| disease | Aortic Valve Stenosis |
| alias | Aortic Stenosis |
The normal mitral valve orifice area exceeds 3.0 cm2. When the orifice area decreases to 1.5 cm2, it is classified as grade I stenosis; at 1.0 cm2, it is grade II stenosis; and when it is less than 1.0 cm2, it is grade III stenosis.
bubble_chart Etiology
Aortic stenosis can be caused by sequelae of wind-dampness heat, congenital stenosis, or senile calcification of the aortic valve. Among patients with aortic stenosis, 80% are male. Pure wind-dampness aortic stenosis is rare and is often combined with aortic regurgitation and mitral valve lesions. The pathological changes include adhesion and fibrosis at the valve commissures, with deformation of the valve membrane exacerbating the damage, leading to calcium deposition and further stenosis.
Congenital aortic stenosis can be unicuspid, bicuspid, or tricuspid. Unicuspid stenosis is present at birth, with progressive fibrosis and calcification of the valve orifice, causing severe left ventricular outflow tract obstruction. Most affected children die within one year. Fifty percent of congenital aortic stenosis cases are bicuspid, and 30% are tricuspid. These two types of valve malformations may not show significant stenosis in childhood, but the abnormal valve structure undergoes degenerative changes due to turbulent flow, leading to leaflet thickening, calcification, stiffness, and eventual stenosis, which may also be accompanied by regurgitation. The aortic root, impacted by turbulent flow, may exhibit post-stenotic dilation (see the section on "Congenital Cardiovascular Diseases" under "Aortic Orifice Stenosis").
Senile calcification of the aortic valve is a degenerative change, accounting for 18% of elderly patients. The valve membrane undergoes degeneration, fibrosis, and calcification, with fusion of the leaflets. The stenosis is relatively mild, and some patients may also have regurgitation.
bubble_chart PathogenesisThe main pathophysiological changes after mitral stenosis are the increased resistance in the left ventricle during systole, which enhances left ventricular contractility to raise the transvalvular pressure gradient and maintain normal cardiac output at rest. This gradually leads to left ventricular hypertrophy, resulting in decreased diastolic compliance and elevated end-diastolic pressure. Although resting cardiac output remains normal, the increase in cardiac output during exercise becomes insufficient. When the valve orifice becomes severely narrowed, the transvalvular pressure gradient decreases, while left atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and right ventricular pressure may all rise, leading to reduced cardiac output. The decrease in cardiac output can cause myocardial hypoxia, hypotension, and arrhythmias. Insufficient cerebral blood supply may result in dizziness, syncope, and other manifestations of cerebral hypoxia. Left ventricular hypertrophy and increased contractility significantly elevate myocardial oxygen consumption, further exacerbating myocardial ischemia.
bubble_chart Clinical Manifestations
(1) Symptoms Due to the significant compensatory capacity of the left ventricle, patients may remain asymptomatic for a considerable period even with noticeable aortic valve stenosis, until the valve orifice area decreases to less than 1 cm2, when clinical symptoms begin to manifest.
1. Exertional Dyspnea This results from reduced left ventricular compliance and left ventricular enlargement, leading to elevated end-diastolic pressure in the left ventricle and left atrial pressure, which in turn increases pulmonary capillary wedge pressure and pulmonary hypertension. As the condition progresses, dyspnea may occur during daily activities, along with orthopnea. Acute pulmonary edema can be triggered by factors such as exertion, emotional stress, or respiratory infections.
3. Exertional Syncope Mild cases may present as blackout, which can be the initial symptom. Episodes often occur during or immediately after physical activity. Possible mechanisms include: failure of cardiac output to increase adequately during exercise due to reduced peripheral vascular resistance; decreased venous return, left ventricular filling, and cardiac output after cessation of exercise; exacerbation of myocardial ischemia during exercise, leading to sudden weakening of myocardial contractility and reduced cardiac output; occurrence of various arrhythmias during exercise, causing sudden decreases in cardiac output. These sudden reductions in cardiac output result in significant cerebral hypoperfusion, leading to syncope.
5. Thromboembolism More common in elderly patients with calcific aortic valve stenosis. Embolism can occur in cerebral vessels, retinal arteries, coronary arteries, and renal arteries.
