Chapter 9. Aortic Valve

Aortic valve replacement (AVR) is the most common valve replacement procedure and the second most common cardiac operation following coronary artery bypass grafting (CABG) in the United States. Intraoperative transesophageal echocardiography (TEE) alters the surgical plan in 13% of patients undergoing aortic valve surgery.1 Furthermore, a consensus statement from the American College of Cardiology, American Heart Association, and American Society of Echocardiography gave intraoperative TEE a class I designation (“evidence and/or general agreement that a given procedure or treatment is useful and effective”) in patients undergoing surgical repair of valvular lesions.2 Thus, a comprehensive TEE evaluation of the aortic valve should be performed in all patients, particularly those undergoing aortic valve procedures.

Intraoperative transesophageal echocardiography is utilized to evaluate aortic valve anatomy, valve function, and hemodynamics. A comprehensive exam includes an evaluation of valvular architecture using two- (2D) and three-dimensional (3D) imaging techniques. Stenotic and regurgitant valvular lesions and their associated hemodynamic perturbations are assessed with pulsed-wave and continuous-wave Doppler echocardiography. TEE evaluation of left ventricular function and ventricular filling yields accurate and rapid assessment in patients with altered left ventricular compliance due to long-standing aortic valve pathology. The immediate post-bypass examination provides rapid assessment of the adequacy of the valve repair/replacement and any associated cardiac complications. Intraoperative examination thus aids surgical decision making, and is especially helpful in determining the feasibility of aortic valve repair versus aortic valve replacement.

A thorough understanding of the anatomy and function of the aortic valve apparatus is necessary to obtain the optimal benefit from transesophageal echocardiographic interrogation of the aortic valve. The aortic valve apparatus is comprised of the left ventricular outflow tract (LVOT), valve cusps, sinuses of Valsalva, and proximal ascending aorta (Figure 9–1). The LVOT consists of the inferior or ventricular surface of the anterior mitral leaflet, the interventricular septum, and the posterior left ventricular free wall.

A normally functioning aortic valve apparatus allows unrestricted blood flow from the left ventricle to the ascending aorta during systole and prevents retrograde blood flow from the aorta to left ventricle during diastole. Stresses during diastole are distributed across the leaflets to the commissures and into the sinuses of Valsalva. The sinuses of Valsalva also play a critical role in systole by allowing the aortic valve to open fully without contacting the walls of the aorta. Disruption in this normal anatomy or mechanisms leads to valve dysfunction. In late diastole and associated LV filling, a 12% expansion of the aortic root is observed immediately prior to aortic valve opening,3-5 which actually initiates leaflet opening prior to ventricular contraction.3,6

Tomographic Views

The proximity of the aortic valve to the upper esophagus yields detailed and high-resolution TEE images. The American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists have published guidelines on obtaining the necessary tomographic views for performing a comprehensive transesophageal echocardiographic examination and are further discussed in the chapter on tomographic views (see Chapter 5). There are four recommended views for evaluation of the aortic valve.7

Midesophageal Short-Axis View

The midesophageal aortic valve short-axis (ME AV SAX) view permits detailed 2D, 3D and color-flow Doppler (CFD) interrogation of the aortic valve and associated root structures. The ME AV SAX view is obtained by anteflexing the TEE probe and rotating the transducer forward to between 30° and 60° in the midesophagus.7

The normal valve consists of three cusps suspended from an associated sinus of Valsalva. The cusps are of similar shape and size with fine, feathery leaflet edges that open fully, creating the appearance of an outwardly bulging equilateral triangle. During diastole the valve leaflets should close or coapt completely. The aortic valve axis is obliquely orientated to the esophageal axis with the right coronary cusp anterior and superior to the noncoronary cusp but inferior to the left coronary cusp. Two-dimensional examination in the ME AV SAX view permits evaluation of individual leaflet architecture and range of motion throughout the systolic (opening) and diastolic (closing) cycle. Since the right coronary cusp is the most anterior cusp, it is displayed below the noncoronary and left cusps on the image display (Figure 9–2). The interatrial septum attaches to the aortic wall near the noncoronary cusp, and the left main coronary artery orifice can frequently be visualized in the left coronary sinus. Thickening, calcification, commissural fusion, and decreased mobility of the leaflets are observed with valvular aortic stenosis. Bicuspid aortic valves have an eccentric circular or “fish mouth” orifice, and often a thickening or raphe that extends from the leaflet edge to the aortic wall. This raphe can be misleading in that it creates the appearance of a fused commissure, suggesting a tricuspid valve. Insertion of the leaflets to the aortic annulus differentiates a bicuspid from a tricuspid valve as the anatomic relationship between the commissures and aortic root are typically altered. Unicuspid and quadricuspid valves can also be identified easily with 2D and 3D imaging in the ME AV SAX view.

The degree of valve opening can be measured by planimetry of the orifice by using the trackball and the caliper and trace functions of the machine (Figure 9–3). Although this method is simple and rapid, it is subject to error, with poor reliability between observers. Overestimation of the valve area by planimetry may occur, particularly in patients with pliable leaflets if the ultrasound beam intersects the leaflets below their tips (Figure 9–4). In addition, in many patients, the leaflets may be so calcified that the orifice cannot be identified. Color-flow Doppler in this view assesses leaflet coaptation and the severity of any associated aortic regurgitation in a semiquantitative fashion.

