Left Parasternal Imaging Planes

Parasternal views of the heart are obtained by positioning the transducer along the left parasternal intercostal spaces. From this position, long- and short-axis images of the heart can be obtained. In the long-axis view, the structures which can be assessed are mitral leaflets and chordal apparatus, right ventricular outflow tract, aortic valve, left atrium, long axis of the left ventricle, and aorta (Fig. 2-2). Rightward angulation allows more complete imaging of the right ventricle. The right ventricular inflow view allows assessment of the right atrium, the proximal portion of the inferior vena cava, and the entry of the coronary sinus, the tricuspid valve, and the base of the right ventricle (Fig. 2-3). The parasternal short-axis images of the heart are obtained as the transducer is rotated 90 degrees from the long-axis plane and swept from a cranial to a caudal position. The most cranial view allows visualization of the aortic valve, atria, right ventricular outflow tract, and proximal pulmonary arteries. The three normal coronary cusps of the aortic valve can be viewed with possible imaging of the proximal right coronary artery arising from the right coronary cusp at the 10 o’clock position, and the left main coronary artery originating from the left coronary cusp at the 3 o’clock position (Fig. 2-4). A series of cross-sectional images of the left and right ventricles are created by moving the transducer caudally. The right ventricle appears as a crescentic structure along the right anterior surface of the left ventricle. At the basal level, the fish-mouthed appearance of the mitral valve is apparent (Fig. 2-5). At the midventricular level, the anterolateral and posteromedial papillary muscles are seen (Fig. 2-6). The most caudal angulation allows visualization of the left ventricular apex (Fig. 2-7).

FIGURE 2-2 Two-dimensional parasternal echocardiographic view of the long axis of the left ventricle. In this diastolic image, the mitral valve leaflets are open and the aortic valve leaflets are closed. The descending aorta can be seen in cross section as it passes beneath the left atrium. AV, aortic valve; dAo, descending aorta; LA, left atrium; AMVL, anterior mitral valve leaflet; LV, left ventricle; RV, right ventricular outflow tract.

FIGURE 2-3 Two-dimensional parasternal echocardiographic view of the long axis of the right heart. The tricuspid valve leaflets (arrowheads) are seen closing in systole. RA, right atrium; RV, right ventricle; TV, tricuspid valve.

FIGURE 2-4 Two-dimensional parasternal short-axis view at the base of the heart. The aortic root with its three aortic sinuses is shown in the center with the left atrium directly posterior to it. A prominent left atrial appendage is present (long arrow), and the left upper pulmonary vein can be seen entering the left atrium. The right ventricular outflow tract lies anterior to the aorta, with the posterior cusp of the pulmonic valve depicted by the short arrow. LA, left atrium; LAA, left atrial appendage; PV, pulmonic valve; pv, pulmonary vein; RA, right atrium.

FIGURE 2-5 Two-dimensional parasternal short-axis view of the left ventricle at the level of the mitral valve. In diastole, the mitral valve leaflets are open in a “fish mouth” pattern. The left ventricle appears circular and the right ventricle is crescentic in shape. IVS, interventricular septum; MV, mitral valve; RV, right ventricle.

FIGURE 2-6 Two-dimensional parasternal short-axis view of the left ventricle at the level of the papillary muscles. Both papillary muscles can be seen projecting into the lumen of the left ventricle. LV, left ventricle; PM, papillary muscles; RV, right ventricle.

FIGURE 2-7 Two-dimensional parasternal short-axis view of the left ventricle at the level of the apex. LV, left ventricle; RV, right ventricle.

Apical Imaging Planes

By placing the transducer at the cardiac apex and orienting the imaging sector toward the base of the heart, it is possible to obtain the apical views of the heart. This allows visualization of all chambers of the heart and the tricuspid and mitral valves. With the transducer oriented in a mediolateral plane at 0 degrees, an apical four-chamber view of the heart is obtained (Fig. 2-8). As the transducer is rotated 45 degrees clockwise to this plane, the apical long-axis view of the heart is obtained (Fig. 2-9), and further clockwise rotation of the transducer to a full 90 degrees produces the apical two-chamber view (Fig. 2-10). The apical two-chamber view is important because it allows direct visualization of the true inferior and anterior wall of the ventricle. Superficial angulation of the scanning plane from the apical four-chamber view brings the left ventricular outflow tract and aortic valve into view, producing the five-chamber view (Fig. 2-11).

FIGURE 2-8 Two-dimensional apical four-chamber echocardiographic view of the heart. To obtain this view, the transducer is placed at the cardiac apex. This produces an image in which the apex and ventricular chambers of the heart are at the top of the image sector and the atria are in the far field of the image. By convention, the left heart structures are positioned to the right of the image. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

FIGURE 2-9 Two-dimensional apical long-axis view of the heart. To obtain this view, the transducer is rotated so that the index marker is pointed toward the suprasternal notch. AV, aortic valve; LA, left atrium; LV, left ventricle.

FIGURE 2-10 Two-dimensional apical two-chamber view of the heart. To obtain this view, the transducer is rotated 45 degree clockwise from the long-axis view. This image plane lies between long-axis view and four-chamber view. In this view, the true anterior (Ant) and inferior (Inf) walls can be seen. LA, left atrium; LV, left ventricle.

FIGURE 2-11 Two-dimensional apical five-chamber echocardiographic view of the heart. From the apical four-chamber view, the transducer is angled superiorly to view the left ventricular outflow tract and aortic valve.

Subcostal Imaging Planes

The subcostal window allows ultrasound access to the heart through the solid tissue of the liver, which readily transmits sound waves. The alignment of the heart relative to this approach permits better visualization of the atrial and ventricular septae because the sound beam strikes these structures in a perpendicular direction. A series of long- and short-axis images are usually obtained from this window. The inferior vena cava and hepatic veins, the liver, and the abdominal aorta can also be evaluated subcostally (Fig. 2-12). Facility with subcostal imaging is important because in some instances, as in the intensive care unit setting, it may be the only viewpoint from which to image the heart in the patient with chest wall injury, hyperinflated lungs, or pneumothorax. In infants and small children the subcostal window provides excellent images of all cardiac structures.

FIGURE 2-12 Two-dimensional subcostal view demonstrating the inferior vena cava and hepatic veins entering the right atrium. A portion of the interatrial septum is present between the right and left atrial chambers. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Suprasternal Imaging Planes

Suprasternal views are obtained by placing the transducer in the suprasternal notch. Both longitudinal and transverse planes of the great vessels can be imaged. The longitudinal plane orients through the long axis of the aorta and includes the origins of the innominate, left common carotid, and left subclavian arteries (Fig. 2-13). The transverse plane includes a cross section through the ascending aorta, with the right pulmonary artery crossing behind. Portions of the innominate vein and superior vena cava are visible anterior to the aorta. The left atrium and pulmonary veins are posterior to the right pulmonary artery (Fig. 2-14).

FIGURE 2-13 Two-dimensional suprasternal long-axis view of the aortic arch. The proximal portions of the brachiocephalic vessels are demonstrated arising from the aortic arch: (1) right brachiocephalic artery, (2) left common carotid artery, and (3) left subclavian artery. The right pulmonary artery (RPA) can be seen in cross section as it passes beneath the ascending aorta (Ao). DAo, descending aorta; LA, left atrium.

FIGURE 2-14 Two-dimensional suprasternal short-axis echocardiographic view of the aortic arch. The right pulmonary artery (RPA) crosses beneath the aorta (Ao) and the pulmonary veins enter the left atrium with a “crablike” appearance. LA, left atrium; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.

Right Parasternal Views

The right parasternal border may also be useful for viewing the heart in either transverse or longitudinal orientations. These views are particularly helpful with medially positioned hearts, right ventricular enlargement, and rightward orientation of the ascending aorta. By allowing direct visualization of the right atrium, both venae cavae, and the interatrial septum, this view is also of particular value in the assessment of interatrial shunt flow, and in the detection of anomalous pulmonary venous drainage.

Parasternal Long-Axis View

In this view, mitral regurgitation is seen as a discrete blue jet in the left atrium during systole (Fig. 2-17). Small jets can be seen with normal valves.

FIGURE 2-17 A parasternal long-axis view of the mitral valve in systole. A large stream of mitral regurgitation (MR) (arrowhead) is seen emerging from the leaflet coaptation point and spreading into the left atrium (LA). The jet is blue (indicating flow away from the transducer) with mosaic of color to reflect turbulent flow. LV, left ventricle.

Aortic regurgitation is seen as blue or red jet emanating from a closed aortic valve. The jet is located in the left ventricular outflow tract and occurs in diastole. The presence of this jet represents an abnormal aortic valve.

Right Ventricular Inflow View

Inferior vena cava inflow is seen as a red jet seen at the inferior margin of the right atrium. It has both systole and diastole phases and flow velocity is normally less than 1.0 m/sec by pulsed Doppler.

Tricuspid inflow is seen as red jet crossing the tricuspid valve. It occurs in diastole with velocities less than 0.6 m/sec. Tricuspid regurgitation is a blue jet in the right atrium which occurs in systole. Small jets are normal. The peak velocity of regurgitant flow can be quantified by continuous wave Doppler.

Parasternal Short Axis

Inferior vena cava inflow is a continuous low-velocity red jet that enters through the right atrial floor adjacent to the interatrial septum. Vigorous caval flow such as seen in children may be confused with left to right interatrial shunt flow. Pulmonary outflow is a systolic blue jet in the pulmonary artery.

