Aortic Stenosis
Praveen Mehrotra
Ira S. Cohen
INTRODUCTION
With the exception of coronary artery bypass grafting procedures, aortic valve replacement (AVR) for critical aortic stenosis (AS) is the most common indication for cardiac surgery in patients past the age of 65 years. Transcatheter aortic valve replacement (TAVR) by either transfemoral or a combined surgical catheter-based technique, assisted by echocardiography, has dramatically increased the number of patients who are candidates for valve replacement. The overwhelming majority of patients in this age group have atherosclerotic degenerative changes of a trileaflet valve as their pathophysiologic substrate. In contrast, most patients undergoing AVR for AS in the 35- to 55-year-old age groups have a bicuspid aortic valve (AV), which typically calcifies early and may be associated with dilation of the ascending aorta (AoA). Rheumatic AV stenosis occurs much less frequently than in the preantibiotic era, typically causes commissural fusion, and is almost invariably associated with mitral valve (MV) disease.
In general, critical AS is diagnosed preoperatively. The development of symptoms (as detected by history or during exercise testing) or left ventricular (LV) dysfunction (i.e., ejection fraction [EF] < 50%) due to AS is currently a class 1 indication for AVR (1). Symptoms of hemodynamically significant AS are congestive heart failure (often starting as exertional dyspnea), exertional syncope, and angina. Provided other potential causes of these symptoms have been excluded, their presence is of paramount clinical significance because failure to operate at the onset of symptoms is associated with a poor prognosis. This is so even if the estimated valve areas are less than “critical.” Calculated AV areas are estimates based on assumptions that apply hydraulic principles to a physiologic system and on gradient measurements that are dependent, to an important degree, on the cardiac output (CO) at the time of measurement.
The rate of progression of stenosis can be fairly rapid and tends to be linear for a given individual, but it is not predictable based on the initial echocardiographic findings (2,3,4). The issue of whether to replace a noncritically stenotic valve prophylactically during other cardiac surgery is also an increasingly important question. Current clinical guidelines support AVR at the time of coronary artery bypass surgery in patients with at least moderate AS, even if asymptomatic, in view of the generally progressive nature of this disorder (1). AVR may also be considered in asymptomatic patients with severe AS with a peak jet velocity >5 m/s and in some patients with severe AS despite low transvalvular gradients (1). The advent of TAVR, however, has modified the decision-making process in these situations as valve replacement can be performed (earlier or later) without the need for open heart surgery. Accordingly, the intraoperative echocardiographer must be adept with the techniques used to assess the severity of AS (Table 12.1).
PATHOPHYSIOLOGY
AS presents a slowly progressive increase in afterload on the ventricle developing over the course of years as the degree of stenosis progresses. The resulting increase in wall stress (force/unit area) induces a variable degree of a concentric hypertrophic response that tends to normalize wall stress.
TABLE 12.1 Grading Severity of Aortic Stenosis | |||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| |||||||||||||||||||||||||||||||||||
Ultimately, this compensatory mechanism fails and typical symptoms develop. The hypertrophied chamber becomes less compliant because of both the stiffness of hypertrophied muscle and concomitant collagen deposition. This results in diastolic dysfunction and increasing preload dependence of the ventricle. Atrial contraction (the “a” kick) can increase the LV end-diastolic pressure to levels as high as 30 to 40 mm Hg to stretch the hypertrophied ventricle at end-diastole before each contraction. Loss of atrial contraction by the development of atrial fibrillation can result in the development of acute pulmonary edema. The need for a relatively high preload (filling pressures) in these noncompliant ventricles is an important key to elective postoperative management.