Midesophageal Long-Axis View

The midesophageal aortic valve long-axis (ME AV LAX) view is perpendicular to the ME AV SAX view and allows imaging of all the components of the aortic valve apparatus, including the left ventricular outflow tract, aortic valve, sinuses of Valsalva, sinotubular junction, and proximal ascending aorta. From the ME AV SAX view, the transducer is rotated forward to 120° to 150° while keeping the aortic valve in the center of view.7 A normal aortic valve appears as two thin lines that open parallel to the aortic walls during systole. The right coronary cusp, being the most anterior cusp, is displayed along the anterior surface of the aortic wall during systole (lower on the image display). The cusp seen at the top of the display is either the noncoronary or left coronary cusp depending upon probe orientation (see Figure 9–4).7

The ME AV LAX view is used to examine leaflet morphology, mobility, thickening, and calcification, and to detect subaortic pathology (eg, subaortic membrane). During systole, normal leaflets move freely, parallel to the axis of flow, and return to the plane of the annulus during diastole. Doming is the characteristic bowing appearance of the leaflets during systole as a result of calcification of the tips but not the bodies of the leaflets (see Figure 9–4). With membranous subaortic stenosis, the LVOT should be examined for the presence of a thin fibrous band or ring stretching from a hypertrophied interventricular septum to the base of the anterior leaflet of the mitral valve (MV) (Figure 9–5), which also may be thickened and stiff. Systolic anterior motion of the anterior leaflet of the MV causing dynamic LVOT obstruction in hypertrophic obstructive cardiomyopathy or after MV repair often is detected in this view. The ME AV LAX view is also used to measure the aortic annulus, sinus of Valsalva, sinotubular junction, and ascending aorta diameters when determining the appropriate size of prosthesis during valve replacement surgery. These measurements are particularly important in homograft implantations where size and geometry have tremendous implications on the success of the procedure.8 Annulus measurement in a normal valve is made from the hinge point of one leaflet to the hinge point of the opposite leaflet of the opened valve during systole (see Figure 9–4; Figure 9–6). However, in heavily diseased valves, better estimations can be made at the junction of the aortic annulus and the LVOT. To improve the estimate, multiple measurements should be made at slightly different scan angles and averaged.

Color-flow Doppler evaluation in the ME AV LAX view identifies systolic blood flow disturbances in the ascending aorta due to aortic stenosis or in the left ventricular outflow tract due to left ventricular outflow tract obstruction (LVOTO) and diastolic flow disturbances due to aortic regurgitation. M-mode measurements also can be made in the ME AV LAX view to examine leaflet mobility, thickness, and tip separation.

Transgastric Long-Axis View

The transgastric long-axis (TG LAX) view is obtained by starting with the transgastric short-axis (TG SAX) view of the left ventricle at the midpapillary level and rotating the transducer forward to 90° to 110°. The mitral valve is visualized on the right side of the display in the near field while the aortic valve is displayed in the far field (Figure 9–7). The far field position of the aortic valve in this view often leads to attenuation of the ultrasound beam, thus limiting 2D imaging. However, parallel alignment of the continuous- or pulsed-wave Doppler beam through the LVOT, aortic valve, and ascending aorta is often possible and allows for the determination of velocities in the outflow tract and through the aortic valve. Acoustic shadowing in the LVOT can also be avoided using this view, making this and the deep TG LAX views invaluable in assessing prosthetic valve function.

Deep Transgastric Long-Axis View

A second view that consistently affords parallel alignment of the Doppler beam with aortic valve blood flow is the deep transgastric long-axis (deep TG LAX) view. This view is developed from the TG SAX view by advancing the probe and utilizing slight leftward flexion and anteflexion. Commonly, the probe is slowly withdrawn until the image is developed. In the deep TG LAX view, the left ventricular apex is located in the near field (top of the screen), the mitral inflow is on the right of the screen, the left atrium is located in the lower right-hand corner, and the aortic valve apparatus is seen in the lower left-hand corner of the display (far field) (Figure 9–8). As with the TG LAX view, the far-field location of aortic valve structures leads to ultrasound attenuation and 2D image degradation. Color-flow Doppler is useful during probe manipulation in order properly align the left ventricular outflow tract, aortic valve, and ascending aorta with the Doppler beam. In aortic stenosis, the continuous-wave Doppler cursor is aligned with the narrow, turbulent, high-velocity jet and the spectral Doppler display is activated. Accurate localization provides a distinctive audible sound and high-velocity (greater than 3 m/s) spectral Doppler recording that exhibits a fine feathery appearance and a midsystolic peak. Planimetry of the spectral envelope yields the velocity-time integral (VTI) and an estimate of mean aortic valve gradient. Transgastric velocity measurements obtained with Doppler imaging correlate well with data obtained by both transthoracic echocardiography (TTE) and cardiac catheterization.9

Skill and practice are necessary to obtain the deep transgastric long-axis and transgastric long-axis views. Stoddard et al demonstrated a significant increase in successful deep transgastric image acquisition with increasing experience (53% feasibility in the first 43 patients, 88% feasibility in the latter 43 patients).10

Aortic Stenosis

Normal aortic valve area is 3 to 4 cm2.11 Obstruction of LVOT flow into the ascending aorta can occur at three distinct anatomical sites: valvular, subvalvular, or supravalvular. Valvular obstruction is discussed in this chapter with a brief introduction to dynamic subvalvular obstruction, while subvalvular and supravalvular obstruction is discussed in the chapters on cardiomyopathies (see Chapter 14) and congenital heart disease (see Chapter 18). Valvular obstruction accounts for the vast majority of LVOT obstruction and is therefore the primary focus of this chapter.