The normal velocity across the pulmonary outflow tract is 0.6 to 0.9 m/sec in adults and 0.7-1.2 m/sec in children.

Apical Views

Transmitral and tricuspid flow are best evaluated in the four-chamber view as a result of the parallel position of the Doppler beam to the direction of blood flow. Likewise, transaortic flow can be assessed in the apical long axis or five-chamber view.

The flows detected in this view are:

FIGURE 2-18 Pulsed Doppler spectral profile of mitral inflow obtained from an apical window. Flow toward the transducer is shown above the baseline in diastole during left ventricular filling. The typical mitral biphasic-filling pattern is seen, with a prominent early filling wave (E wave) and smaller late diastolic filling wave (A wave).

FIGURE 2-19 Pulsed Doppler spectral profile of aortic outflow obtained from an apical window. Flow velocities are plotted below the baseline to indicate that the direction of flow is away from the apically positioned transducer. The typical aortic flow profile is a systolic flow with rapid upstroke to a peak velocity in midsystole and rapid decline in velocity during late systole.

Other Views

Subcostal views are useful for assessing flow within the inferior vena cava, hepatic veins, and abdominal aorta. The suprasternal window is used for recording flow in the ascending and descending aorta and in the superior vena cava.

Myocardial Doppler Tissue Imaging

The transducer properties can be manipulated so that myocardium (low velocity) is the target of ultrasound reflection rather than blood cells (high velocity). Similar Doppler principles can be applied with color saturation of the tissue to indicate direction and velocity of the myocardium. A sample volume (similar to pulsed Doppler) is placed within the myocardium or valvular annulus to obtain a quantitative spectral profile of myocardial motion (Fig. 2-20). From the fundamental parameter of velocity, strain or strain rate imaging that measures tissue deformation can be derived (Fig. 2-21). Dopplerderived tissue velocity, strain and strain rate have been demonstrated to improve evaluation of myocardial mechanics when compared to previous measures such as wall thickening or motion.

FIGURE 2-20 Tissue Doppler imaging shows myocardial velocity in a target sample region. In this case the sample volume is placed at the septal mitral annulus. The systolic motion of the annulus (s′) and the diastolic motion (e′ and a′) are shown.

FIGURE 2-21 Tissue velocity derived radial strain of the left ventricle shown from the midventricular short axis. The two areas of interest are shown by ovals superimposed on the myocardium. The peak strain value for normal myocardium (anteroseptum, yellow curve) has a higher positive strain (myocardial lengthening) than dysfunctional myocardium (inferior wall, green curve) during systole.

Contrast Echocardiography

Contrast echocardiography uses intravenous agents that result in increased echogenicity of blood or myocardium with ultrasound imaging.

Contrast agents form small microbubbles, which at low ultrasound power, output disperse ultrasound at the gas and liquid interface, thus increasing the signal detected by the transducer. Right heart contrast is performed with injection of agitated saline and enables detection of right to left intracardiac shunts (Fig. 2-22). Left heart contrast agents consist of air or fluorocarbon gas encapsulated with stabilizing substances such as denatured albumin or monosaccharides. The microbubbles that are formed are small enough to pass through the pulmonary capillary bed, thus allowing opacification of the left heart following intravenous injection. The opacification of left ventricular cavity enhances endocardial border and cardiac mass identification particularly in cases of suboptimal acoustic windows (Fig. 2-23). Contrast echocardiography improves analysis of regional wall abnormalities. Real-time myocardial contrast echocardiography is being investigated as a tool for quantitative analysis of myocardial perfusion.

FIGURE 2-22 Apical four-chamber view recorded after the injection of agitated saline into an upper limb vein. Agitated saline contrast is seen to fill the right atrium (RA) and right ventricle (RV) before entering the left atrium (LA) and left ventricle (LV). The image is acquired after a Valsalva maneuver that transiently increases the right atrial pressure. This is reflected in the leftward displacement of the interatrial septum (IAS) resulting in increased right to left flow through the patent foramen ovale.

FIGURE 2-23 Apical four-chamber view recorded of a patient with left ventricular apical pseudoaneurysm (PSA) following left ventricular contrast agent injection showing complete cavity opacification and delineation of all left ventricular walls. IVS, interventricular septum; LV, left ventricle; RV, right ventricle.

Three-Dimensional Echocardiography

Volumetric imaging using a complex multi-array transducer to acquire three-dimensional pyramidal volume data is used to obtain images of the cardiac structures in three spatial dimensions. The structures may be viewed as a three-dimensional image or displayed simultaneously in multiple two-dimensional tomographic image planes. Postacquisition processing involves cropping that allows different views of the interior structures of the heart to be displayed. The structure studied can be manipulated so that it is viewed from multiple angles such as the surgical enface view of the mitral valve from the left atrium (Fig. 2-24). Quantitative volumetric data obtained by tracing the endocardial borders increases the accuracy of left ventricular volume assessment and allows for assessment of the right ventricular shape and volume (Fig. 2-25). Real-time three-dimensional transesophageal echocardiography (TEE) is currently being used to assist with device implantation in the catheter laboratory (Fig. 2-26). The current limitations of this technique, which is continually improving, include image quality, ultrasound artifact, and temporal resolution.

FIGURE 2-24 A three-dimensional enface view of the mitral valve from the left atrial perspective. There is prolapse of the middle scallop of the anterior mitral leaflet (pAMVL).

FIGURE 2-25 A three-dimensional left ventricular volume assessment allows all regions of the ventricular myocardium to be incorporated into the volume assessment. Each region is depicted by the different color code representing the 17-segment model. The image is from a patient with dilated cardiomyopathy and thus the ventricular shape is more globular in structure.

FIGURE 2-26 A three-dimensional study recorded during an atrial septal defect closure procedure. The image is recorded from the left atrial aspect showing the catheter traversing the atrial septal defect (ASD). The Amplatzer Atrial Septal Closure device (AMP) is seen at the tip of the catheter (CATH) as it is being positioned along the interatrial septum.

Two-Dimensional (Speckled) Strain Echocardiography

A new measure of myocardial strain analyzes motion by tracking speckles in the ultrasound image of the myocardium in two dimensions. The geometric shift of each speckle represents focal myocardial deformation. Software is available to process the temporal and spatial information and thus by tracking the speckles, two-dimensional tissue velocity, strain, and strain rate can be calculated. This technique, unlike Doppler measurement of strain, is not angle dependent (Fig. 2-27).

FIGURE 2-27 Two-dimensional radial speckle strain calculated from a short axis recording at the level of the mitral annulus. On the top left (A), the left ventricular short-axis view with the region of interest divided into six color-coded segments is displayed. The right panel (B) shows the graphical representation of the radial strain of all accepted segments. The myocardium thickens during systole and hence there is a positive deflection in the value of radial strain during systole.

Normal Linear Dimensions

By convention, most laboratories report the size of the left atrium, aortic root, and left ventricle from the measurement of the linear dimensions of each structure in the parasternal long-axis view of the heart (Table 2-1). All linear dimensions have been shown to bear a direct linear relation to body height. Normal chamber dimensions have also been determined for each of the standard two-dimensional views to allow quantitative assessment of each chamber or great vessel from any view.

TABLE 2-1 Normal linear dimensions^*

* Obtained from parasternal long-axis view.

Left Ventricular Volume

There are a number of methods for calculating left ventricular volume from two-dimensional echocardiographic images that require the assumption of a geometric shape of the left ventricle (Fig. 2-28).

FIGURE 2-28 Diagrammatic representations of the left ventricle showing the geometric models that have been used to calculate left ventricular volume. The shaded figure indicates the true chamber volume with the superimposed solid figure demonstrating the geometric shape described by the formula. The Simpson’s rule method comes closest to approximating the true shape of the ventricle. A, area; D, diameter; L, length; LAX, long axis length; LVID, left ventricular internal dimension.

Rights were not granted to include this figure in electronic media. Please refer to the printed book.

(From Weyman AE: Principles and Practice of Echocardiography, ed 2, Philadelphia, 1994, Lea & Febiger.)

The ellipsoid formula requires measuring the length of the ventricle and its diameter at the base. This volume estimation is valid in normal (symmetric) left ventricles, but it is less reliable when there is a distortion of ventricular shape (e.g., following myocardial infarction).

Simpson’s rule requires measuring the length of the ventricle from apical views and then determining the volume of a predefined number of disklike cross-sectional segments from base to apex.

Three-dimensional volume measurement makes no geometric assumptions and thus can determine the volume of both normal and distorted ventricles (see Figure 2-25).

Left Ventricular Systolic Function from Two-dimensional Images

Real-time echocardiographic assessment of endocardial motion and the degree of wall thickening during systole allows excellent qualitative assessment of global and regional ventricular function. Using this method, systolic function can be described as either normal or depressed, and regional function is either normal, hyperkinetic, hypokinetic, akinetic, or dyskinetic.

Quantitative assessment of ventricular function is available by estimating the global ejection fraction, determined by calculating the change in volume of the ventricle between diastole and systole.

The simplest method of estimating ejection fraction is to assume that the change in area at the base of the ventricle is representative of global ventricular function. In this way:

where LVIDD = the internal diameter of the base of the ventricle in diastole, and LVISD = the internal diameter of the ventricle in systole. Because this formula fails to account for apical function, 10% is empirically added if function at the apex is normal, 5% is added if the apex is hypokinetic, and 5% to 10% is subtracted if the apex is dyskinetic. The development of automated endocardial border detection now makes it possible to obtain an online estimate of ejection fraction based on changes in cavity area.