AS can cause angina in the absence of significant epicardial coronary artery disease. The prevailing theory as to the mechanism of angina in AS has been that the tissue turgor of the hypertrophic wall compromises coronary flow reserve by restricting the dilatory capacity of penetrating coronary vessels. AV pressure gradients, LV mass, female sex, LV filling pressure (septal E/é), and myocardial fibrosis have univariate associations with reduced myocardial perfusion reserve. Of these, LV mass index and late gadolinium enhancement on magnetic resonance imaging (a marker of fibrosis) appear to be the most important (5). Cardiac catheterization is therefore required to exclude critical coronary artery disease (which coexists in approximately 50% of cases) in patients both with and without angina, as silent coronary disease is potentiated by the physical limitation on activity caused by the stenosis. Syncope is a consequence of the inability to increase CO in response to the peripheral vasodilation associated with exercise, to arrhythmia or to acute heart failure. Pulmonary congestion results from the increasingly high preload (left atrial pressure) required for adequate function in a noncompliant ventricle with diastolic dysfunction and the shortening of the diastolic filling period by exerciseinduced tachycardia.
ECHOCARDIOGRAPHIC EVALUATION OF THE AORTIC VALVE
The AV can be evaluated by M-mode, two-dimensional (2D), Doppler, and three-dimensional (3D) transesophageal echocardiography (TEE) to assess valve morphology and severity of disease. Two-dimensional TEE imaging of the AV is generally superior to transthoracic echocardiography (TTE) because of the improved resolution of the higher frequency TEE probe 
(Video 12.1). Three-dimensional imaging shares the limits inherent to all ultrasound techniques determined by the interrelation of sector (volume) size, frame rate, and depth on image resolution. The reduced temporal and spatial resolution of 3D imaging frequently results in dropout of the thin leaflets of a normal AV 
(Video 12.2). With the thickening and calcification of the leaflets seen with the development of valvular stenosis, 3D imaging is often better but may also be impaired by the associated acoustic shadowing 
(Video 12.3). Nevertheless, data suggest that 3D TEE evaluation of the AV can provide more accurate estimation of AV area by planimetry (6). Both 2D and 3D TEE imaging of the AV are best performed from the mid-esophageal (ME) short-axis (SAX) or longaxis (LAX) views. Updated guidelines for the assessment of AS by echocardiography including TEE have recently been published (7,8). The following discussion follows the recommended priority of methods for evaluation outlined therein.
(Video 12.1). Three-dimensional imaging shares the limits inherent to all ultrasound techniques determined by the interrelation of sector (volume) size, frame rate, and depth on image resolution. The reduced temporal and spatial resolution of 3D imaging frequently results in dropout of the thin leaflets of a normal AV (Video 12.2). With the thickening and calcification of the leaflets seen with the development of valvular stenosis, 3D imaging is often better but may also be impaired by the associated acoustic shadowing (Video 12.3). Nevertheless, data suggest that 3D TEE evaluation of the AV can provide more accurate estimation of AV area by planimetry (6). Both 2D and 3D TEE imaging of the AV are best performed from the mid-esophageal (ME) short-axis (SAX) or longaxis (LAX) views. Updated guidelines for the assessment of AS by echocardiography including TEE have recently been published (7,8). The following discussion follows the recommended priority of methods for evaluation outlined therein.Quantitative Doppler Assessment of Aortic Stenosis
The severity of AS is assessed quantitatively with Doppler echocardiography in two ways: measuring the gradient across the valve with the modified Bernoulli equation and estimating the AV area with the continuity equation. Both techniques require that the ultrasound beam be as parallel to the transvalvular blood flow as possible.
Transesophageal Echocardiographic Doppler Views for Assessing Aortic Stenosis
In AS, aligning the TEE transducer parallel to the left ventricular outflow tract (LVOT) and AV can be challenging. The deep transgastric (TG) and TG LAX views are commonly used depending on which one offers the optimal window for interrogation parallel to the stenotic jet. Advancing the probe from a TG SAX view with continued anteflexion may allow acquisition of the deep TG view from near the LV apex. Occasionally, clockwise or counterclockwise rotation of the probe and varying the angle of interrogation over a wide range may facilitate this. The TG LAX view is obtained with the probe at the mid-papillary level or slightly above and the imaging plane angle of interrogation increased from 120 to 140° where the LVOT, AV, and AoA come into view. Both techniques offer an excellent approach to AV flow dynamics; however, the patient’s
anatomy will dictate which view provides the best interrogation of transvalvular blood flow. For this reason, it is advised that both views be sought out and the highest velocities obtained are used in calculations of AS severity. In a small minority of individuals, the ME LAX view (at 120°) allows the best alignment to the transaortic flow.
anatomy will dictate which view provides the best interrogation of transvalvular blood flow. For this reason, it is advised that both views be sought out and the highest velocities obtained are used in calculations of AS severity. In a small minority of individuals, the ME LAX view (at 120°) allows the best alignment to the transaortic flow.