The most common cause of aortic stenosis in the United States is calcific aortic stenosis of the elderly (Figure 9–9), followed by congenital abnormalities, including bicuspid and rarely unicuspid or quadricuspid valves (Figure 9–10). Bicuspid aortic valves account for approximately 50% of the aortic valve replacements performed in the United States and Europe, while progressive calcification of a tricuspid valve accounts for the remainder.12 The mechanism of aortic stenosis in the elderly and in congenital cases is distorted flow through the diseased valve leading to degenerative changes in the cusps, which predisposes the valve to calcification. The rate of calcification and stenosis varies widely, although elderly men with associated coronary artery disease and individuals with a history of smoking, hypercholesterolemia, and elevated serum creatinine levels demonstrate a more rapid disease progression.13-15 Many experts believe that the development of aortic stenosis is an active process, which involves chronic inflammation fueled by atherosclerotic risk factors.16 An infrequent cause of aortic stenosis in the United States is rheumatic disease, which produces commissural fusion; however, rheumatic disease remains a common cause of aortic stenosis worldwide.

Calcific aortic stenosis of the elderly characteristically occurs in patients greater than the age of 65, while patients between the ages of 35 and 55 with aortic stenosis typically have a congenital bicuspid aortic valve. Four percent of the elderly U.S. population has significant aortic stenosis,17 and approximately 1% to 2% of the population has a bicuspid aortic valve.18 Patients with a bicuspid aortic valve may also have coarctation of the aorta, dilation of the aortic root, or aortic dissection. In patients with a bicuspid aortic valve, aortic root dilation can develop irrespective of hemodynamics and age, and has been shown to continue after valve repair, suggesting a common developmental defect.19 Concomitant replacement of the ascending aorta should be considered if the ascending aortic diameter is greater than or equal to 4.5 cm, given the tendency for progressive aortic root dilation even after aortic valve replacement.20

The European Association of Echocardiography and the American Society of Echocardiography recently published guidelines and standards regarding the echocardiographic assessment of valve stenosis.11 Methods graded as appropriate and recommended for all patients (level 1) with aortic stenosis (AS) include measurement of:

• AS jet velocity
• Mean transaortic gradient
• Valve area by continuity equation (utilizing velocity-time integrals)

Methods considered reasonable when additional information is needed in select patients (level 2) include:

• Simplified continuity equation (utilizing maximum velocities)
• Velocity ratio or dimensionless index
• Aortic valve area planimetry

Two-Dimensional Measures

Two-dimensional imaging of a stenotic aortic valve in the ME AV SAX and ME AV LAX views will typically demonstrate leaflet restriction, calcification, commissural fusion, and failed leaflet coaptation. The ME AV SAX view can be used for measuring the aortic valve orifice area by planimetry, which has been shown to correlate well with other quantitative methods,21 but is also subject to error in the presence of highly pliable or heavily calcified leaflets.22 A cross section that is oblique or inferior to the leaflet tips overestimates the orifice size (see Figure 9–4). It is important, therefore, to develop an image with the smallest orifice size to ensure that the imaging plane transects the leaflet tips. To do so, the aortic valve is first imaged in the ME AV LAX, and the smallest orifice seen on the long axis is centered on the image display screen. The transducer position is then stabilized within the esophagus as the multiplane angle is rotated backward to the short-axis view. In a true short-axis cross section, the valve should appear relatively circular and all three cusps appear equal in shape. Planimetry for aortic valve area is a level 2 recommendation by expert consensus and is considered reasonable when additional information is needed in selected patients.11

The ME AV LAX view provides imaging of the left ventricular outflow tract, aortic valve, and aortic root, and is useful in differentiating valvular from subvalvular and supravalvular pathology. Reduced leaflet separation and doming with the curvature towards the aortic wall are sufficient for the qualitative diagnosis of aortic stenosis. Maximal cusp separation of less than 8 mm in a long-axis view suggests critical stenosis, whereas greater than 12 mm separation suggests noncritical disease.23 Measurements of aortic valve separation can be made with M-mode techniques where a characteristic “box car” pattern is seen on M-mode display when the aortic valve is open, with leaflet separation represented by the width of the box car. In patients with membranous subaortic stenosis, M-mode assessment may show early systolic closure of the valve (Figure 9–11).

Pressure Gradients

The primary echocardiographic technique used to quantify the severity of aortic stenosis is Doppler echocardiography for determination of pressure gradient and aortic valve area. Valvular stenosis produces a decrease in pressure distal or downstream from the stenosis. This pressure gradient or pressure drop across the valve stenosis is proportional to the velocity of flow as described by the Bernoulli equation:

ΔP = 4 (V22 − V12)+ Local Acceleration + Viscous Losses

Where ΔP = Pressure gradient (mm Hg)

V2 = Velocity of flow (m/s) distal to the stenosis (aortic valve)

V1 = Velocity of flow (m/s) proximal to the stenosis (LVOT)

Given that local acceleration is only significant for long tubular lesions, and viscosity losses are only important when hematocrit is extremely high, these factors can be disregarded in clinical practice. Typically, V1 or the LVOT velocity is less than 1 m/s and therefore can be disregarded as well. This yields the commonly applied simplified Bernoulli equation:

ΔP = 4 (V2)2

ΔP = 4 (VAortic Valve)2

When V1 exceeds 1.5 m/s (eg. LVOT flow acceleration or obstruction), the modified Bernoulli equation should be utilized:

ΔP = 4 (V22 – V12)

V1 is commonly elevated in the presence of aortic regurgitation, volume overload, or other high output states. Failure to use the modified Bernoulli equation in these conditions when LVOT velocity exceeds 1.5 m/s will overestimate the pressure gradient and the severity of aortic stenosis.