You can also estimate the ejection fraction by assessing the change in ventricular volume during the cardiac cycle using a simple formula, which assumes that the left ventricle is spherical:

Methods that estimate ejection fraction based on a single dimension obtained at the base of the heart, however, tend to overestimate global function in patients with apical infarction, and underestimate global function in patients with inferior basal infarctions.

Simpson’s rule generally provides a more accurate estimate of ejection fraction because it removes some of the assumptions about ventricular geometry. With current echocardiographic instrumentation, online and offline measurement capabilities provide easy access to this quantitative method. To perform the Simpson’s rule calculation, outline the full ventricular contour from the apical view in diastole. The automated measurement package will then draw a midline between the ventricular apex and the midpoint of the mitral annular plane and divide the ventricle into a series of small parallel disks of equal height, which run perpendicular to the midline. Because the radius and height of each disk is known, the volume of each disk can be computed. Summing the volume of each disk allows calculation of the diastolic ventricular volume. The same process is repeated for the end-systolic ventricular volume, and the ejection fraction is calculated as the difference in volume from diastole to systole, divided by the diastolic volume. The major limitation in this method is the inability to image the complete endocardial surface or the true length of the ventricle in some patients. The accuracy can be improved by using the biplane Simpson’s method, which averages the estimates of ventricular volume, obtained in orthogonal planes from apical four-chamber views and apical two-chamber views.

Two-dimensional echocardiographic estimates of ejection fraction make a number of assumptions about ventricular shape; they are most useful in normal or symmetrically dilated hearts. The application of three-dimensional technology can overcome the problems of estimating left ventricular ejection fraction in distorted ventricles.

Left Ventricular Systolic Function from Doppler Echocardiography

Doppler echocardiography makes it possible to estimate stroke volume and cardiac output by measuring volumetric flow through the heart. Stroke volume is calculated by measuring the cross-sectional area of a vessel or valve and then integrating the flow velocities across that specific region in the vessel or valve throughout the period of flow. The product of stroke volume and heart rate then gives an estimate of cardiac output (Fig. 2-29).

FIGURE 2-29 The Continuity equation for a region of narrowing is based on the volumetric flow on each side of the narrowing being equal (Q₁ = Q₂). The flow rate is equal to the product of the mean velocity and the cross sectional area. Thus CSA₁ × V₁ = CSA₂ × V₂. The mean velocity increases to maintain a constant flow rate through a region of narrowing. CSA₁, the area of the lumen of the cylinder; CSA₂, area of the stenosis; V₁, velocity; V₂, velocity of flow through the stenotic region.

Although cardiac output can be determined from the pulmonary, mitral, or tricuspid transvalvular flows, the aortic valve diameter and flow velocities are the most accurate. Further, there is excellent correlation between Doppler and roller pump estimates of stroke volume. In clinical practice, inaccuracies in measurement of the area of the outflow tract limit the use of Doppler estimates of cardiac output. This technique is successful, however, in following relative changes in cardiac output following pharmacologic intervention because the area of the outflow tract is assumed to remain constant.

Left Ventricular Diastolic Function

Impairment of left ventricular diastolic filling has been increasingly recognized as a clinical problem, either in association with systolic dysfunction or as an isolated entity. Two-dimensional echocardiography assesses left ventricular size, volumes, ejection fraction, and hypertrophy. The presence of an enlarged left atrium is found in more than 90% of patients with diastolic dysfunction.

Echocardiographic Doppler assessment of left ventricular filling properties includes transmitral velocity and pulmonary vein flow characterization. Measurements of peak early (E) and late (A) diastolic flow velocities, isovolumic relaxation time, and deceleration time of early diastolic filling are all useful measures of diastolic function, but are limited by reduced accuracy for detection of high left atrial pressure in patients with normal ejection fraction or left ventricular hypertrophy, and poor ability to separate the effects of preload from relaxation. Flow propagation velocity by color M-mode and diastolic myocardial velocity by tissue Doppler (Ea) are measurements of diastolic function/impaired relaxation that are independent of the effects of preload. Flow propagation velocity relates inversely with the time constant of left ventricular relaxation. However, it can be difficult to measure and thus is less reproducible and may give erroneous results in patients with concentric left ventricular hypertrophy, small left ventricular cavity, and high filling pressures. Annular velocity is an index of myocardial relaxation and multiple studies have shown the ratio of transmitral E velocity to annular velocity Ea relates well with mean pulmonary capillary wedge pressure. However, it is a regional index and thus can vary between sampling sites and in patients with abnormal regional wall motion. The typical patterns observed with each of these methods in various forms of diastolic dysfunction are depicted in Fig. 2-30. A simplified algorithm for the use of E/Ea ratio in the clinical assessment of diastolic function is shown in Fig. 2-31. In addition, all diastology quantification measurements are not applicable for patients not in sinus rhythm or for those who have inflow obstruction (mitral stenosis, prosthetic valves).

FIGURE 2-30 Diagrammatic representation of Doppler transmitral flow velocities, pulmonary venous flow velocities, tissue Doppler velocity patterns, and color flow propagation in various states of left ventricular diastolic dysfunction. CMM-Vp, color M-mode velocity of propagation; PV, pulmonary venous flow; TDE, tissue Doppler echocardiography.

(Reproduced with permission from J.D. Thomas, MD.)

FIGURE 2-31 A suggested clinical algorithm for assessment of diastolic dysfunction for patients with normal systolic function (LVEF ≥ 50%). The assessment is integrated from tissue Doppler velocities at the mitral annulus (Ea), mitral inflow E velocity (E), mitral valve deceleration time and two-dimensional assessment of the left atrium (LA) and left ventricle (LV). LVEF, left ventricular ejection fraction; LVH, left ventricular hypertrophy; MV, mitral valve.

(Reproduced with permission from J. Hung, MD.)

Left Atrium

It is conventional to measure the anteroposterior dimension of the atrium at end systole in the parasternal long-axis view from a line drawn through the plane of the aortic valve. Measurement of the medio-lateral dimension and supero-inferior dimension can be made from the apical four-chamber view. Atrial enlargement may occur as a consequence of either an increase in atrial pressure (resulting from mitral stenosis or elevated left ventricular end-diastolic pressure), an increase in volume (as in mitral regurgitation), or as a consequence of primary atrial dysfunction (as in atrial fibrillation).

The left atrial appendage is a “dog ear”-shaped extension of the atrium situated along the lateral aspect of the chamber near the mitral annulus. Although usually inconspicuous, it is easily visible in the parasternal short-axis and apical two-chamber views of the atria when there is a dilated left atrium. Definitive imaging of the atrial appendage is usually performed with transesophageal imaging for the most accurate visualization of thrombus. It is important to realize that the appendage is a trabeculated structure. These trabeculae may be confused with thrombus, which may form within the appendage (Fig. 2-32).

FIGURE 2-32 A two-dimensional transesophageal echocardiogram showing the left ventricle (LV), left atrium (LA), left atrial appendage (LAA), and large thrombus (arrowheads).

Right Ventricle

Morphologically, the right ventricle can be divided into an inflow portion that includes the heavily trabeculated body of the ventricle, and an outflow portion that includes the infundibulum. The inflow portion extends from the tricuspid valve to the apex. The right ventricle generally has a crescentic shape when viewed in short axis, with its medial border formed from the convexity of the interventricular septum. The lateral or free wall of the right ventricle normally has a radius of curvature approximately equal to the left ventricular free wall. Because of the complex shape of the right ventricle, it is less amenable to geometric modeling than the left ventricle. Therefore, although there are simple, valid two-dimensional echocardiographic criteria for estimating right ventricular volume in nondistorted hearts, newer three-dimensional echocardiographic techniques are more reliable in assessing right ventricular volume.

Right ventricular enlargement may occur as a consequence of right ventricular volume loading, right ventricular infarction, or as part of a generalized cardiomyopathic process. In each instance, as dilatation progresses, the anteroposterior dimension of the ventricle increases and interventricular septal motion becomes increasingly abnormal. Specifically, in diastole the septum may appear to flatten, especially at the base, and in early systole the septum may move rightward (paradoxically) rather than leftward.

Pressure loading of the right ventricle results in progressive hypertrophy (Fig. 2-33). This may be difficult to discern with confidence because of the degree of trabeculation of the chamber. A free wall thickness of greater than 5 mm is a quantitative criterion for right ventricular hypertrophy. Marked pressure overloading typically produces systolic flattening of the interventricular septum.

FIGURE 2-33 Apical four-chamber view of a patient with severe primary pulmonary hypertension. The right ventricle (RV) is enlarged. There is hypertrophy of the free wall (RVH). The right atrium (RA) is enlarged and high right atrial pressures cause displacement of the interatrial septum (IAS) to the left. The left atrium (LA) and left ventricle (LV) are underfilled as a result of the reduced output from the right heart and are thus small.

Right Atrium

Assessment of right atrial size is usually made qualitatively by comparing it to the left atrium in the apical four-chamber view and quantitatively by measuring the maximal mediolateral and supero-inferior dimensions in this view. There are several normal structures within the right atrium. These include the Eustachian valve, which crosses from the inferior vena cava to the region of the foramen ovale, and the crista terminalis. In the apical four-chamber view, the crista can be seen as a ridge of tissue that separates the smooth-walled portion of the right atrium from its trabeculated anterior portion, often noted as a small mass of echoes located adjacent to the superior border of the right atrium. The right atrial appendage is a broad-based triangular structure that lies anterior to the atrial chamber near the ascending aorta. It is most visible in the parasternal views of the right atrium and readily visualized by TEE.