6. Other Symptoms Advanced aortic valve stenosis may present with manifestations of reduced cardiac output, such as marked fatigue, weakness, and peripheral cyanosis. Signs of left heart failure may also appear, including orthopnea, paroxysmal nocturnal dyspnea, and pulmonary edema. Severe pulmonary hypertension may lead to right heart failure, manifesting as systemic venous hypertension, hepatomegaly, atrial fibrillation, tricuspid regurgitation, etc.
(2) Sign
1. Cardiac auscultation: A rough, loud ejection systolic murmur can be heard at the second right intercostal space near the sternum, presenting as a crescendo-decrescendo "water calptrop base peel" type. It appears after the first heart sound, reaches its peak intensity during the intermediate stage [second stage] of systole, and gradually diminishes before the closure of the aortic valve (second heart sound). It is often accompanied by a systolic thrill. The murmur may intensify after inhaling amyl nitrite. The murmur radiates to the carotid artery and subclavian artery, sometimes extending to the lower sternum or the apex of the heart. Generally, the longer and louder the murmur, and the later its peak occurs during systole, the more severe the aortic valve stenosis. However, in cases complicated by heart failure, the blood flow velocity across the valve slows down, making the murmur softer and shorter. An early systolic ejection sound may be heard, particularly common in congenital non-calcified aortic valve stenosis, but this sound disappears when the valve becomes calcified and rigid. When valve mobility is restricted or calcification is significant, the aortic component of the second heart sound weakens or disappears, and paradoxical splitting of the second heart sound may also occur. A fourth heart sound is often audible at the apex, indicating left ventricular hypertrophy and elevated end-diastolic pressure. A third heart sound (diastolic gallop rhythm) may be heard when left ventricular dilation and failure are present.
2. Other signs: The pulse is flat and weak. In cases of severe stenosis, due to reduced cardiac output, systolic blood pressure decreases, and pulse pressure narrows. Elderly patients often have concomitant atherosclerosis, so the decrease in systolic blood pressure is not obvious. The cardiac dullness border may be normal, but it expands to the left in cases of heart failure. A systolic heaving impulse can be palpated in the apical region, and a double impulse may be observed in the left lateral decubitus position—the first being atrial contraction to increase left ventricular filling, and the second being ventricular contraction, which is sustained and forceful. At the base of the heart, the supraclavicular fossa, and the neck, a systolic tremor can be palpated.
bubble_chart Auxiliary Examination
(1) X-ray Examination The left heart border is rounded, and the cardiac silhouette is not enlarged. Common findings include post-stenotic dilation of the aorta and aortic calcification. In adults, the absence of aortic valve calcification generally indicates no severe aortic stenosis. In heart failure, the left ventricle is significantly enlarged, and signs such as left atrial enlargement, prominence of the pulmonary artery trunk, widening of pulmonary veins, and pulmonary congestion may also be observed.
(2) Electrocardiogram (ECG) Examination In grade I aortic stenosis, the ECG may be normal. In severe cases, ECG shows left ventricular hypertrophy and strain. Worsening ST-segment depression and T-wave inversion suggest progressive ventricular hypertrophy. Left atrial enlargement is often evident. Severe aortic valve calcification may lead to left anterior fascicular block and varying degrees of atrioventricular or bundle branch block.
(3) Echocardiography M-mode echocardiography reveals thickening of the aortic valve, reduced motion amplitude, and an opening amplitude of less than 18 mm. Enhanced echo reflections suggest valve calcification. The aortic root is dilated, and the left ventricular posterior wall and interventricular septum show symmetric hypertrophy. Two-dimensional echocardiography demonstrates concentric doming of the aortic valve during systole and can identify congenital valve malformations. Doppler ultrasound shows slow and diminishing blood flow across the aortic valve and can calculate the maximum transvalvular pressure gradient.
(4) Left Heart Catheterization This procedure directly measures pressures in the left atrium, left ventricle, and aorta. Left ventricular systolic pressure increases, while aortic systolic pressure decreases. As aortic stenosis worsens, this pressure gradient widens. The left atrial pressure curve shows a tall a wave during atrial contraction. It should be considered in the following cases: young patients with congenital aortic stenosis who are asymptomatic but require assessment of left ventricular outflow obstruction; suspected left ventricular outflow obstruction unrelated to valvular causes; differentiation between aortic stenosis and coexisting coronary artery disease (requiring concomitant coronary angiography); and preoperative evaluation for multivalvular disease.
bubble_chart Treatment Measures
(1) Medical Treatment Appropriately avoid excessive physical labor and strenuous exercise, prevent infective endocarditis, and regularly follow up with echocardiographic reexamination. Rehmannia-based drugs can be used for patients with heart failure; when using diuretics, attention should be paid to preventing volume depletion. Nitrate esters can relieve symptoms of angina.