In order to measure transvalvular blood velocity, continuous-wave Doppler (CWD) is used in either the TG LAX or deep TG LAX view. The CWD cursor is aligned with the narrow, turbulent, high-velocity jet and the spectral Doppler display is activated. Accurate localization provides a distinctive high-velocity (>3 m/s) spectral Doppler recording that exhibits a fine feathery appearance and a midsystolic peak (Figure 9–12). Planimetry of the spectral envelope yields the velocity-time integral and an estimate of mean aortic valve gradient. The mean gradient is a derived measurement obtained by all ultrasound systems by averaging the instantaneous gradients over the entire ejection period. The peak pressure gradient (also provided by all ultrasound systems) can be estimated from the peak velocity measurement using the simplified Bernoulli equation:

Peak Aortic Valve Pressure Gradient (PGAV) = 4 (Aortic Valve Velocity)2

Peak gradients are calculated from velocity information and therefore do not provide additional clinical information in comparison to peak velocity. A peak velocity greater than 4 m/s and a mean gradient greater than 40 mm Hg are suggestive of severe aortic stenosis (Table 9–1).

Gradients derived in the operating room may be significantly different from those obtained during preoperative echocardiographic studies or in the cardiac catheterization laboratory. Stenotic orifice gradients are flow dependent, and an increase in cardiac output across the aortic valve will increase the gradient. Conditions that increase systolic blood flow through the aortic valve such as hyperdynamic left ventricular function, sepsis, severe aortic regurgitation, and hyperthyroidism will also increase the pressure gradient. Conversely, conditions that decrease systolic blood flow through the aortic valve such as severe LV dysfunction, severe mitral regurgitation, mitral stenosis, and a left to right shunt will decrease the aortic transvalvular pressure gradient (Table 9–2). Thus, pressure gradients should be measured under constant and optimal loading conditions, and cardiac output should be determined whenever possible to ensure estimation of true gradients. If necessary, the cardiac output should be increased to the normal range by using an agent such as dobutamine (start at 2.5 or 5 mcg/kg/min and increase every 3 to 5 minutes to a maximum of 10 to 20 mcg/kg/min). Further, in the presence of irregular heart rhythms, such as premature ventricular contractions and atrial fibrillation, an averaged VTI from at least five consecutive beats should be used for all calculations. If patients are being mechanically ventilated, measurements should be made at the end of exhalation. In heavily calcified and stenotic valves, the VTI can be difficult to obtain, and peak velocities may be underestimated if the CWD beam does not pass through the orifice. Color-flow Doppler can be helpful in aligning the CWD beam by identifying the location of the flow through the valve. Aortic stenosis jets also can be confused with mitral regurgitant jets when measured in the deep TG LAX view. Differentiating the two jets involves recognition that the aortic stenosis jet begins later (after isovolumic contraction: mid to latter portions of the QRS complex) and ends earlier than the mitral regurgitant jet and that the peak velocity of a mitral regurgitant jet is always higher than that of an AS jet. When subvalvular velocities exceed 1.5 m/s, the modified rather than the simplified Bernoulli equation must be used to avoid overestimating the true pressure gradient.

Differences in gradients between the intraoperative echocardiography examination and catheterization data are also commonly seen. It should be remembered that catheterization reports frequently present peak-to-peak gradients, which is the difference between the peak LV pressure and the peak aortic pressure (Figure 9–13). Because the peak aortic pressure is attained (a fraction of a second) later than the peak LV pressure, it is not an actual physiologic measurement, whereas Doppler measurements reflect peak instantaneous gradients. Thus, Doppler-derived gradients may be greater than catheter-derived gradients when peak-to-peak gradients are reported. Doppler-derived gradients may also be greater than catheter-derived gradients when the phenomenon of pressure recovery (reconversion of kinetic energy not completely dissipated as turbulence back to pressure energy distal to a stenosis, resulting in decrease in the pressure gradient) is present. Pressure recovery appears to be clinically relevant only in patients with a small (<3 cm) aorta or a small (<19 mm) bileaflet tilting disk prosthesis.

Nonvalvular Stenosis Left ventricular outflow tract gradients can also occur from subvalvular or supravalvular pathology. Subvalvular stenosis may present as a fixed or a dynamic (different degrees of obstruction during systole) lesion. In membranous subaortic stenosis (also discussed in Chapter 18), there is a fibrous band or ring just below the AV causing obstruction to LV outflow that remains fixed (unchanged) throughout systole. In hypertrophic obstructive cardiomyopathy (also discussed in Chapter 14), hypertrophy of the basal segment of the interventricular septum produces dynamic LVOT obstruction, typically peaking late in systole. Thus, valvular aortic stenosis produces a rounded spectral Doppler pattern with a midsystolic peak, while dynamic left ventricular outflow tract obstruction produces a late systolic peak with a “dagger-shaped” or “shark's tooth” spectral pattern (Figure 9–14). Turbulent flow in the LVOT on color-flow Doppler imaging is usually the first clue of the existence of subvalvular obstruction.

