dimensional echo aortic regurgitation (AR) 95–6 aortic stenosis (AS) 90–1 endocarditis 107–10 left ventricular (LV) systolic function 36–7 mitral stenosis 77–8 pulmonic stenosis (PS) 105 tricuspid regurgitation (TR) 102 tricuspid stenosis (TS) 101 two-dimensional imaging 3–5 diastolic function 53–4 185 . cardiac masses 158 rhabdomyosarcomas. 70. 38 sinus venosus ASDs. 146 TAPSE see Tricuspid Annular Plane Systolic Excursion TDI see tissue Doppler imaging TEE vs. TEE. 70. parasternal window 15–18 sample volume 6 sarcoidosis 133–4 secondary cardiac tumors. left ventricular (LV) systolic function 37. 134 vs. 134 rhabdomyomas. constrictive pericarditis (CP) 145 endomyocardial fibrosis (EMF) 130–1 hemochromatosis 133. left ventricular (LV) systolic function 39 tetralogy of Fallot (TOF). TTE. 72. congenital cardiac malformations 176 short axis view coronary artery disease 64. congenital cardiac malformations 177–9 Tricuspid Annular Plane Systolic Excursion (TAPSE). 169 sound 1–2 spectral Doppler 6 diastolic function 54–60 MR 85 strain and strain rate. 46–7 tricuspid annular plane systolic excursion (TAPSE) 43–4 RV inflow tract view. endocarditis 110 Tei index. diastolic function 54–6 transposition of the great vessels (TGV). congenital cardiac malformations 170–2 TGC see time gain compensation TGV see transposition of the great vessels three-dimensional echocardiography 9. right ventricular (RV) function 43–4 tricuspid regurgitation (TR) 101–3 assessment 102–3 Doppler 102–3 two-dimensional echo 102 tricuspid stenosis (TS) 100–1 Doppler 101 M-mode 101 two-dimensional echo 101 tricuspid valve anatomy 100 tricuspid regurgitation (TR) 101–3 tricuspid stenosis (TS) 100–1 valvular heart disease 100–3 TS see tricuspid stenosis TTE vs.

coronary artery disease 62–6 Waterston shunt surgical technique. congenital cardiac malformations 169–70. coronary artery disease 72–4 VSDs see ventricular septal defects wall motion abnormalities (WMAs).INDEX two-dimensional imaging (cont.) mitral regurgitation (MR) 84 Uhl’s anomaly 134. congenital cardiac malformations 178. 134 univentricular atrioventricular connection. 171 ventricular septal rupture. endocarditis 107–10 ventricular septal defects (VSDs). 179 valvular heart disease 75–115 aortic valve 87–100 endocarditis 106–10 mitral valve 75–87 nonbacterial thrombotic endocarditis (NBTE) 110 prosthetic heart valves 111–15 pulmonic valve 104–6 surgical treatment 111–15 tricuspid valve 100–3 vegetation. congenital cardiac malformations 176 WMAs see wall motion abnormalities 186 .

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