 FIGURE 12.1 Deep transgastric view with parallel continuous wave Doppler beam alignment in a patient with severe aortic stenosis. Aortic stenosis tracing is labeled with a maximal aortic valve velocity of 4.7 m/s and Bernoulli equation-derived peak and mean aortic valve gradient of 89 and 48 mm Hg, respectively. Aortic valve time-velocity integral (TVI) is 86 cm. |
Doppler Determination of the Aortic Valve Gradient: The Modified Bernoulli Equation
Once the appropriate view is obtained, the mean and peak transaortic gradients are obtained using continuous wave Doppler (CWD). The velocity profile should be a dense signal with a smooth outer edge and clear maximal velocity. The peak gradient is obtained from measuring the maximal velocity of the AV spectral Doppler profile, while the mean gradient is obtained by tracing the velocity profile and using the analysis program of the ultrasound machine (Fig. 12.1). Care should be taken to avoid tracing or measuring faint linear signals at the peak of the velocity profile. The modified Bernoulli equation is used to calculate transaortic valve pressure gradients from aortic velocities (Table 12.2). The modified Bernoulli equation states that the maximal pressure gradient equals four times the square of the peak jet velocity and allows calculation of the peak instantaneous gradient across any orifice. Thus, if the peak blood flow velocity across the AV is 4 m/s, the calculated peak gradient = 4 × 42 = 64 mm Hg. The mean gradient is calculated by averaging the instantaneous gradients over time. The mean velocity cannot be used to estimate the mean gradient in the Bernoulli equation. A less accurate alternative mean gradient can be calculated from the peak velocity as 2.4 (Vmax)2.
The mean gradient, in particular, correlates well with invasively determined gradients and is most often used in evaluating the severity of AS.
The mean gradient, in particular, correlates well with invasively determined gradients and is most often used in evaluating the severity of AS.
TABLE 12.2 Doppler Equations for Aortic Transvalvular Gradients and Flow | |||||
|---|---|---|---|---|---|
|
TABLE 12.3 Calculation of Aortic Valve Area With the Continuity Equation | ||||
|---|---|---|---|---|
|
Hemodynamically significant AS is generally associated with a mean gradient of 40 mm Hg or more or a maximal velocity of 4 m/s or more. The exception is in patients with a low EF or stroke volume who may not be able to generate a high gradient. These patients are described as having low-flow, low-gradient severe AS (see below) which is an increasingly recognized entity. In these patients, mean gradients as low as 20 to 30 mm Hg may be associated with critical stenosis, and the valve area by continuity equation and planimetry, as well as a dobutamine challenge in some patients should be considered to further evaluate the significance of AS. In these situations, recently published AS guidelines recommend estimation of transvalvular flow by calculation of Doppler stroke volume index (SVI) (Table 12.3) (7). In AS, low transvalvular flow is defined as <35 mL/m2. Systemic hypertension during echocardiographic assessment also impacts both on the apparent gradient and the left ventricular ejection fraction (LVEF) and must also be considered in evaluating the validity of the assessment of the gradient. (See below.)
The peak gradient can be influenced by the flow velocity on the ventricular side of the valve plane. Remember that the simplified Bernoulli equation ignores the impact of the LVOT blood flow velocity. However, the Bernoulli equation must factor in the LVOT blood flow velocity when it exceeds 1.5 m/s, as commonly occurs in associated aortic insufficiency and other high-output states, to avoid overestimation of the pressure gradient (see Table 12.2). For example, if the outflow tract velocity is 1.7 m/s and the peak transvalvular velocity is 4 m/s, the actual gradient is 4 × (42 – 1.72) = 4 × (16 – 2.89) = 52.4 mm Hg, instead of the 64 mm Hg predicted by the simplified Bernoulli equation.