Low-Gradient Aortic Stenosis A particularly challenging perioperative dilemma is the evaluation of the patient with aortic stenosis and low cardiac output, or “low-flow, low-gradient aortic stenosis.” Patients with low-gradient aortic stenosis typically have a valve area less than 1.0 cm2, impaired systolic function, and a mean transvalvular pressure gradient less than 30 mm Hg. Mortality rates for aortic valve replacement in this setting are as high as 18% if the ejection fraction is less than 30% to 35%,24–26 but the 4-year survival without intervention is less than 20%.27,28 Intraoperative echocardiography combined with dobutamine stress testing plays an important role in assessing perioperative risk by determining contractile reserve. A 20% stroke volume increase from baseline to peak dobutamine dose identifies the existence of contractile reserve,29 and operative mortality is reported to be 5% and 32%, respectively, in patients with or without contractile reserve.28 In addition to assessing risk, dobutamine administration normalizes cardiac output for a more accurate estimation of transvalvular gradients.30 Alternatively, aortic valve area in patients with low ejection fraction and cardiac output can be estimated using the continuity equation method or the dimensionless index (see below).

Aortic Valve Area—Continuity Equation

The continuity equation method to calculate aortic valve area is based upon the concept of conservation of mass and continuity of flow. The flow of blood through the left ventricular outflow tract must equal flow through the aortic valve into ascending aorta:

SVAV = SVLVOT

SVAV = CSAAortic Valve × VTIAortic Valve

SVLVOT = CSALVOT × VTILVOT

Where SV = Stroke volume

CSA = Cross-sectional area

Thus,

CSAAortic Valve × VTIAortic Valve = CSALVOT × VTILVOT

Aortic valve area is then calculated as:

Assuming that the LVOT is circular:

CSALVOT = π × (d/2)2

CSALVOT = π/4 × d2

CSALVOT = 0.785 × d2

Where d = LVOT diameter

The valve area calculated with the continuity equation is the effective orifice area or the cross-sectional flow area of blood as it passes through the valve. It should be remembered that this effective orifice area is smaller than the anatomic valve area due to contraction of the flow stream, but the calculated effective orifice area is accepted as a measure of aortic valve area and is the primary predictor of clinical outcome.11

To obtain the three measurements required to solve the continuity equation for aortic valve area, one must utilize three different echocardiographic techniques and tomographic views:

In the setting of stenosis, CWD is used to measure aortic valve velocity because velocities encountered are usually greater than 2 m/s. Proper alignment of the Doppler beam with flow through the aortic valve is essential as any deviation from a parallel intercept angle leads to velocity underestimation. Orientation of the CWD beam using color-flow Doppler and audible signaling may be helpful. If the intercept angle is within 20° of parallel, the degree of underestimation is 6% or less and clinically acceptable. The resulting CWD spectral envelope is solid or shaded in character, reflecting nonlaminar flow, and demonstrates a high-velocity midsystolic peak. Planimetry is then utilized to trace the spectral envelope and obtain the aortic valve velocity-time integral (VTI) and peak velocity. Although both VTI and peak velocity are considered acceptable by some experts, a recent consensus statement indicated that the utilization of peak velocities may be less reliable for determination of aortic valve area using the continuity equation.11,31

The LVOT VTI is determined by placing the pulsed-wave Doppler sample volume in the LVOT just proximal to the aortic valve and tracing the spectral Doppler envelope. The pulsed-wave sample volume should first be placed at the level of the valve and slowly withdrawn into the LVOT until a smooth spectral pattern without aliasing is obtained. In patients with AS, the sample volume may need to be withdrawn 0.5 to 1.0 cm apically to obtain a laminar flow curve due to the flow acceleration in close proximity to the valve.11 The spectral profile should demonstrate laminar flow as demonstrated by a hollow or unshaded spectral envelope. Normal peak velocities in the LVOT range from 0.8 to 1.5 m/s.

An accurate determination of aortic valve area using the continuity method requires that the LVOT diameter be measured at the same point in the LVOT as where the LVOT spectral velocity was recorded. This measurement is usually obtained with the ME AV LAX view, because 2D imaging is optimal when the ultrasound beam intersects its target perpendicularly. The LVOT annular diameter is obtained during midsystole with electronic calipers placed along the inner edges of the endocardium. Normal values for the LVOT diameter are a mean of 2.0 cm with a range of 1.8 to 2.2 cm.

Accurate measurement of the LVOT diameter is essential because this measurement is squared to determine CSALVOT and is the greatest source for error in determining aortic valve area with the continuity equation. Underestimation of LVOT diameter will result in underestimation of the aortic valve area. A second source of error is introduced when the LVOT diameter and the LVOT velocity are not measured in the same location. A technical limitation of TEE is that the best view for 2D imaging of the LVOT (ME AV LAX) is not the best view for Doppler interrogation of LVOT velocity (TG LAX or deep TG LAX). Similarly, the LVOT and aortic valve velocity measurements should be acquired from the same heartbeat to minimize the effect of beat-to-beat variability in stroke volume. The most common clinical scenario of beat-to-beat variability is the patient with an irregular cardiac rhythm, eg, atrial fibrillation. In patients with atrial fibrillation, it is recommended that at least five consecutive beats be analyzed and averaged. Alternatively, CWD through both the aortic valve and the left ventricular outflow tract often yields two spectral envelopes, the higher velocity related to the aortic valve and a lower, denser pattern consistent with the left ventricular outflow tract velocity (Figure 9–15). This “double-envelope” technique circumvents the problem of different stroke volumes by allowing both velocity-time integrals to be determined on the same beat.32 Another potential source of error is the inability to align the Doppler beam to be parallel with flow. Ensuring that axial alignment deviates less than 20° from parallel minimizes this error. A final limitation is the inability to obtain adequate tomographic views, leading to an inability to estimate aortic valve area in up to 6% of patients.33,34 Epicardial echocardiography (see Chapter 20) can overcome this limitation in 100% of patients and demonstrates excellent correlation with TEE, TTE, and cardiac catheterization–derived measures.35

Velocity Ratio or Dimensionless Index

The ratio of the LVOT velocity-time integral to the aortic valve velocity-time integral is termed the dimensionless index (DI) and is used as an estimate of aortic stenosis severity.