Mitral Stenosis

Echocardiography assists with the diagnosis and timing of intervention for mitral stenosis by providing accurate assessment of valve area, valve morphology, and the degree of pulmonary hypertension.

Acquired mitral stenosis is almost invariably caused by scarring and inflammation of the valve and chordal apparatus from past rheumatic fever. As a consequence of the disease, the mitral leaflets and chordal apparatus become diffusely thickened. Subsequently the valvular apparatus may shorten, fuse together at the commissural margins, and finally calcify. This results in a reduction in leaflet excursion so that the mitral leaflets appear to dome during diastole (Fig. 2-34). As the degree of valvular obstruction increases, flow through the valve decreases, left atrial pressure begins to rise, left atrial size increases (in the apical views, the interatrial septum is seen to bow to the right), and the potential for atrial thrombus formation is increased. Typically, the left ventricular size is normal or even small. If there is severe mitral stenosis, there may be paradoxical motion of the interventricular septum as a consequence of slow ventricular filling. Further, if there is pulmonary hypertension, the right heart and the pulmonary arteries may dilate and there may be severe tricuspid regurgitation. Almost all of these morphologic features are evident from the parasternal long-axis view of the heart; however, parasternal short-axis images are essential for planimetry of the mitral valve orifice (Fig. 2-35).

FIGURE 2-34 Parasternal long-axis echocardiographic view in a patient with rheumatic heart disease demonstrating marked calcification of the mitral valve leaflet tips. Instead of opening widely, the leaflets dome in diastole and the mitral orifice is severely restricted (arrowheads). LA, left atrium; LV, left ventricle; MV, mitral valve.

FIGURE 2-35 Parasternal short-axis echocardiographic view of the right and left ventricles at the mitral valve level. The mitral valve leaflets are thickened and the valve orifice is eccentrically restricted (arrowheads). The medial commissure is more tightly fused than the lateral commissure resulting in a larger orifice along the lateral aspect of the valve. LV, left ventricle; MVO, mitral valve orifice; RV, right ventricle.

Echocardiographic grading of the severity of mitral stenosis is possible by assessing the degree of leaflet thickening, calcification, mobility, and the degree of chordal thickening and shortening (Table 2-2). When systematically graded, a low value of 1 to a high value of 4 is given for each of these characteristics. It is then possible to derive a numeric “score” that describes the extent of the mitral valve disease. This system is helpful in predicting the likelihood of successful balloon dilatation of the valve, with scores greater than 8 predicting a poor outcome following percutaneous dilatation.

Direct planimetry of the valve orifice in the short-axis plane can provide an accurate measurement of the mitral valve area. Three-dimensional echocardiography can improve the accuracy of detecting the smallest mitral orifice by providing simultaneous, perpendicular on axis views of the valve orifice.

Continuous wave Doppler can help assess the severity of mitral stenosis because it enables calculations of the peak and mean transmitral gradients and the mitral valve area. For this purpose, the apical four-chamber view is preferable so that the Doppler beam can be directed through the mitral valve plane, parallel to the direction of left ventricular inflow. In contrast to the Doppler profile through a normal mitral valve, the continuous wave Doppler signal in patients with mitral stenosis demonstrates an increased velocity of flow in early diastole, with a prolonged descent of the early filling wave (deceleration time) that may merge into the late filling wave (Fig. 2-36). In patients with atrial fibrillation, the A wave, which reflects atrial contraction, is absent. The degree of prolongation of the phase of early filling relates directly to mitral valve area and to the severity of mitral stenosis.

FIGURE 2-36 Parameters that can be measured from the continuous wave Doppler assessment of the mitral valve include the mean pressure gradient and the mitral valve area from the pressure half-time measurement. Integration of the overall pressure gradient beneath the spectral display will calculate the mean pressure gradient (dotted curve). For the pressure half-time method, the time required for the pressure to decay from its peak value to one half of that value is determined. The velocity at which the pressure gradient has declined to one half of its peak can be calculated as 0.7 × V_max. The time taken for this velocity to be reached is the pressure half-time (Pt_1/2), which can be entered into the equation Mitral Valve Area = 220/Pt_1/2.

Once you obtain the continuous wave Doppler profile, it is possible to calculate the transmitral gradient by converting the velocity information provided by the Doppler signal into an estimate of pressure using the simplified Bernoulli equation. In essence, the Bernoulli theorem states that the velocity (V) of flow across a stenosis relates to the pressure difference (P) across the stenosis. Specifically, the simplified Bernoulli equation predicts that the pressure gradient across a valve approximates a value four times the square of the velocity of flow across the valve (P = 4V²). Knowing the peak velocity of flow across the mitral valve, therefore, enables calculation of the peak pressure gradient across the valve. Similarly, the average of the velocities throughout all of diastole yields the mean gradient. Most commercial echocardiographic Doppler equipment contains software that can automatically integrate the velocity profile once it is traced, and then calculate the mean gradient using the Bernoulli equation. In general, the gradient across the mitral valve obtained by Doppler correlates well with that obtained at catheterization.

Doppler estimates of mitral valve area rely on the observation that the degree of prolongation of early filling relates directly to the degree of mitral stenosis. Quantification of this is possible by calculating the time for the pressure gradient across the mitral valve to fall to half its peak value, the pressure half-time. Pressure half-time is obtained from the continuous wave Doppler profile by determining the velocity half-time, measuring the time interval between peak transmitral velocity and the point where transmitral velocity has fallen to half its peak value.

In normal subjects, the pressure half-time is less than 60 ms. In contrast, in patients with mitral stenosis the half-time is usually in excess of 200 ms, with higher values in patients with more severe disease. An empirical formula that relates pressure half-time to the mitral valve area is as follows: Area = 220/Pressure Half-Time. This is fairly accurate compared with estimates of valve area determined by catheterization. From this empirical formula, patients with a pressure half-time of greater than 220 ms have a mitral valve area equal to or less than 1.0 cm².

Rheumatic Mitral Regurgitation

Although the incidence of rheumatic mitral regurgitation is decreasing, the disease is still prevalent in older patients. Typically, the echocardiogram confirms mitral leaflet and chordal thickening in association with aortic valve disease. As the disease progresses and the leaflets become less mobile, valvular stenosis may also be evident. In these cases, echocardiography is most useful in determining whether the valve is predominantly stenotic or incompetent. This information is invaluable for determining the optimal clinical and corrective approach to the valvular lesion.

Myxomatous Mitral Valve Prolapse

Mitral valve prolapse is a degenerative disorder that primarily affects the collagen of the mitral leaflets and chordae; however, it may also affect the aortic and tricuspid valve. Although often diagnosed clinically by the presence of a murmur or click, echocardiography is frequently used to confirm the diagnosis.

Echocardiographically, mitral valve prolapse is suggested by the superior displacement of one or both of the mitral valve leaflets into the atrium during systole (Fig. 2-37). Because of the complex saddle shape of the mitral annulus, minor degrees of superior displacement of the anterior leaflet may normally be recorded from the apical four-chamber view. Therefore, the diagnosis of mitral valve prolapse should only be made when the long-axis views (parasternal or apical long axis) show leaflet displacement. Color Doppler usually shows an eccentric jet of regurgitation that is in the opposite direction to the leaflet which is prolapsed (see Figure 2-37B). In patients with more advanced disease, there is also evidence of leaflet thickening, which relates to the presence of myxomatous infiltration of the valve. There may also be redundant or ruptured chordae.

FIGURE 2-37 (A) Parasternal long-axis echocardiographic view of the left atrium and left ventricle demonstrating prolapse of the mitral valve anterior leaflet. The anterior cusp (AMVL) bows into the left atrium behind the coaptation point of the mitral leaflets. (B) The color Doppler shows the resultant eccentric posterior directed jet (MR, arrowheads). LV, left ventricle; RV, right ventricle.

There is an important relationship between the appearances of the mitral valve in this condition and both the degree of mitral valve dysfunction and patient prognosis. Specifically, patients with marked displacement, thickening, and deformity of the leaflets are more likely to have severe mitral regurgitation and to be at greatest risk of valve-related complications including valve surgery and endocarditis.

As in any patient with mitral regurgitation, left atrial size increases with increasing severity of the regurgitant lesion and left atrial dimension can act as an index of the severity and duration of the mitral regurgitation. Left ventricular size may be normal or dilated. Systolic function is typically hyperdynamic in patients with primary compensated valvular mitral regurgitation of moderate severity. Although no single echocardiographic index yet accurately predicts the correct timing of mitral valve surgery in patients with primary chronic valvular mitral regurgitation, those with a left ventricular end-systolic diameter greater than 40 mm tend to have less recovery of ventricular function following surgery.

Mitral Annular Calcification

Calcification of the mitral annulus is common in the elderly. It begins as a focal process, affecting the posterior portion of the annular ring, then extends laterally and finally anteriorly (Fig. 2-38). As the process evolves, the base of the mitral leaflets and chordal apparatus thicken and calcify. This impairs the normal mechanism of coaptation leading to mitral regurgitation. It may also result in restriction of mitral inflow with the development of a small transmitral gradient. Although annular calcification is visible in almost any view, the parasternal short-axis image at the base of the heart is the most useful view for defining the circumferential extent of the disease.

FIGURE 2-38 Parasternal long-axis view of the left ventricle showing a focal dense area of calcification is present along the posterior mitral annulus (PMAC).

