Aortic Valve Stenosis
Abnormal narrowing of the aortic valve orifice.
The prevalence of aortic valve stenosis, the most clinically significant valvular lesion in the elderly, increases with age. The severity of the stenosis is often underestimated because its progression is so gradual and because symptoms may be attributed to normal aging.
In the elderly, common causes of aortic valve stenosis are calcification of a congenital bicuspid aortic valve and degenerative aortic stenosis. Rheumatic heart disease is the cause in 20%; mitral valve disease often coexists. Regardless of the cause, calcification occurs in patients with aortic valve stenosis by age 65. A congenital bicuspid valve, if present, tends to become calcified in patients aged 45 to 60, and typically, the aortic aspect of the tricuspid semilunar aortic valve is calcified in patients > 75.
Pathophysiology
In aortic valve stenosis, the systolic gradient across the aortic valve during systole produces turbulence, which results in a systolic ejection murmur. The increased left ventricular systolic pressure leads to concentric left ventricular hypertrophy, and these two changes lead to an increase in myocardial oxygen demand. As the aortic valve narrows to < 0.8 cm2, aortic pressure takes longer to reach its peak, and systolic pressure may decrease. During systole, tissue pressure on the coronary microvasculature increases coronary vascular resistance and decreases blood flow into the midmyocardium and epicardium. These factors decrease myocardial blood flow, especially to the subendocardium, and result in myocardial ischemia, subendocardial fibrosis, angina pectoris, and ventricular arrhythmias. Significant coronary artery disease (CAD) develops in almost 50% of elderly patients.
During exercise, systemic vascular resistance decreases normally. If stroke volume cannot increase, systolic blood pressure can decrease. This drop in blood pressure plus transient and rapid ventricular arrhythmias can result in exertional syncope.
Symptoms and Signs
Most patients with aortic valve stenosis are asymptomatic. Those with symptoms have an extremely poor prognosis without valve replacement. Chest discomfort, which is usually characteristic of angina pectoris, is an early symptom. During exertion, presyncope (transient alteration of consciousness) or syncope occurs in about one third of symptomatic patients. Exertional dyspnea may progress to pulmonary edema, or pulmonary edema may occur suddenly without previous symptoms. If aortic valve stenosis is severe, the left ventricle becomes stiff, and the left atrium may become dilated, resulting in atrial fibrillation. Absence of an atrial contraction markedly decreases the late filling of the noncompliant left ventricle, and stroke volume may decrease, resulting in a marked worsening of symptoms and in heart failure. Heart failure develops in about one half of elderly patients with severe aortic valve stenosis. Because of vascular stiffening, systolic hypertension may coexist with severe aortic stenosis in elderly patients. About one fourth of deaths due to aortic stenosis occur suddenly.
Physical findings may include a narrow pulse pressure, especially when stroke volume decreases, and a slow-rising, small-volume carotid pulse. However, the poorly compliant arterial wall may mask these abnormalities, so that the carotid pulse appears relatively normal. The cardiac apex impulse is forceful and sustained, but this finding may be masked by kyphosis (in which the anteroposterior diameter of the chest is increased). The first heart sound is soft. The aortic component of the second heart sound is also soft; it may be inaudible when stenosis is severe and the valve is heavily calcified. Reverse splitting of the second heart sound may occur in patients with left ventricular failure. A fourth heart sound is common but disappears in the one fourth of elderly patients who develop atrial fibrillation. Ejection sounds are rare because the valve cusps are immobile.
A harsh, loud crescendo-decrescendo systolic murmur, often associated with a thrill, is maximal at the upper right sternal border. The murmur peaks in mid to late systole and often radiates throughout the precordium and into the neck. This late peaking is often the best clue to severe aortic stenosis. The murmur's high-frequency components are often transmitted to the lower left sternal border and the cardiac apex during most of systole and may resemble the murmur of mitral regurgitation. In patients with heavily calcified aortic valves, the murmur sometimes has a musical high-pitched quality (termed seagull murmur). The murmur's intensity does not correlate with the severity of the obstruction. Basal diastolic murmurs of aortic regurgitation are heard in more than one half of patients with aortic valve stenosis.
