Aortic stenosis is caused by congenital valve malformations or rheumatic lesions that lead to thickening and adhesion of the aortic valve leaflets, resulting in valvular stenosis. Long-standing cases may develop calcification or be complicated by infective endocarditis. Rheumatic heart disease often coexists with aortic regurgitation and mitral valve disease.
Pathophysiology
The normal aortic valve area is 3 cm2. Due to the strong contractile force and compensatory capacity of the left ventricle, mild stenosis typically does not produce significant hemodynamic changes. However, when the valve area decreases to below 1 cm2, left ventricular outflow becomes restricted, leading to an increase in left ventricular systolic pressure, prolonged left ventricular ejection time, and delayed closure of the aortic valve. Resting cardiac output may remain near-normal, but it cannot adequately increase during exertion. A systolic pressure gradient develops between the left ventricle and the aorta, with its magnitude reflecting the severity of the stenosis.
For moderate stenosis, the pressure gradient is usually 30–50 mmHg, while in severe cases it may reach 50–100 mmHg or higher. Progressive left ventricular wall hypertrophy eventually leads to left ventricular failure. Severe stenosis cases are often complicated by significant left ventricular hypertrophy, resulting in increased myocardial oxygen consumption. Additionally, diastolic aortic pressure may fall below normal levels, reducing coronary artery blood flow and causing symptoms of myocardial ischemia.
Clinical Manifestations
Mild stenosis cases are often asymptomatic. Patients with moderate to severe stenosis may experience fatigue, dizziness or syncope, angina pectoris, exertional dyspnea, orthopnea, and acute pulmonary edema. Complications such as infective endocarditis or sudden cardiac death may also occur.
Physical Examination
A systolic thrill may be palpable in the second intercostal space along the right sternal border. A coarse systolic ejection murmur can be heard in the aortic valve area and radiates to the neck. The second heart sound in the aortic valve area is delayed and diminished. Severe stenosis often presents with weak pulses, low blood pressure, and narrow pulse pressure.
Auxiliary Examinations
Electrocardiography (ECG)
Findings may show left axis deviation, left ventricular hypertrophy with strain, and T-wave inversion. Some cases may also present with left bundle branch block, atrioventricular block, or atrial fibrillation.
X-ray Examination
Cardiac silhouette changes may be absent in early-stage cases. As the condition progresses, left ventricular enlargement becomes evident, with elongation of the left cardiac border downwards and leftwards. Post-stenotic dilation of the ascending aorta may also be visible.
Echocardiography
Echocardiography is the most effective method for evaluating the severity of the disease. M-mode echocardiography shows reduced opening amplitude of the aortic valve leaflets, widened valve leaflet curves, and multiple lines visible during diastole. Two-dimensional or cross-sectional echocardiography demonstrates thickening, deformation, or calcification of the valve leaflets, along with reduced mobility and narrowed valve orifice.
Treatment
Patients presenting with angina, syncope, or heart failure often experience rapid disease progression after symptom onset, with a high incidence of sudden death within 2–3 years. Early surgical intervention is therefore recommended, involving aortic valve replacement with a prosthetic valve.
In recent years, transcatheter aortic valve replacement (TAVR), performed via peripheral arterial or transapical access, has been introduced into clinical practice. This technique offers advantages such as reduced trauma and faster recovery. However, it is associated with higher rates of perioperative complications such as paravalvular leakage and permanent pacemaker implantation. Whether the long-term outcomes of TAVR surpass those of conventional surgical aortic valve replacement (SAVR) remains to be determined through further longitudinal follow-up studies.