Flail Mitral Leaflet

Complete or partial disruption of the support of one or both of the mitral leaflets usually presents suddenly with the development of a new murmur or acute pulmonary edema. In either setting, the echocardiogram in association with the clinical picture may provide direct insight into the nature of the underlying disease process. Specifically, the echocardiogram can demonstrate systolic prolapse of the entire leaflet into the left atrium (Fig. 2-39) and significant mitral regurgitation by color Doppler. A flail leaflet is caused by infective endocarditis, underlying myxomatous mitral valve disease (mitral valve prolapse), or papillary muscle rupture in association with acute myocardial infarction.

FIGURE 2-39 In this apical four-chamber echocardiographic image, the mitral valve leaflets are thickened. A portion of the posterior leaflet is flail and everts into the left atrium (arrow). The left atrium is significantly enlarged secondary to severe mitral regurgitation. LA, left atrium; pv, pulmonary veins.

Functional Mitral Regurgitation

In some patients the mitral valve may appear morphologically normal but is clearly incompetent, as evidenced by clinical or echocardiographic signs of moderate to severe mitral regurgitation (Fig. 2-40). In these patients the mitral regurgitation is caused by abnormal (incomplete) coaptation of the mitral leaflets caused by either annular dilatation or papillary muscle dysfunction. In both instances, the pattern of leaflet closure appears abnormal in the parasternal and apical views; the mitral leaflets appear to coapt only at their tips, rather than along the distal third of the leaflet. The appearance may range from leaflet and chordal tethering to complete failure of coaptation. There is often associated ventricular dilatation and global or regional wall motion abnormality.

FIGURE 2-40 In this two-dimensional echocardiography image, the left ventricle and left atrium are dilated consistent with dilated cardiomyopathy. There is tethering of the subvalvular mitral apparatus. Mitral annular dilatation and tethering resulting from left ventricular remodeling can both contribute to functional mitral regurgitation. MR, mitral regurgitation.

Assessment of Mitral Regurgitation

Color Doppler readily demonstrates mitral regurgitation. In general it is sensitive to regurgitant flow through the atrioventricular valves, and small jets of regurgitation are common in normal hearts because of retrograde flow induced by valve closure. Regurgitant jets usually appear as a localized stream of flow emerging from the valve leaflets at valve closure that then expand into the distal chamber. From most sampling windows, the jets of mitral regurgitation are predominantly blue because they are directed away from the transducer. The introduction of yellow and greens in the color flow map indicates high-velocity turbulent flow and results in a pattern referred to as “mosaic.” Regurgitation can be confirmed by either pulsed or continuous wave Doppler.

Regurgitant flow characteristically begins at the peak of the R wave on the electrocardiogram (ECG) and continues throughout systole. The peak velocity of these jets reflects the atrioventricular gradient, which can be calculated using the simplified Bernoulli equation described earlier. Therefore, the continuous wave Doppler signal in patients with mitral regurgitation usually has a peak velocity of about 5 m/sec, reflecting a peak atrioventricular gradient of 100 mm Hg.

Semiquantitative assessment of the severity of mitral regurgitation involves integration of many echocardiographic and Doppler variables. Initially, it is helpful to consider the appearance of the valve leaflets, chordae, and the pattern of leaflet coaptation. This may provide insight into both the mechanism and likely severity of regurgitation. It is useful to determine whether the valvular apparatus appears normal or thickened and deformed and to determine whether the pattern of coaptation is normal, incomplete, or asymmetric (as a result of complete or partial leaflet flail). With this preliminary assessment, it is possible to gain a sense of whether the degree of regurgitation is likely to be mild, moderate, or severe. For example, it is unlikely with a normal valvular apparatus and a normal pattern of coaptation to have more than mild regurgitation, yet it is highly likely that with a partially flail leaflet there will be moderate to severe mitral regurgitation.

Following assessment of valve morphology and the pattern of coaptation, the color Doppler signals yield further insight into the degree of regurgitation. Color flow Doppler provides a color map of the net instantaneous velocity of blood flow within the atria at varying time points during systole. From this map it is possible to describe the size (area, length, width at the orifice) and direction (central or eccentric) of the regurgitant jet. Descriptors of jet size, particularly the size of the proximal jet at the vena contracta relate to the angiographic degree of regurgitation (Fig. 2-41). Unfortunately, many factors affect the accurate assessment of the degree of regurgitation. For example, changing either the gain or the pulse repetition frequency of the Doppler system may alter the relationship between jet size and the degree of regurgitation, resulting in either an artificial increase or decrease in jet size (particularly jet area and length). Further, detection of the regurgitant jet may not be possible in all instances, such as in patients with prosthetic valves that block out or reflect the interrogating Doppler signal and prohibit its passage into the atrium. Finally, the relationship between jet size and severity of regurgitation may be underestimated if the jet is directed eccentrically along the atrial wall, as often occurs with more severe regurgitation.

FIGURE 2-41 Diagrammatic representation of an apical four-chamber echocardiographic view indicating a method for quantifying the severity of mitral regurgitation. With the transducer placed at the cardiac apex, the mitral insufficiency flow stream is detected within the left atrium by color flow mapping (shaded area). The extent of jet penetration within the atrial chamber and the jet area relative to the left atrial area are used to qualitatively assess the degree of regurgitation. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

In an effort to overcome some of the limitations related to analysis of the distal jet, investigators have analyzed the size of the converging flow stream proximal to the valve (i.e., on the ventricular side of the valve) (Fig. 2-42). Analysis of the size of this proximal isovelocity surface area (PISA) provides accurate assessment of the regurgitant flow rate but requires careful technical manipulation and high quality imaging to record a PISA that can be accurately measured.

FIGURE 2-42 Diagrammatic depiction of proximal isovelocity surface area (PISA) formed as flow accelerates to pass through a discrete orifice. Regurgitant flow can be calculated by multiplying the aliasing flow velocity by the area of the hemispherical shell (2πr²). r, radius.

Flow reversal in the pulmonary veins by pulsed Doppler offers additional evidence that the degree of mitral regurgitation is likely to be severe. Because it is the atria that bear the burden of chronic regurgitation, assessment of atrial size may also be valuable in determining its severity and chronicity. However, because other parameters such as atrial fibrillation and left ventricular end-diastolic pressure may also influence atrial size, chamber size alone may be a misleading marker of the severity of regurgitation.

Aortic Stenosis

Aortic stenosis is any abnormality of the aortic valve in which the leaflets restrict the lumen of the outflow tract. The three cardinal features of aortic stenosis are (1) leaflet thickening, deformity, and calcification; (2) decreased mobility or doming of the leaflets, or both; and (3) an absolute decrease in size of the valve orifice resulting from reduced cusp separation (Fig. 2-45).

FIGURE 2-45 Parasternal short-axis echocardiographic view at the base of the heart in a patient with calcific aortic stenosis. The aortic valve leaflets are calcified highlighting the commissural margins (arrowheads). Immobility of the cusps results in only a slitlike aortic valve orifice in systole.

Aortic stenosis may be acquired or congenital. In congenital aortic stenosis, the aortic valve may be unicuspid, bicuspid, or rarely, quadricuspid (Fig. 2-46). Typically, the leaflets are thin but appear to dome. This is evident in the parasternal long-axis views in midsystole. Specific characterization is possible by imaging the valve in the short-axis plane to determine the number of cusps and commissures. Although bicuspid valves are by nature stenotic, they may also predispose to significant aortic regurgitation. Identification of a bicuspid valve may be difficult in older patients if the valve has begun to calcify.

FIGURE 2-46 Echocardiographic views of the aortic valve in a patient with a bicuspid aortic valve. The panel on the left is a parasternal short-axis view of the aortic valve in diastole showing a single commissural line across the aortic root. In the central panel, the valve is shown in systole forming an elliptical orifice, which is classical for a bicuspid aortic valve. The panel on the right is a parasternal long-axis view, which demonstrates the aortic leaflets forming a dome in systole (arrows). Ao, aorta; LV, left ventricle.

Unlike congenital aortic valve disease, which usually presents before the fourth decade, acquired calcific aortic stenosis presents in the patient’s sixth or seventh decade. Typically, the valve is thickened and calcified and there is reduced cusp separation. Detection of some residual leaflet motion usually indicates that the valve area is greater than 0.6 cm².

None of the typical features of aortic stenosis is necessarily specific for the diagnosis of hemodynamically significant disease. Leaflet thickening is common in the elderly and rarely associated with significant obstruction to outflow. Focal thickening may represent vegetation rather than fibrosis. Although reduced cusp separation and doming of the leaflets are more specific for hemodynamically significant disease, this may also occur in patients with a low cardiac output. Direct measurement of the valve orifice is rarely accurate by transthoracic echocardiography; however, direct planimetry of the aortic valve area from TEE can provide an accurate estimate in patients with normal left ventricular function. In patients with significant aortic stenosis, left ventricular size and systolic function are typically normal; however, left ventricular hypertrophy is usually evident (wall thickness >12 mm).

Accurate assessment of the degree of stenosis is usually possible using continuous wave Doppler, which allows estimation of the peak and mean aortic gradient and the aortic valve area. To determine the peak and mean gradient across the valve, you must first obtain accurate profiles of flow emanating from the valve, usually from apical windows. It is also important to interrogate flow through the valve from the right parasternal window because deformation of the aortic leaflets may eccentrically direct the jet of blood flow toward the right sternal border as it enters the aorta. The typical continuous wave Doppler profile of aortic stenosis begins after the R wave on the ECG and is not holosystolic. Noting the time of onset and the duration of flow helps to differentiate the aortic stenosis profile from the continuous wave Doppler profile of mitral regurgitant flow.