The ECG shows evidence of left ventricular hypertrophy, but hyperinflated lungs may mask increased left ventricular voltage. Even when left ventricular hypertrophy is severe, heart size often remains normal until heart failure develops; the heart then enlarges. Poststenotic aortic dilation is common.
Diagnosis
Dense calcification of the aortic valve, best seen on a lateral chest x-ray, suggests hemodynamically significant aortic stenosis. If calcification is not seen on the chest x-ray or echocardiogram, the diagnosis of critical (very severe) aortic valve stenosis is virtually excluded.
Two-dimensional echocardiography is used to assess cardiac chamber size, wall thickness, wall motion, valve leaflet motion, valve orifice size, and valvular calcification. Doppler echocardiography is used to measure intracardiac blood velocity, from which the severity of valvular regurgitation or obstruction can be calculated. Serial measurements can determine progression of the disorder. If the anteroposterior diameter of the chest is increased, the echocardiographic views of the heart may be limited, and the technician may have to spend a long time getting the maximum jet velocity to reflect the maximum aortic systolic gradient. For this reason, the severity of aortic stenosis can be underestimated in the elderly.
Frequently, the severity of aortic stenosis can be determined on the basis of Doppler-echocardiographic findings. However, if surgery is being considered for an elderly patient, catheterization is usually performed to determine whether CAD is present and, if present, how severe it is. Stress testing to the level of the patient's ordinary activity with ECG monitoring may be used to check for ischemic changes and arrhythmias, especially in patients with moderate aortic stenosis. However, if severe aortic stenosis is suspected, exercise testing is contraindicated because exercise-related syncope and death are risks.
Two-dimensional echocardiography and Doppler studies help differentiate aortic valve stenosis from benign aortic sclerosis, which occurs in one third to one half of elderly persons. Benign aortic sclerosis typically produces no symptoms and is not hemodynamically significant; the basal systolic murmur is short and peaks early, and the carotid pulse is normal.
Because the chest discomfort of aortic valve stenosis is due to myocardial ischemia, aortic valve stenosis cannot be distinguished from angina pectoris due to CAD on the basis of symptoms. Syncope due to aortic valve stenosis must be distinguished from that due to atrioventricular block or tachyarrhythmias, both common among elderly patients. Ventricular tachyarrhythmias may be due to CAD or to ischemia produced by severe aortic valve stenosis. Severe aortic valve stenosis should be suspected and ruled out in all elderly patients with heart failure and a systolic ejection murmur, especially if they have unexplained left ventricular hypertrophy.
Prognosis and Treatment
Elderly patients with noncritical aortic valve stenosis require serial surveillance because stenosis often progresses at an unpredictable pace.
Asymptomatic elderly patients with severe aortic stenosis can usually be managed medically; surgery is justified only if the risk of perioperative mortality is less than that of sudden death. However, a detailed history is very important for verifying that the patient is active and asymptomatic before concluding that the patient can be safely managed medically.
Aortic valve replacement is indicated for symptomatic patients with hemodynamically significant aortic valve stenosis, because their expected life span is reduced. The 3-year mortality rate for untreated symptomatic patients is about 50%; life span is shorter for such patients if they have heart failure and longer if they have angina pectoris. Elderly patients with severe aortic stenosis may have a worse prognosis. In one series, the mortality rate was 50% at 1 year and 65% at 2 years.
Percutaneous balloon valvuloplasty is used only for symptomatic palliation of severely ill patients who are not candidates for surgery, because valvuloplasty has high rates of restenosis and mortality after hospital discharge. Ultrasonic debridement of calcium is no longer performed.
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