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Aortic stenosis: overview
Last reviewed: 12.07.2025
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Aortic stenosis is a narrowing of the aortic valve that limits blood flow from the left ventricle into the ascending aorta during systole. Causes of aortic stenosis include congenital bicuspid aortic valve, idiopathic degenerative sclerosis with calcification, and rheumatic fever.
Progressive aortic stenosis without treatment eventually leads to the classic triad of syncope, angina, and exertional dyspnea; heart failure and arrhythmias may occur. Characteristic features include a low-amplitude, delayed-peaking carotid pulse and a crescendo-decrescendo ejection murmur. Diagnosis is by physical examination and echocardiography. Asymptomatic aortic stenosis often requires no treatment. In children, balloon valvotomy is used for progressively severe aortic stenosis or for clinical symptoms; valve replacement is indicated in adults.
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The prevalence of aortic stenosis, according to different authors, fluctuates from 3-4 to 7%. With age, the frequency of this defect increases, amounting to 15-20% of people over 80 years old, and with an increase in the life expectancy of the population, the incidence of this defect in the population will increase. The predominant sex is male (2.4: 1), but in the older age subgroup, women predominate. Aortic stenosis is divided by origin into congenital and acquired, by the extent of the lesion - into isolated and combined, by localization - into valvular, supravalvular, infravalvular or caused by hypertrophic cardiomyopathy.
Causes of aortic stenosis
Aortic sclerosis, thickening of the valve structures with fibrosis and calcification (initially without stenosis) are the most common causes of aortic stenosis in the elderly; with age, aortic sclerosis progresses to stenosis in at least 15% of patients. Aortic sclerosis is also the most common cause of aortic stenosis leading to the need for surgical treatment. Aortic sclerosis resembles atherosclerosis, with lipoprotein deposition, active inflammation and calcification of the valves; risk factors are the same.
The most common cause of aortic stenosis in patients under 70 years of age is congenital bicuspid aortic valve. Congenital aortic stenosis is detected in 3-5 per 1000 live births, more often in boys.
In developing countries, the most common cause of aortic stenosis is rheumatic fever in all age groups. Supravalvular aortic stenosis may be caused by a congenital membrane or hypoplastic narrowing above the sinuses of Valsalva, but is rare. A sporadic variant of supravalvular aortic stenosis is associated with characteristic facial features (high and broad forehead, hypertelorism, strabismus, upturned nose, long philtrum, wide mouth, abnormal dental growth, chubby cheeks, micrognathia, low-set ears). When associated with early idiopathic hypercalcemia, this form is known as Williams syndrome. Subvalvular aortic stenosis is caused by a congenital membranous or fibrous ring located below the aortic valve; it is also rare.
Aortic regurgitation may be associated with aortic stenosis. Approximately 60% of patients over 60 years of age with significant aortic stenosis also have mitral annular calcification, which can lead to significant mitral regurgitation.
As a consequence of aortic stenosis, left ventricular hypertrophy gradually develops. Significant left ventricular hypertrophy causes diastolic dysfunction and, if progressed, may lead to decreased contractility, ischemia, or fibrosis, any of which can cause systolic dysfunction and heart failure (HF). Left ventricular enlargement occurs only when the myocardium is damaged (eg, during myocardial infarction). Patients with aortic stenosis are more likely to suffer from bleeding from the gastrointestinal tract or other localizations (Gade syndrome, hepatorenal syndrome), since a high degree of trauma in the area of stenotic valves increases the sensitivity of von Willebrand factor to activation of plasma metalloprotease and can increase platelet clearance. Gastrointestinal bleeding may also be a consequence of angiodysplasia. Hemolysis and aortic dissection occur more often in such patients.
Symptoms of aortic stenosis
Congenital aortic stenosis is usually asymptomatic until at least 10 to 20 years of age, after which symptoms of aortic stenosis may begin to progress rapidly. In all forms, untreated progressive aortic stenosis eventually leads to syncope during exercise, angina, and shortness of breath (the so-called SAD triad). Other symptoms of aortic stenosis may include heart failure and arrhythmias, including ventricular fibrillation, which can lead to sudden death.
Fainting during physical exertion develops because the functional state of the heart cannot provide the necessary level of blood supply during physical activity. Fainting without physical exertion develops due to altered baroreceptor reactions or ventricular fibrillation. Angina pectoris occurs in approximately two-thirds of patients. About a third have significant atherosclerosis of the coronary arteries, in half the coronary arteries are intact, but there is ischemia caused by left ventricular hypertrophy.
There are no visible signs of aortic stenosis. Palpable symptoms include changes in the pulse in the carotid and peripheral arteries: the amplitude is reduced, there is a divergence with the contractions of the left ventricle (pulsus parvus et tardus) and increased contractions of the left ventricle (a push instead of the first heart sound and a weakening of the second heart sound) due to its hypertrophy. The palpable area of the left ventricular contraction does not change by palpation until the development of systolic dysfunction in heart failure. Palpable IV heart sound, which is easier to detect at the apex, and systolic thrill, coinciding with the murmur of aortic stenosis and determined better at the left upper border of the sternal can sometimes be determined in severe cases. Systolic blood pressure can be high with minimal or moderate aortic stenosis, but it decreases as the severity of aortic stenosis increases.
On auscultation, S1 is normal and S2 may be single because the aortic valve closure is distended by fusion of the aortic (A) and pulmonary (P) components of S or (in severe cases) A is absent. As severity increases, S1 weakens and may eventually disappear. S4 is occasionally heard . An ejection click may be heard immediately after in patients with aortic stenosis due to congenital bicuspid aortic valve disease, where the valve leaflets are rigid but not completely immobile. The click does not change with stress testing.