Once you obtain optimal Doppler profiles, you can use the simplified Bernoulli equation to estimate the instantaneous aortic gradient (Fig. 2-47). This may produce a different gradient from the peak-to-peak gradient obtained in the catheterization lab that is derived by comparing peak aortic and left ventricular systolic pressure irrespective of time.

FIGURE 2-47 The Bernoulli equation is based on the principle of the conservation of energy. In the presence of a narrowing, the velocity distal to the narrowing must accelerate or increase to maintain energy. The inverse relationship between velocity and pressure dictates that the pressure distal to the stenosis must drop. This results in a pressure gradient between the region proximal to the narrowing and the region distal to the narrowing that is determined by the Bernoulli equation. P₁, proximal pressure; P₂, distal pressure; V₁, proximal velocity; V₂, distal velocity.

Doppler techniques can also be used to estimate aortic valve area using the continuity equation. The continuity theorem states that the volume of flow entering a cylinder equals the volume of flow passing through an obstruction within the cylinder, which in turn equals the volume of flow exiting from the cylinder (see Figure 2-29). Because the rate of flow (ml/min) in the cylinder relates to both the velocity (V₁) of flow and to the area of the lumen of the cylinder (CSA₁), it should be possible to estimate the area of the stenosis (CSA₂) if you know the velocity of flow through the stenotic region (V₂):

This concept allows calculation of the area of a stenotic valve (CSA₂):

Aortic Regurgitation

Aortic valve abnormalities associated with aortic regurgitation include bicuspid valve, heavily calcified leaflets, leaflet prolapse, and mobile echodensities suggestive of endocarditis vegetations. Aortic pathology associated with aortic regurgitation includes dilatation of the aortic sinuses or aortic root (Marfan syndrome), ascending aortic aneurysm, and aortic root dissection (Fig. 2-48). Impingement of an aortic regurgitant jet directly into the mitral leaflets may create a high frequency diastolic fluttering of one or both of the mitral leaflets. If regurgitation is severe, early diastolic closure of the mitral valve may occur.

FIGURE 2-48 Parasternal long-axis view showing jet of central aortic regurgitation (blue jet) originating from the aortic valve. The width of the jet in relation to the diameter of the left ventricular outflow tract can be used to semiquantitatively assess regurgitation severity. A central jet that fills less than 25% of the outflow tract is consistent with mild aortic regurgitation. Ao, aorta; AR, aortic regurgitation; LV, left ventricle.

As the severity of aortic regurgitation increases, the left ventricle dilates and hypertrophies. Systolic function is usually preserved until late in the course of the disease. Patients in whom the left ventricular systolic dimension reaches 55 mm tend to have a worse outcome following surgery. Conversely, significant ventricular remodeling and restoration of systolic function may occur following surgery.

In the parasternal long-axis views, aortic regurgitation appears by color Doppler as a diastolic red or blue jet emanating from the region of the aortic valve and directed into the left ventricular cavity. Sometimes the jet tracks along the anterior leaflet of the mitral valve. Parasternal short-axis, the apical five-chamber, and apical long-axis views may also allow detection of regurgitation, which appears as a red jet because it is directed toward the transducer. Despite the ready detection of aortic regurgitation by color Doppler, assessing the severity of regurgitation is more difficult and at best only semiquantitative. It is preferable to assess regurgitant jet size by evaluating proximal jet width rather than jet length, which may be misleading as even small jets may coalesce with mitral inflow and appear large. An alternative is to consider the cross-sectional area of the jet in the short-axis plane. More severe regurgitation tends to fill a greater portion of the outflow tract in early diastole.

Pulsed Doppler can assess the severity of aortic regurgitation by detecting the presence of late diastolic flow reversal in the descending aorta, which invariably occurs with severe regurgitation. Finally, measurement of the regurgitant pressure half-time derived from the continuous wave Doppler profile reflects the instantaneous pressure gradient between the aorta and the left ventricle. Therefore, more rapid pressure half-times reflect rapid increases in diastolic pressure within the left ventricle and reflect more severe regurgitation. In general, a pressure half-time below 200 ms is indicative of severe aortic insufficiency; however, the use of this method is limited by the effects of other factors which may raise left ventricular diastolic pressure unrelated to the degree of aortic regurgitation (Fig. 2-49).

FIGURE 2-49 Continuous wave Doppler spectral trace in a patient with aortic insufficiency. The aortic flow is sampled from the apex with systolic outflow shown below the baseline and diastolic regurgitant flow above the baseline. With normal aortic and left ventricular diastolic pressures, the pressure difference between aorta and left ventricle remains high and the slope of the regurgitant velocities drops off gradually (arrows). AR, aortic regurgitation; AS, aortic stenosis.

Assessing Left Ventricular Regional Wall Motion

Echocardiographic assessment of regional wall motion depends on the ability to assess both the degree of endocardial motion and the degree of myocardial thickening. In practice, the assessment of endocardial excursion is simple, but it may be misleading in the presence of noncardiac motion (rotation, translation). Although assessment of myocardial thickening is unaffected by these factors, its use may be limited if visualization of the epicardial and endocardial contours is inadequate.

Regional wall motion is most frequently described qualitatively as being normal, hypokinetic (moving in the proper direction but at a slower rate and to a smaller extent than normal), akinetic (not moving), or dyskinetic (moving outward in systole). The Cardiac Imaging Committee of the American Heart Association has recommended a system with 17 segments to standardize echocardiographic segmental assessment with that of other cardiac imaging techniques (Fig. 2-54). If one assigns a functional “score” to each segment based on qualitative visual assessment (normal = 0, hypokinesis = 1, akinesis = 2, dyskinesis = 3), an estimate of the extent of segmental dysfunction can be made.

FIGURE 2-54 Diagrammatic representation of myocardial segments of the left ventricle as viewed from the standard echocardiographic views. Thickening and excursion of each of these segments is assessed to indicate areas of hypokinesis, akinesis, dyskinesis or normal function. The 17 segments are also color coded according to the most common coronary vasculature supply.

Acute Complications of Myocardial Infarction

The acute mechanical complications of myocardial infarction, including papillary muscle and ventricular septal rupture, are most common after large inferoposterior and inferoseptal infarctions. Clinically, both conditions present with a sudden deterioration in hemodynamic status and the development of a new pansystolic murmur.

In patients with papillary muscle rupture, one or the other mitral leaflet becomes flail and the head of the ruptured papillary muscle prolapses in and out of the left atrium with each cardiac cycle. Further, as a consequence of the acute onset of regurgitation, the noninfarcted myocardium is hyperdynamic and color Doppler confirms a large, usually eccentric jet of mitral regurgitation into a slightly dilated atrium. In contrast, in patients with acute septal rupture, the mitral apparatus is intact and color Doppler can help accurately locate the septal defect (Fig. 2-55). Continuous wave Doppler can determine the peak velocity of interventricular shunt flow, and thus predict the gradient between the left and right ventricles (by using the simplified Bernoulli equation). From this information the pulmonary artery pressure can be estimated.

FIGURE 2-55 There is a large gap in the basal aspect of the interventricular septum (IVS). Color Doppler shows blood shunting (blue jet) from the left ventricle (LV) through a ventricular septal defect (VSD) into the right ventricle.

Rupture of the free wall of the ventricle, which may occur even after small infarctions, is most often rapidly fatal as a result of acute pericardial tamponade. In some instances, however, pericardial adhesions can limit the extent of pericardial bleeding (either from past pericarditis or prior coronary surgery) and result in a localized pseudoaneurysm. In contrast, true aneurysms usually form after large infarctions affecting either the anterior septal wall, or less commonly, the inferior base of the heart. Aneurysms are characteristically thinned, dyskinetic, and predispose to thrombus formation. Apical thrombus is usually evident as a collection of echogenic material in the region of abnormal wall motion (Fig. 2-56). Thrombus may either embolize acutely or become organized, layering along the wall or calcifying with time. The left ventricular remodeling can occur after myocardial infarction, resulting in ventricular size and shape change that may have adverse effect on cardiac function.

FIGURE 2-56 This two-chamber view of the left ventricle shows an apical mural thrombus. The thrombus has a speckled appearance and is brighter than the surrounding the myocardium. It is adherent to the left ventricular apex that is dilated and akinetic.

Dilated Cardiomyopathy

Despite the large number of recognized causes of dilated cardiomyopathy, there is rarely a specific etiologic factor and most cases are assumed to be a consequence of viral infection. Typically, all chambers of the heart are dilated and both the right and left ventricles appear diffusely hypokinetic. The feature that most distinguishes idiopathic dilated cardiomyopathy (IDCM) from ischemic cardiomyopathy is the presence of global, rather than regional, dysfunction (Fig. 2-57). In some patients, however, regional dysfunction may be evident because of preservation of systolic function at the base of the left ventricle or because of the presence of left bundle branch block, which causes paradoxical septal motion. Nonetheless, whereas right ventricular function is often preserved in patients with ischemic cardiomyopathy, this is not typical of other causes.

FIGURE 2-57 The four-chamber apical view in a patient with dilated cardiomyopathy shows significant left ventricular (LV) dilatation with spherical remodeling. The increased LV and left atrial (LA) pressures result in displacement of the interventricular and interatrial septum (arrows). RA, right atrium; RV, right ventricle.