(2) Surgical Treatment The key to treatment is relieving aortic valve stenosis and reducing the transvalvular pressure gradient. Commonly used surgical methods include: ① Percutaneous balloon aortic valvuloplasty. This can immediately reduce the transvalvular pressure gradient, increase cardiac output, and improve symptoms. Indications include: congenital aortic stenosis in children and adolescents; patients who cannot tolerate surgery; life-threatening grade III stenosis; and severe stenosis with significant left ventricular dysfunction as a preoperative bridge. ② Open aortic valve commissurotomy. This effectively improves hemodynamics, with a surgical mortality rate of less than 2%. However, secondary valve calcification and restenosis may occur after 10–20 years, requiring reoperation. It is suitable for children and adolescents with congenital aortic stenosis without calcification who have developed symptoms; or those without symptoms but with significant left ventricular outflow tract obstruction; normal cardiac output but a peak systolic pressure gradient exceeding 6.7 kPa (50 mmHg); or a valve area less than 1.0 cm2. ③ Prosthetic valve replacement. Indications include: grade III aortic stenosis; calcific aortic stenosis; and aortic stenosis combined with regurgitation. Performing the surgery before clinical symptoms appear yields better long-term outcomes and lower surgical mortality. Even if clinical symptoms such as angina, syncope, or left ventricular decompensation occur, prosthetic valve replacement should be performed as early as possible. Although the surgical risk is relatively high, symptom improvement and long-term outcomes are superior to non-surgical treatment. For significant aortic stenosis combined with coronary artery disease, simultaneous prosthetic valve replacement and coronary artery bypass grafting are recommended.
(1) Congestive heart failure 50-70% of patients die from congestive heart failure.
(2) Embolism Most commonly seen in calcific aortic valve stenosis. Cerebral embolism is the most frequent, but it can also occur in the retina, limbs, intestines, kidneys, spleen, and other organs.
(3) Subacute infective endocarditis Can occur in bicuspid aortic valve stenosis.
The detection of an ejection systolic murmur in the aortic valve area at the base of the heart can diagnose aortic valve stenosis, and echocardiography can confirm the diagnosis. Clinically, aortic valve stenosis should be differentiated from the following conditions with systolic murmurs in the aortic valve area:
(1) Hypertrophic obstructive cardiomyopathy (HOCM), also known as idiopathic hypertrophic subaortic stenosis (IHSS). A systolic murmur can be heard at the fourth intercostal space along the left sternal border, with rare systolic clicks and normal aortic second heart sound (A2). Echocardiography reveals asymmetric hypertrophy of the left ventricular wall, significant thickening of the interventricular septum (with a ratio of septum to posterior wall ≥ 1.3), anterior motion of the septum during systole, narrowing of the left ventricular outflow tract, and possible mitral regurgitation due to anterior displacement of the mitral valve leaflet.
(2) Aortic dilation, caused by conditions such as hypertension or syphilis. A short systolic murmur may be heard at the second intercostal space along the right sternal border, with a normal or accentuated A2 and no splitting of the second heart sound. Echocardiography can confirm the diagnosis.
(3) Pulmonary valve stenosis. A rough, loud systolic murmur can be heard at the second intercostal space along the left sternal border, often accompanied by a systolic click. The pulmonary second heart sound (P2) is weakened and split, while A2 remains normal. Right ventricular hypertrophy and dilation are present, with post-stenotic dilation of the pulmonary artery.
(4) Tricuspid regurgitation. A high-pitched holosystolic murmur is heard at the lower left sternal border, which intensifies during inspiration due to increased venous return and weakens during expiration. Jugular venous distension and hepatomegaly may be present, along with significant enlargement of the right atrium and ventricle. Echocardiography can confirm the diagnosis.
(5) Mitral regurgitation. A holosystolic blowing murmur is heard at the apex, radiating to the left axilla. The murmur diminishes after inhalation of amyl nitrite. The first heart sound (S1) is weakened, A2 is normal, and the aortic valve shows no calcification.