The continuous-wave VTI of a normal aortic valve will equal the VTI of the LVOT, and therefore the DI will equal 1. With progression of aortic stenosis, the aortic valve velocity increases while the left ventricular outflow tract velocity remains unchanged. Severe aortic stenosis is present when the DI is less than 0.25.36 Patients with a normal LVOT diameter of 2.0 cm, have a calculated LVOT area of 3.14 × (1)2 = 3.14 cm2. A DI less than 0.25 thus corresponds to an aortic valve area that is 25% of the LVOT area or approximately 0.25(3.14) = 0.8 cm2 (see Table 9–1).

Associated Echocardiographic Findings

Pressure overload from the increased resistance to ejection initially results in concentric hypertrophy of the LV, thus allowing the ventricle to preserve SV by increasing the contractile mass. Posterior wall thickness should be measured in aortic stenosis using the caliper function in the TG SAX view, at end-diastole (excluding the papillary muscles). Wall thickness 1.0 cm or greater in women and 1.1 cm or greater in men is considered abnormal. Septal hypertrophy as a consequence of aortic stenosis can lead to the development of systolic anterior motion (SAM) of the mitral valve after AVR (see Chapters 8 and 14). Diastolic dysfunction also is commonly seen in these patients because relaxation is impaired in the hypertrophied ventricle and optimal ventricular filling becomes dependent to a greater degree on atrial contraction. Mitral inflow velocities typically demonstrate a decrease in the velocity of early diastolic inflow (decrease in E-wave amplitude), an increase in the velocity of late diastolic inflow due to atrial contraction (increase in A-wave amplitude), a decrease in E/A velocity ratio, and a prolonged deceleration time (see Chapter 12). Early in aortic stenosis, LV end-systolic volume and end-diastolic volume remain unchanged; however, an increase in LV end-diastolic pressure may be present from abnormal relaxation and stiffness of the hypertrophied ventricle. Chronic increases in LV end-diastolic pressure result in elevated left atrial (LA) pressures and LA enlargement, predisposing to the development of atrial fibrillation. Loss of the atrial contraction can then further impair LV filling, thus producing dramatic decreases in SV and cardiac output. Ventricular dilatation, resulting in an elevated LV end-diastolic volume and LV end-systolic volume, occurs late in the disease. Dilation of the ascending aorta may be a consequence of long-standing aortic stenosis from an adaptive mechanism promoting left ventricular ejection, or may be due to intrinsic disease within the aortic wall. A comprehensive examination of the ascending aorta, including epiaortic scanning, is recommended to determine the need for surgical repair and to guide cannulation and perfusion strategies. Finally, mitral regurgitation is common in patients with aortic stenosis and is related to either LV pressure overload or intrinsic mitral disease. In the majority of patients without intrinsic mitral disease, mitral regurgitation improves after aortic valve replacement, but the evidence supporting this intuitive clinical reasoning is sparse.

Aortic Regurgitation

Aortic regurgitation is caused by intrinsic disease of the aortic valve leaflets or diseases that affect the integrity of the ascending aorta. Intrinsic disease of the aortic cusps includes calcific, rheumatic, myxomatous, congenital, infectious, and traumatic abnormalities. Conditions that alter the structural support of the aortic annulus include annular dilatation, aortic dissection, and aneurysmal disease. Assessment of aortic regurgitation by TEE requires determination of the etiology of valve dysfunction, classification of the severity of aortic regurgitation, and associated cardiovascular changes. El Khoury et al have proposed a classification system describing the mechanism of aortic regurgitation.37 This classification system, similar to the Carpentier classification system for mitral regurgitation,38 was developed to provide insight into the mechanism of aortic regurgitation, guide repair techniques, and provide a framework for the assessment of long-term outcomes. Type I lesions are associated with normal leaflet motion and are subclassified according to the segment of the aortic root that is dilated or by the presence of cusp perforation. Type Ia lesions are caused by dilation of the sinotubular junction and ascending aorta; type Ib lesions are caused by dilation of the sinus of Valsalva and sinotubular junction; and type Ic lesions are caused by isolated dilation of the aortic annulus. Type Id lesions have normal leaflet mobility and normal aortic root dimensions, but are characterized by leaflet perforation. Type II lesions are caused by leaflet prolapse secondary to excessive cusp tissue or commissural disruption, and type III lesions are caused by leaflet restriction (Figure 9–16).37

Two-Dimensional Measures

The four standard TEE views of the aortic valve (ME AV SAX, ME AV LAX, TG LAX, and deep TG LAX) are also utilized to evaluate an insufficient aortic valve. The ME AV LAX view will identify prolapsing aortic valve cusps, an aortic aneurysm, or aortic dissection with loss of aortic valve cusp suspension from the aortic annulus. Leaflet perforations secondary to endocarditis may be visible in both the ME AV SAX and ME AV LAX views. The ME AV SAX view allows for planimetric assessment of the end-diastolic gap between the aortic cusps as an estimate of the severity of aortic regurgitation. A gap area less than 0.2 cm2 (small), 0.2 to 0.4 cm2 (moderate), and greater than 0.4 cm2 (large) demonstrates good angiographic correlation with mild, moderate, and severe aortic regurgitation, respectively.39

Doppler Color-Flow Mapping

Doppler echocardiography provides several quantitative estimates of the severity of aortic regurgitation (Table 9–3). The ME AV SAX view allows visualization of all aortic valve cusps during interrogation with color-flow Doppler and is useful for identifying the location of regurgitant flow. Color-flow Doppler applied to the ME AV LAX view allows assessment of the width of the AR jet relative to the LVOT during diastole. Central jets are more common with aortic annular dilatation, whereas an eccentric jet implies underlying leaflet pathology, whether intrinsic to the valve or secondary to disruption of the valve suspension mechanism (Figure 9–17, 9–18 and 9–19).