In most instances, both the mitral and tricuspid valves appear normal. Despite this, there may be significant central atrioventricular regurgitation resulting from incomplete closure of the mitral and tricuspid leaflets consequent to annular dilatation and leaflet tethering as a result of papillary muscle displacement with remodeling. The presence of cavitary thrombus increases the risk of systemic emboli.

Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathies are familial in nature and genetically determined. Pathologically, they are characterized by ventricular hypertrophy, which may be diffuse or localized to the septum, apex, or ventricular free wall. Patients with septal hypertrophy are classified further into those with or without evidence of dynamic obstruction to left ventricular outflow.

The most common form of hypertrophic cardiomyopathy is associated with septal hypertrophy. Typically, the ratio of septal to posterior free wall thickness is in excess of 1.3:1. The left ventricular cavity usually appears small, and the ventricular apex may be completely obliterated in systole. The mitral valve may be morphologically normal, but there are often subtle anomalies of the mitral apparatus. These include anterior displacement of the papillary muscles, redundancy of the mitral chordae or leaflets, and in some instances, prolapse of the mitral valve. Mitral regurgitation occurs frequently and relates to the anatomy of the mitral apparatus and to the degree of outflow tract obstruction.

A hallmark of asymmetric hypertrophic cardiomyopathy with outflow tract obstruction is systolic anterior motion (SAM) of the anterior leaflet of the mitral valve (Fig. 2-58). The interposition of this leaflet tissue causes obstruction to left ventricular emptying in mid-to-late systole. This is reflected in aortic valve motion, with a closure pattern in midsystole. Doppler sampling of the left ventricular outflow tract demonstrates increased velocity at the site of leaflet-septal contact, and the continuous wave Doppler profile typically has a late-peaking systolic pattern (see Figure 2-57B). The peak velocity of this outflow signal can be used to predict the outflow tract gradient.

FIGURE 2-58 (A) Two-dimensional echocardiographic view of a patient with hypertrophic cardiomyopathy. There is anterior displacement of the anterior mitral valve leaflet (AMVL) into the left ventricular outflow tract in systole creating dynamic subaortic stenosis. (B) Continuous wave Doppler spectral tracings from the cardiac apex in a patient with hypertrophic cardiomyopathy and dynamic left ventricular outflow obstruction. Placement of the sample volume in the left ventricular outflow tract (LVOT) shows systolic flow below the baseline with a late rise to peak velocity indicating that obstruction occurs as systole progresses. (C) M-mode tracing through the mitral valve leaflets showing systolic anterior motion (SAM) of the mitral valve. The interventricular septum (IVS) and posterior wall of the left ventricle (PW) are significantly thickened. There is normal opening of the mitral leaflets in diastole (E) and systole (A). Ao, aorta; LA, left atrium; LV, left ventricle.

Left atrial enlargement is almost invariable in hypertrophic cardiomyopathy. In the presence of atrial fibrillation, both atria are typically dilated. Thickening of the aortic valve, the mitral annulus, anterior mitral leaflet, and upper septum is common, especially in older patients. Asymmetric septal hypertrophy should be differentiated from discrete upper septal hypertrophy, which is common in elderly hypertensive persons and is not associated with either midseptal hypertrophy or evidence of outflow obstruction.

Restrictive Cardiomyopathy

The characteristic morphologic features of restrictive cardiomyopathy are marked ventricular hypertrophy, a small ventricular cavity, and biatrial enlargement. Typically, systolic function is normal or even hyperkinetic. Valvular leaflets may be thickened and there is usually significant mitral and tricuspid regurgitation. The pericardium also appears normal. The most prominent physiologic derangement is impaired diastolic relaxation reflected in the alteration of the pattern of left ventricular filling on the Doppler profile of mitral inflow. Typically, the initial filling wave is large with rapid deceleration consequent to increased early filling, and the late filling wave is either small or absent owing to a reduced late diastolic filling capacity (see Figure 2-30). Although a specific cause is rarely determined, consideration should be given to the possibility of an infiltrative process such as amyloidosis and hemochromatosis.

Endomyocardial Fibrosis

Endomyocardial fibrosis is characterized by thickened endocardium, apical obliteration, global biventricular systolic and diastolic dysfunction, and mitral regurgitation. It is associated with hypereosinophilic syndrome and the changes result from endocardial inflammation and thrombus formation which predominately affects the apex.

Noncompaction Cardiomyopathy

The echocardiographic diagnosis is made by detection of thickened left ventricular walls with two distinct layers of noncompacted and compacted myocardium with deep intertrabecular recesses. The prominent trabecular meshwork typically involves the apex or midventricular segments of the inferior and lateral wall with hypokinesis of the affected and adjoining segments. A ratio of noncompacted-to-compacted myocardial thickness of greater than 2:1 measured at end systole is characteristic of left ventricular noncompaction. This form of cardiomyopathy is caused by intrauterine arrest of compaction of the myocardial fibers and meshwork. Clinically, the patients are at increased risk of heart failure, arrhythmias, and embolic events (Fig. 2-59).

FIGURE 2-59 This pediatric apical four-chamber view is from an infant with noncompaction cardiomyopathy. The right ventricular (RV) and left ventricular (LV) walls consist of a thick layer of noncompacted myocardium with deep intertrabecular recesses (arrows) and thinner layer of compacted myocardium. LA, left atrium; RA, right atrium.

Arrhythmogenic Right Ventricular Dysplasia

Patients with arrhythmogenic right ventricular dysplasia (ARVD) are predisposed to ventricular arrhythmias and sudden cardiac deaths. The right ventricular myocardium is replaced by adipose tissue and collagen. This leads to the characteristic echocardiographic features of focal right ventricular motion defects and aneurysm formation, right ventricular dilatation and hypokinesis, and the presence of brightly echogenic areas in the right ventricular myocardium indicative of fatty/fibrous tissue replacement (Fig. 2-60).

FIGURE 2-60 Subcostal image showing focal outpouching of the right ventricular (RV) free wall (arrowheads) reflecting focal aneurysmal formation, which is a major criterion for arrythmogenic right ventricular dysplasia. The RV free wall is also brightly echogenic, suggestive of fibro fatty infiltration. The RV chamber size appears dilated. LV, left ventricle.

Pericardial Effusions and Pericardial Tamponade

Echocardiography is a sensitive technique for the detection and localization of pericardial effusions. Serous pericardial fluid does not reflect ultrasound and therefore appears as an echolucent area within the boundaries of the pericardial sac (Fig. 2-61). The size of the pericardial effusion is usually described semiquantitatively as being small, moderate, or large. When large, the heart swings freely in the pericardial space. The distinction between large fluid collections in the pleural space and pericardial fluid can be made on the parasternal long-axis view. Pericardial fluid extends between the descending thoracic aorta and left atrium. In contrast, the aorta remains closely apposed to the atrioventricular groove in the presence of pleural fluid.

FIGURE 2-61 Two-dimensional echocardiographic view in a patient with both a pleural and pericardial effusion. The echo-free space anterior and immediately posterior to the heart is pericardial fluid. The parietal pericardial layer divides the posterior pericardial fluid from the pleural fluid. The location of the descending thoracic aorta in relation to the fluid is often helpful in distinguishing pleural from pericardial fluid. The descending aorta is seen in cross section behind the heart. Pericardial fluid lies between the heart and the aorta while pleural fluid is seen posterior to both the heart and the aorta. Ao, aorta; dAo, descending aorta; LA, left atrium; LV, left ventricle.

In some circumstances the echocardiographic image may suggest the presence of a specific pericardial abnormality such as tumor, fibrin, or organized hematoma. For example, the presence of discrete masses of echoes adherent to the visceral surface of the heart suggests pericardial tumor, whereas discrete strands between the visceral and parietal layers of the pericardium suggest fibrin.

Echocardiography is also useful in determining the hemodynamic significance of pericardial fluid collections. An increase in intrapericardial pressure relative to atrial and ventricular pressure causes inversion of the right atrial free wall at the end of atrial systole (early ventricular diastole), and inversion of the right ventricular free wall in early diastole (Fig. 2-62A). Right ventricular inversion is both sensitive and specific for clinically apparent cardiac tamponade. In contrast, right atrial inversion is a more sensitive but less specific marker of tamponade. Doppler ultrasound is useful in the assessment of the hemodynamic significance of pericardial effusions. In particular, it is possible to detect exaggerated respiratory phase variation in right and left ventricular inflow and aortic and pulmonary outflow, consequent to the inability of the heart to both fill normally and eject a normal stroke volume in the presence of a tense fluid-filled pericardium (see Figure 2-62B).

FIGURE 2-62 (A) Right atrial (RA) free wall inversion (arrowheads) occurs when intrapericardial pressure exceeds right atrial systolic pressure. The longer the duration of RA inversion relative to the cycle length, the greater the likelihood of cardiac tamponade. (B) Pulsed Doppler spectral tracings of flow velocity across the mitral valve in a patient with large pericardial effusion (eff). With inspiration, the right ventricular (RV) early diastolic filling velocity is augmented while the left ventricular (LV) filling decreases. Reciprocal changes occur during expiration. Arrows highlight the large variation in mitral inflow (minimum and maximum) with respiration. (C) M-mode echocardiogram in a patient with pericardial tamponade, demonstrating right ventricular outflow tract compression. The right ventricular free wall contracts in systole and moves posteriorly in parallel with the interventricular septum on the M-mode trace. However, when the mitral valve opens in diastole, the wall remains compressed (arrows) by the pressure in the pericardial space. LA, left atrium; RA, right atrial.