Discrepancies often occur between catheterization and echocardiographic pressure gradients in AS. The peak echocardiographic gradient measures the peak instantaneous gradient between the LV and aorta. This is generally higher than the invasively determined “peak-to-peak gradient” (between the peak LV pressure and the generally later peak aortic pressure) routinely entered on cardiac catheterization reports (Fig. 12.2). In addition, the phenomenon of pressure recovery (PR), the recovery of pressure energy from the kinetic energy of acceleration through the narrowed orifice that occurs distal to the stenotic valve, can cause an elevation in the estimated transvalvular gradient by Doppler as compared to measurements by catheterization. In general, this phenomenon only becomes a factor in patients with small aortas (sinotubular junction ≤3 cm). (See below.)
Doppler Estimation of the Aortic Valve Area: The Continuity Equation
The continuity equation is based on the law of conservation of mass and states that the volume of blood that enters the stenotic aortic orifice through the LVOT is equal to the volume of blood that exits it (Fig. 12.3). If we can calculate the volume of flow entering a stenotic AV through the LVOT and measure the velocity at which it exits the stenotic valve, then the equation can be rearranged to solve for the area of the stenotic valve (see Table 12.3). The AV area derived from the continuity equation is the effective area, the area of the orifice at the vena contracta which is immediately distal to the anatomic area, which is derived from planimetry of the valve. The effective area has been clinically validated even though it is slightly smaller than the anatomic area as the primary predictor of clinical outcome (7,9). The area of the normal AV is between 3 cm2 and 4 cm2 (Fig. 12.4). Guidelines viewing the disease as a continuum based on hemodynamic and
natural history data define severe stenosis as an AV area <1 cm2, a mean gradient >40 mm Hg, or peak jet velocity >4 m/s (see Table 12.1) (7).
natural history data define severe stenosis as an AV area <1 cm2, a mean gradient >40 mm Hg, or peak jet velocity >4 m/s (see Table 12.1) (7).
 FIGURE 12.2 Example of left ventricular (LV) and aortic (Ao) pressures measured with fluid-filled catheters in a patient with severe aortic stenosis. The maximal instantaneous gradient is greater than the peak-to-peak gradient. The shaded area indicates the mean gradient. (From Otto CM. Textbook of Clinical Echocardiography. 2nd ed. Philadelphia, PA: WB Saunders; 2000:238, with permission.) |
When determining AV area by continuity equation, one first calculates the cross-sectional area of the LVOT. In the ME AV LAX view, the LVOT or annular diameter is obtained by measuring the inner dimension (endocardium to endocardium) of the LVOT generally at the insertion point of the AV leaflets in midsystole with the electronic calipers (Fig. 12.5, top). However, measurement of the outflow tract should ideally be performed where the optimal outflow tract velocity profile is obtained by pulsed-wave Doppler (PWD) in
the apical (by transthoracic echo) or TG (by transesophageal echo) view (see below). This is generally either at, or within a centimeter of, the aortic leaflet insertions into the valve annulus. The diameter of the LVOT is generally 2.0 ± 0.2 cm and varies somewhat in proportion to body size. Inaccuracies in measurement of the outflow tract can account for much of the error in this technique because the radius is squared in the continuity equation. The most common discrepancies occur during the imaging of elderly women, who often have a smaller outflow tract (and body surface area) than average, and large men, who often have a larger outflow tract (and body surface area). Another source of error occurs in the presence of upper septal hypertrophy which results in tapering of the proximal LVOT; in these situations, the annular dimension can be utilized as it is less affected by this phenomenon (10).
the apical (by transthoracic echo) or TG (by transesophageal echo) view (see below). This is generally either at, or within a centimeter of, the aortic leaflet insertions into the valve annulus. The diameter of the LVOT is generally 2.0 ± 0.2 cm and varies somewhat in proportion to body size. Inaccuracies in measurement of the outflow tract can account for much of the error in this technique because the radius is squared in the continuity equation. The most common discrepancies occur during the imaging of elderly women, who often have a smaller outflow tract (and body surface area) than average, and large men, who often have a larger outflow tract (and body surface area). Another source of error occurs in the presence of upper septal hypertrophy which results in tapering of the proximal LVOT; in these situations, the annular dimension can be utilized as it is less affected by this phenomenon (10).