One method for estimating aortic regurgitation that demonstrates good correlation with angiographic determinants of aortic regurgitation is the ratio of the jet width measured at the origin of the jet (within 1 cm of the aortic valve) to the width of the LVOT.31 A jet width/LVOT width ratio of less than 0.25 is mild AR, while a ratio greater than 0.64 is indicative of severe AR. An alternative estimate for the severity of aortic regurgitation is based upon the ratio of the cross-sectional area of the regurgitant jet (within 1 cm of the valve) to the cross-sectional area of the LVOT. A ratio of jet area–to–LVOT area less than 5% represents mild AR, while a ratio greater than 60% represents severe AR.40 It is important to remember that the length of the aortic regurgitation jet into the left ventricle does not correlate with severity because of the dependence of this measure upon loading conditions and ventricular compliance.

Vena Contracta Width

The vena contracta is the narrowest portion of the regurgitant jet and is located at or just proximal to the orifice. It is obtained in the ME LAX view with the imaging depth reduced to optimize imaging size. The largest diameter of the vena contracta during any portion of diastole should be measured. Vena contracta width correlates well with the severity of AR by angiography; a width greater than 6.0 mm is severe, while a width less than 3.0 mm represents mild aortic regurgitation (Figure 9–20).41 Vena contracta width is a load-independent determinant of AR severity, as it is not affected by changes in afterload or volume loading.

Pressure Half-Time and Deceleration Slope

Continuous-wave Doppler is utilized to determine the severity of aortic regurgitation by measuring the pressure half-time (PHT) and the deceleration slope of the regurgitant jet. A parallel intercept between the regurgitant jet and Doppler beam is typically obtained using the deep TG LAX or TG LAX views. Color Doppler is then used to identify the location and direction of the AR jet, and the Doppler cursor is placed within the jet to obtain the continuous-wave spectral Doppler velocity profile. A large regurgitant orifice allows for a more rapid equalization of the aortic and left ventricular pressures, yielding a more rapid decline in the regurgitant jet velocity, thus generating a steep deceleration slope and a short pressure half-time (time for the diastolic pressure gradient to fall to half its initial value) (Figure 9–21). A deceleration slope greater than 3 m/s2 or a pressure half-time shorter than 200 milliseconds is indicative of severe (3 to 4+) aortic regurgitation.42 A pressure half-time of greater than 500 milliseconds is indicative of mild aortic regurgitation (Figure 9–22). In patients with elevated LV end-diastolic pressure (e.g. ischemia, cardiomyopathy, chronic AR) the use of PHT may overestimate the true severity of regurgitation because the elevated ventricular pressure will decrease the time required for equalization of pressures between the aorta and the left ventricle. Similarly, decreased SVR (e.g. sepsis, post-CPB) results in a steeper deceleration slope.

Descending Aortic Flow Reversal

The presence of holodiastolic flow reversal on pulsed-wave Doppler (PWD) examination of the descending aorta indicates severe AR (Figure 9–23). The PWD sample is placed in the descending aorta, just beyond the aortic arch, in the longitudinal plane of the descending aorta (multiplane angle at 90°), with the sample volume in the center of the aorta. However, better alignment with aortic flow may be obtained in the distal descending aorta. Holodiastolic flow reversal in the proximal descending aorta is sensitive but not specific for detection of severe AR, whereas flow reversal in the abdominal aorta is sensitive and specific for AR.43,44 False-positive results in the proximal aorta can be due to the presence of a patent ductus arteriosus, Blalock-Taussig shunt, or a descending aortic aneurysm.

Regurgitant Volume, Regurgitant Fraction, and Effective Regurgitant Orifice Area

Patients with mild aortic regurgitation as determined by jet width, vena contracta size, and pressure half-time require no further assessment of AR severity. However, if any of these parameters suggest more than mild AR, other quantitative measures such as regurgitant volume, regurgitant fraction, and effective regurgitant orifice area should be assessed (see Table 9–3).40 Regurgitant volume is the difference between the volume of blood flowing antegrade through the regurgitant valve compared to the volume of blood flowing antegrade through a different but nonregurgitant cardiac valve. For example, in the absence of intracardiac shunts and mitral regurgitation, the aortic valve regurgitant volume is the difference between aortic valve systolic flow and systolic flow through the pulmonic valve or diastolic flow through the mitral valve.

Regurgitant Volume (RV) = SVRegurgitant Valve − SVCompetent Valve

RVAortic Valve = SVAortic Valve − SVPulmonic or Mitral Valve

RVAortic Valve = (VTIAortic Valve × CSAAortic Valve) − (VTIPulmonic or Mitral Valve × CSAPulmonic or Mitral Valve)

Pulmonary artery blood flow is reliably measured with TEE and is typically favored over mitral inflow because the mitral valve annulus is saddle shaped and not circular as required for the calculation of CSA. In the absence of aortic stenosis, SVLVOT can be substituted for SVAortic Valve.

Regurgitant fraction is the proportion of aortic flow that is regurgitant and equals the aortic valve regurgitant volume divided by the aortic valve systolic volume.