Pericardial Constriction

The diagnosis of constrictive pericarditis by two-dimensional echocardiography is difficult, but it may be suggested by abnormal pericardial thickening or calcification in association with impaired ventricular filling. Typically, pericardial thickening is visible as a thick, uniformly bright echogenic layer surrounding all or part of the left ventricle. In the presence of constriction, ventricular filling occurs early and ceases abruptly in middiastole because of the restraining effect of the pericardium, which prevents the ventricular chambers from enlarging as they fill. This pattern of rapid early diastolic filling and reduced late diastolic filling may also be inferred from the mitral inflow Doppler profile, which typically shows a large early filling wave, and a small or absent late filling wave.

Other two-dimensional echocardiographic features that may be visible include the lack of respiratory variation in the size of the inferior vena cava and a specific pattern of motion of the interventricular septum. This “septal bounce” pattern is an initial diastolic leftward movement of the septum, which is a consequence of the increased right ventricular inflow during peak inspiration followed by a rapid rightward shift as left ventricular filling begins.

Although none of these signs are either sensitive or specific for the diagnosis of pericardial constriction, with a compatible clinical picture they provide support for the diagnosis. Further, although some Doppler features may prove useful in distinguishing pericardial constriction from restrictive cardiomyopathy, the absence of signs of restrictive cardiomyopathy may in itself provide more useful clinical information.

Pericardial Cysts

Pericardial cysts are rare benign developmental abnormalities that are usually asymptomatic, but which may come to your attention on a routine chest x-ray. Echocardiographically, they appear as a unilocular fluid-filled thin-walled structure located adjacent to the right atrium or along the lateral border of the right or left side of the heart.

Intracardiac Tumors

Intracardiac tumors may be either primary or secondary. Secondary tumors are significantly more frequent than primary tumors and result from aggressive local intrathoracic malignancies that invade the myocardium directly or spread into the atria from the pulmonary vessels. Secondary hematologic spread of disease may also occur from the abdomen, retroperitoneal space, breast, or skin. In keeping with their aggressive nature and means of spread, secondary tumors grow within the myocardium, appearing as distinct, usually brightly echogenic masses. Rarely, secondary tumors may seed the endocardium and appear to grow into the ventricular cavity. Finally, secondary invasion of the pericardium may be visible as discrete regions of thickening of the visceral pericardium in association with a pericardial effusion.

Primary tumors of the heart are distinctly rare and most often benign. These include fibromas, fibroelastomas, rhabdomyomas, and myxomas. The most common tumor is the atrial myxoma. These frequently arise from the left side of the fossa ovalis, but they may arise anywhere in the atria and occasionally involve the mitral or tricuspid leaflets. They can be either sessile or pedunculated, single or multiple. Myxomas have been associated with other noncardiac conditions including lentiginosis and pituitary tumors (usually familial). Echocardiographically, myxomas are discrete, multilobulated masses. Although usually homogeneous in appearance, they may contain focal areas of lucency as a result of areas of hemorrhage that occur when the tumor outgrows its blood supply. When large and pedunculated, atrial myxomas may prolapse across the mitral or tricuspid valve in diastole and impair ventricular filling (Fig. 2-63).

FIGURE 2-63 Transesophageal four-chamber echocardiographic view of a large left atrial myxoma prolapsing through the mitral valve. LA, left atrium; LV, left ventricle; MV, mitral valve; RA, right atrium; RV, right ventricle.

Another benign tumor seen more commonly in children and infants is the rhabdomyoma. These tumors are frequently multiple and may first be detected by fetal ultrasound as multiple echogenic foci in the myocardium. Although they may be quite large at birth and can cause significant obstruction to intracardiac flow, most rhabdomyomas regress with time. There is a strong association of rhabdomyomas with tuberous sclerosis.

A number of malignant primary tumors may arise in the heart. Rhabdomyosarcomas arise from striated muscle and infiltrate diffusely into the myocardium, particularly the interventricular septum. They may also grow into and obliterate the cardiac chambers. In contrast, angiosarcomas are the most common primary cardiac malignancy in adults and are more common in males. They most often arise in the right atrium in the region of the interatrial septum and may be polypoid. Fibrosarcomas arise from endocardial structures and tend to be large fleshy tumors, which may infiltrate and involve more than one cardiac chamber.

Intracardiac Thrombus

Intracardiac thrombus forms as a result of low flow within the heart or as a result of endocardial injury. Thrombus formation most commonly occurs in atrial fibrillation, mitral stenosis, dilated cardiomyopathy, and recent myocardial infarction.

Ventricular thrombi appear as focal echo producing masses adjacent to the normal endocardial contour and may be laminar, sessile, or independently mobile. They can have a speckled appearance and when organized may contain areas that are brighter than the surrounding myocardium (see Figure 2-56). Thrombi should be differentiated from false tendons, apical scar, and chest wall artifacts. This is usually possible because thrombi are typically seen in at least two views, do not appear as distinct linear midventricular structures, and tend to form in regions of abnormal wall motion. The risk of systemic embolism following myocardial infarction is greater in patients with echocardiographic evidence of thrombus, and in these patients the risk relates to the size and mobility of the thrombus.

Atrial thrombi have morphologic characteristics similar to those of ventricular thrombi. They most frequently arise in the atrial appendage. Transesophageal imaging is often required to confirm or exclude the presence of thrombus with certainty. It is important to differentiate thrombus from the normal trabeculae of the appendage and from the ridge between the appendage and the lower left pulmonary vein (see Figure 2-32).

A number of normal anatomic structures can produce the appearance of a mass lesion in the atria. Specifically, thickening of the tricuspid annulus, prominence of trabeculae along the roof of the atria, and a prominent eustachian valve may all be misdiagnosed as a right atrial tumor. Finally, compression of the atrial wall by an intrathoracic mass or hiatal hernia may also produce the appearance of a left atrial tumor.

Proximal Aortic Disease

An increase in aortic root dimension is typical of proximal aortic root disease. In patients with Marfan syndrome, dilatation typically occurs at the level of the aortic sinuses and the ascending aortic root appears relatively normal. In contrast, in patients with either an atherosclerotic or luetic aortic aneurysm, the aorta appears diffusely thickened and dilatation occurs beyond the level of the sinotubular junction; discrete atheromatous plaques may be seen as irregular thickening of the vessel wall or as areas of discrete calcification. On occasion, there may be evidence of focal plaque rupture, with linear mobile echodensities attached to the abnormal vessel wall.

Aortic dissection is suggested by aortic root dilatation and a discrete dissection flap, which partitions the aortic lumen (Fig. 2-64). Typically the true lumen is smaller than the false lumen, increases in size during systole, and has high velocity flow within it. Once aortic dissection is confirmed, it is important to determine the involvement of the ostia of either the coronary or head and neck vessels, aortic valve (resulting in aortic regurgitation), and pericardial space (resulting in effusion and tamponade). Transesophageal imaging allows the diagnosis of aortic dissection with much higher sensitivity and almost complete specificity. Finally, a rare but echocardiographically distinct condition of the proximal aorta is the development of an aneurysm of the sinus of Valsalva. This may be clinically silent, but detectable during routine echocardiography as a discrete membranous structure prolapsing into either the right atria (if the aneurysm arises from the noncoronary sinus) or right ventricle (if the aneurysm arises from the right coronary sinus). Rupture of the aneurysm may occur spontaneously or as a consequence of infection and presents clinically with the development of a continuous murmur. Color Doppler reveals evidence of abnormal aortoatrial or aortoventricular continuous shunt flow. Occasionally, the degree of left-to-right shunt flow may be significant and require surgical correction.

FIGURE 2-64 Echocardiographic view of the aortic arch showing an extensive aortic dissection. The dissection flap is seen as a mobile linear echodensity extending from the anterior ascending aortic wall to the branches of the aortic arch. AsAo, ascending aorta; PA, pulmonary artery.

Disease of the Thoracic and Abdominal Aorta

Dissection of the thoracic aorta may occur as a consequence of atheromatous disease or as a result of chest trauma. In cases of suspected dissection, transesophageal imaging is usually required to confirm the diagnosis by echocardiography. The features of dissection are the same as those described for the ascending aorta. Abdominal scanning will detect atheromatous disease of the abdominal aorta, including accurate assessment of the size of abdominal aortic aneurysms.

The Doppler profile seen in the abdominal aorta may suggest a coarctation; with a significant coarctation, there is continuous systolic and diastolic flow in the aorta. Further, continuous wave Doppler directed through the descending thoracic aorta can determine the gradient across the coarctation, and the suprasternal window may allow accurate visualization and location of the coarctation itself, especially in the pediatric patient (Fig. 2-65).

FIGURE 2-65 (A) Suprasternal notch two-dimensional echocardiographic view of the aortic arch demonstrating a discrete narrowing at the aortic isthmus (arrow) indicative of an aortic coarctation. Color flow Doppler of the same view shows flow acceleration and turbulence at the site of the coarctation, where the low-velocity blue color seen in the transverse arch turns to a bright blue and yellow jet through the discrete obstruction (arrow). (B) Continuous wave Doppler tracing in the descending thoracic aorta showing the typical Doppler pattern for coarctation, with high velocity systolic flow and a slurring of the flow profile (arrowheads), which reflects a continued gradient across the coarctation into diastole. AA, aortic arch; dAo, descending aorta.