Blase A. Carabello, MD, FACC

1. What is the most common cause of aortic stenosis (AS) in developed countries today, and what is the current thinking about its pathogenesis?

    Although rheumatic fever was once the most common cause of AS, today calcific disease of either bicuspid or tricuspid AS is the leading cause. Once considered a degenerative disease, it is now clear that calcific AS is an inflammatory process with many similarities to atherosclerosis. A normal aortic valve, and AS as a result of congenital bicuspid aortic valve, rheumatic AS, and calcific AS, are shown in Figure 30-1.

2. What is the pathophysiology of AS, and what effect does it have on the left ventricle (LV)?

    AS exerts a pressure overload on the LV. Normally, pressure in the LV and aorta are similar during systole, as the normal aortic valve permits free flow of blood from LV to aorta. However, in AS, the stenotic valve forces the LV to generate higher pressure to drive blood through the stenosis, causing a pressure difference (gradient) from LV to aorta. The LV compensates for this pressure overload by increasing its mass (left ventricular hypertrophy [LVH]). The ways in which the transvalvular gradient are measured and quantified are shown in Figure 30-2.

3. How is left ventricular hypertrophy compensatory?

    The Law of Laplace states that systolic wall stress (σ) is equal to:

    As the pressure term in the numerator increases, it is offset by an increase in thickness in the denominator, thus normalizing afterload. Because afterload is a key determinant of ejection, LVH helps to maintain ejection fraction and cardiac output.

4. Are there downsides to LVH?

    Yes. Although LVH is initially compensatory, as it progresses it takes on pathologic characteristics, leading to increased morbidity and mortality.

5. What are the classic symptoms of AS, and why are they important?

    The classic symptoms of AS are angina and syncope and those of heart failure (dyspnea, orthopnea, paroxysmal nocturnal dyspnea, edema, etc.). Their importance is graphically displayed in Figure 30-3. In the absence of symptoms, survival is nearly the same as that of an unaffected population. However, at the onset of symptoms there is a dramatic demarcation such that mortality increases to 2% per month, so that three-quarters of all AS patients are dead within 3 years of symptom onset unless proper therapy is instituted. It should be noted that when the data for this figure were compiled, the etiology of AS was usually rheumatic or congenital heart disease and the average age of the patients was 48 years. Since then the etiology of AS has changed (as noted above) and with it the age at symptom onset has increased by about 15 years.

6. What are findings of AS on physical examination?

    AS is usually recognized by the presence of a harsh systolic ejection murmur that radiates to the neck. In mild disease, the murmur peaks in intensity early in systole, peaking progressively later as severity of disease increases. The carotid upstrokes become delayed in timing and reduced in volume because the stenotic valve steals energy from the flow of blood as it passes the valve. The apical beat is forceful. Palpation of this strong apical beat with one examining hand while the other hand palpates the weakened delayed carotid upstroke is dynamic proof of the obstruction that exists between the LV and the systemic circulation. Because the severely stenotic aortic valve barely opens, there is little valve movement upon closing. Thus, the A2 component of S2 is lost, rendering a soft single second sound. An S4 is usually present in patients in sinus rhythm, reflecting impaired filling of the thickened, noncompliant LV.

7. How is echocardiography used to assess the patient with AS?

    Currently, echocardiography is the central tool in diagnosing the presence and severity of AS. In severe AS, the aortic valve is calcified and has limited mobility. The amount of LVH and the presence or absence of LV dysfunction can be established. Because

as the valve area decreases, velocity of flow must increase for flow to remain constant (Fig. 30-4). This increase in blood velocity at the valve orifice is detected by Doppler ultrasound. The severity of AS is assessed using the factors given in Table 30-1. In general, if a patient has the symptoms of AS and assessment indicates severe disease, then the symptoms are attributed to AS. However, it must be emphasized that the benchmarks listed here are only guidelines to severity, and some patients exhibit exceptions to them.

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