 FIGURE 12.3 Demonstrates the concept of parallel beam alignment and the concept of “what goes in has to come out.” Hence LVOTTVI × LVOTCSA = ASTVI × aortic valve area (AVA). |
 FIGURE 12.4 Mid-esophageal short-axis view of a normal aortic valve with a planimetered area of 3.0 cm2 obtained from a 3D zoom acquisition. Planimetry was performed with multiplanar reconstruction software (left). Volume rendering of the same normal aortic valve (right). |
Lastly, in the continuity equation, we assume that the LVOT exhibits circular geometry with the cross-sectional area calculated utilizing the formula πr2 (or π[D/2]2). However, recent observations of LVOT geometry by computed tomography (CT) angiography and 3D echocardiography (11,12,13), have shown that it is often not circular but elliptical (Fig. 12.5, bottom) and that its true size is best determined by direct planimetry. While the assumption of a circular LVOT by 2D imaging can result in up to a 20% underestimation of the true LVOT area compared to planimetry (13), routine planimetry of the LVOT area with 3D imaging for the continuity equation-derived AVA is not recommended, as doing so results in potentially much larger AVA values which can potentially lead to erroneous assessment of disease severity (9). Three-dimensional planimetry of the outflow tract, on the other hand, is very important for appropriate transcatheter valve sizing, while the continuity equation utilizing the circular assumption has held up well for clinical assessment of severity and cutoffs based on this technique have shown to be strong predictors of outcomes (7,14). Nevertheless, 3D multiplanar images of the LVOT are still useful to ensure that the maximal anteroposterior LVOT and annular diameter are measured for the continuity equation (see Fig. 12.5, bottom).
Secondly, the LVOT time-velocity integral (TVI) is then determined with PWD. The sample volume is placed just proximal to the AV cusps and then gradually moved away from the AV in the LVOT until a smooth velocity profile with a narrow range of velocities at each time point is obtained (Fig. 12.6). PWD is essential for this flow measurement because the profile should be obtained at the level of the outflow tract where the LVOT dimension was measured. If the profile is obtained just below the aortic leaflet insertion point, then the LVOT dimension should be remeasured at the same place. The internal calculation package available on all echocardiographic machines calculates the TVI after the LVOT velocity profile is traced. A second alternative method, which is less well validated, uses CWD interrogation through the AV. If the alignment is correct, a more intense lower velocity inner envelope representing the lower-velocity LVOT flow is imaged within the higher velocity aortic jet envelope. This inner profile
can be traced as previously described to calculate the LVOT TVI. However, the inner envelope peak can be erroneously high because the subaortic jet accelerates into the stenotic orifice to form a proximal isovelocity surface area as it narrows to fit into the orifice which can result in an overestimation of the AV area.
can be traced as previously described to calculate the LVOT TVI. However, the inner envelope peak can be erroneously high because the subaortic jet accelerates into the stenotic orifice to form a proximal isovelocity surface area as it narrows to fit into the orifice which can result in an overestimation of the AV area.
 FIGURE 12.5 Mid-esophageal short-axis view of a stenotic trileaflet aortic valve. Biplane imaging of the aortic valve is utilized with biplane cursor positioned through commissure (between left and noncoronary sinus) and right sinus (top, left). An orthogonal view is created which generally produces the largest anteroposterior left ventricular outflow tract (LVOT) and annular measurement as the LVOT is being bisected along its minor dimension. LVOT imaging can be performed with three-dimensional multiplanar imaging (bottom). The LVOT is elliptical with small minor (anteroposterior) dimension (shown in red) and a larger major (medial-lateral) dimension (shown in green).
Related posts:
Full access? Get Clinical Tree
Get Clinical Tree app for offline access
|