Effective regurgitant orifice area (EROA) is calculated by dividing the regurgitant volume by the velocity-time integral of the regurgitant jet recorded by continuous-wave Doppler.41

Associated Echocardiographic Findings

The size of the left ventricle is an indirect indicator of the severity of aortic regurgitation in patients with chronic AR. A dilated ventricle usually excludes mild AR, instead favoring moderate to severe chronic aortic regurgitation. In cases of acute aortic regurgitation, a normal-sized ventricle does not exclude severe AR because the left ventricle has not had the time to remodel and dilate. Late in the disease course after long-standing dilation, left ventricular systolic function will irreversibly deteriorate; therefore, surgical intervention is recommended before LV systolic function declines. An aortic regurgitation jet may also cause a diastolic fluttering and premature closure of the anterior mitral leaflet. An eccentric AR jet may cause diastolic doming of the mitral valve towards the left atrium.

Effect of AR on Associated Valvular Lesions

As described earlier, AS severity may be overestimated in patients with AR if elevated subvalvular velocities are ignored by applying the simplified instead of the modified Bernoulli equation. Patients with both moderate aortic stenosis and moderate aortic regurgitation are considered to have severe valvular disease.11 Similarly, mitral valve area (MVA) is overestimated in patients with both mitral stenosis and aortic regurgitation when the pressure half-time (PHT) method is used. The PHT method utilizes the deceleration of mitral valve inflow to estimate mitral valve area. Deceleration is based on the equalization of pressure between the left atrium and left ventricle, and deceleration time increases (shallow slope) as mitral valve area decreases. In the absence of aortic insufficiency, left ventricular pressure rise occurs from diastolic mitral inflow alone. With aortic insufficiency, however, left ventricular pressure rise occurs more rapidly, leading to a steeper mitral inflow slope and an overestimation of mitral valve area (Table 9–4).

The introduction of three-dimensional echocardiography into clinical practice has allowed a more detailed evaluation of the left ventricular outflow tract and aortic valve apparatus, compared with two-dimensional echocardiography (Figure 9–24, 9–25 and 9–26). Incorporation of a three-dimensional LVOT area produces less deviation from invasively or planimetrically measured aortic valve areas than conventionally (2D) calculated areas using the continuity equation.45 Real-time intraoperative three-dimensional echocardiography is also useful for identifying aortic valve abnormalities that may be missed with two-dimensional echocardiography.46

The technique of geometric aortic valve analysis, which employs pattern recognition to generate a dynamic analysis of the aortic valve area, LVOT diameter, sinotubular junction, and ascending aorta, has also recently been introduced into clinical practice (Figure 9–27) and may offer greater quantification of aortic valve function.

Aortic Valve Repair Versus Replacement

Just as with the mitral valve, aortic valve repair techniques are always preferred when feasible, as compared to replacement procedures. The vast majority of aortic valves suitable for repair, however, have regurgitant rather than stenotic lesions. Aortic regurgitation that results from aortic dissection is easily repaired by resuspension of the cusps and is highly successful in the absence of additional leaflet pathology. Unfortunately, calcific aortic stenosis is rarely amenable to repair. Boodhwani et al evaluated a series of 264 patients presenting for aortic valve repair for greater than moderate aortic regurgitation. Sixty-four percent of patients in this study had a single type of AR as classified by El Khoury et al,37 30% had two types, and 6% had three different types. The majority of patients had type I or functional aortic annular dilation, 35% had type II or leaflet prolapse, and 15% had restricted leaflet mobility or type III AR (see Figure 9–16). Patients with type III AR had a higher risk for recurrent AR at follow-up, and therefore these patients need to be considered for valve replacement rather than repair.47 Data from the Cleveland Clinic also suggest that repair of regurgitant bicuspid aortic valves is superior (0% immediate replacement rate after repair) to that of a tricuspid aortic regurgitant valve (15% immediate post-repair replacement rate).48 Compared to mitral valve repair, the aortic valve repair failure rate is higher (14% vs 6.6%) due to the greater technical difficulty of aortic valve repair.49

Cardioplegia Delivery

Moderate to severe aortic regurgitation necessitates an altered myocardial perfusion strategy during aortic cross clamping to keep the LV empty and avoid the increase in wall tension and oxygen demand during cardioplegic arrest. Milder degrees of aortic regurgitation have also been described on occasion to produce greater than expected degrees of incompetence during cardiopulmonary bypass, perhaps from an alteration of the three-dimensional architecture of the valve when the LV is decompressed. Cardioplegia is most often provided in this setting via selective antegrade delivery into each coronary ostia or retrograde through the coronary sinus.

Aortic valve disease will become more prevalent as our population ages. Intraoperative TEE has been demonstrated to be safe, effective, and instrumental in the management of patients undergoing aortic valve surgery. TEE confirms the preoperative diagnosis, evaluates the severity of aortic valve disease, determines the feasibility of aortic valve repair versus replacement, and evaluates the success of surgical correction. Two-dimensional imaging combined with pulsed-wave, continuous-wave, and color Doppler allow for quantitative evaluation of stenotic and regurgitant lesions, as well as identification of the etiology of valve dysfunction. The recent introduction of real-time three-dimensional TEE will undoubtedly enhance the ability of the echocardiographer to better define aortic valve pathology, communicate a more accurate description of the valve dysfunction to the surgeon, and provide for safer deployment of percutaneous valves (see Chapter 11).

The authors would like to thank Drs. Stephen R. Strelec and Saket Singh for their insight, review, and recommendations regarding this chapter.