Auscultatory findings include a crescendo-decrescendo ejection murmur heard best with the stethoscope diaphragm at the left upper sternal border with the patient sitting and leaning forward. The murmur is usually conducted to the right clavicle and both carotid arteries (often louder on the left than on the right) and has a harsh or grating timbre. In older patients, vibration of the non-contiguous leaflet tips of the calcified aortic valve may produce a louder, high-pitched "cooing" or musical murmur at the apex, with softening or absence of the murmur parasternally (Gallavardin phenomenon), thus simulating mitral regurgitation. The murmur is softer when the stenosis is less severe, but as the stenosis progresses, it becomes louder, longer, and peaks in late systole (ie, the crescendo phase becomes longer and the decrescendo phase becomes shorter). As left ventricular contractility decreases in critical aortic stenosis, the murmur diminishes and may disappear before death.
The murmur of aortic stenosis typically increases with maneuvers that increase left ventricular volume (eg, leg raise, squat, after ventricular extrasystole) and decreases with maneuvers that decrease left ventricular volume (Valsalva maneuver) or increase afterload (isometric handgrip). These dynamic maneuvers have the opposite effect in the murmur associated with hypertrophic cardiomyopathy, which in other circumstances may resemble the murmur of aortic stenosis.
Diagnosis of aortic stenosis
A presumptive diagnosis of aortic stenosis is made clinically and confirmed by echocardiography. Two-dimensional transthoracic echocardiography is used to detect aortic valve stenosis and its possible causes. This study allows quantification of left ventricular hypertrophy and the degree of diastolic or systolic dysfunction, as well as detection of associated valvular disorders (aortic regurgitation, mitral valve pathology) and complications (eg, endocarditis). Doppler echocardiography is used to quantify the degree of stenosis by measuring aortic valve area, flow velocity, and supravalvular systolic pressure gradient.
A valve area of 0.5-1.0 cm or a gradient > 45-50 mmHg indicate severe stenosis; an area < 0.5 cm and a gradient > 50 mmHg indicate critical stenosis. The gradient may be overestimated in aortic regurgitation and underestimated in left ventricular systolic dysfunction. Aortic valve flow velocity < 2-2.5 m/s in the presence of valvular calcification may indicate aortic sclerosis rather than moderate aortic stenosis. Aortic valve sclerosis often progresses to aortic stenosis, so careful monitoring is necessary.
Cardiac catheterization is performed to determine whether coronary artery disease is the cause of angina or when there is discrepancy between clinical and echocardiographic findings.
An ECG and chest radiography are performed. The ECG shows changes characteristic of left ventricular hypertrophy, with or without ischemic changes in the STv segment of the T wave. Chest radiography may reveal aortic valve calcification and signs of heart failure. Left ventricular dimensions are usually normal unless there is terminal systolic dysfunction.
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Treatment of aortic stenosis
Asymptomatic patients with a peak systolic gradient < 25 mmHg and valve area > 1.0 cm have low mortality and a low overall risk of requiring surgery within the next 2 years. Annual monitoring of symptom progression is performed by echocardiography (to assess gradient and valve area).
Asymptomatic patients with a gradient of 25–50 mmHg or a valve area < 1.0 cm have a higher risk of developing clinical manifestations over the next 2 years. Management of these patients is controversial, but most are candidates for valve replacement. This procedure is mandatory for patients with severe asymptomatic aortic stenosis requiring CABG. Surgery may be indicated in the following cases:
- development of arterial hypotension during a treadmill exercise test;
- LV ejection fraction < 50%;
- moderate or severe valvular calcification, peak aortic velocity > 4 m/s and rapid progression of peak aortic velocity (> 0.3 m/s per year).
Patients with ventricular arrhythmias and significant LV hypertrophy are also often treated surgically, but the efficacy is less clear. Recommendations for patients without either condition include more frequent monitoring of symptom progression, LV hypertrophy, gradients, valve area, and drug therapy when needed. Drug therapy is mainly limited to β-blockers, which slow the heart rate and thus improve coronary blood flow and diastolic filling in patients with angina or diastolic dysfunction. Statins are also used in older patients to stop the progression of aortic stenosis caused by aortic sclerosis. Other drugs may cause harm. Use of drugs that reduce preload (eg, diuretics) may reduce left ventricular filling and impair cardiac performance. Drugs that reduce afterload (eg, ACE inhibitors) may cause hypotension and reduce coronary blood flow. Nitrates are the drugs of choice for angina, but rapidly acting nitrates may precipitate orthostatic hypotension and (occasionally) syncope because the ventricle, with its severely limited output, cannot compensate for the sudden fall in blood pressure. Sodium nitroprusside has been used as an afterload reducer in patients with decompensated heart failure for several hours before valve replacement, but because this drug may have the same effect as rapidly acting nitrates, it must be used cautiously and under close supervision.
Symptomatic patients require valve replacement or balloon valvotomy. Valve replacement is indicated for virtually all patients who can tolerate surgery. Sometimes the native pulmonary valve can be used for optimal function and durability; in this case, the pulmonary valve is replaced with a bioprosthesis (Ross procedure). Sometimes, in patients with associated severe aortic regurgitation in the setting of a bicuspid valve, the aortic valve can be repaired (valvular repair) rather than replaced. Preoperative assessment of coronary artery disease is necessary so that, if necessary, CABG and valve replacement can be performed in the same operation.
Balloon valvotomy is used primarily in children and young adults with congenital aortic stenosis. In older patients, balloon valvuloplasty results in frequent restenosis, aortic regurgitation, stroke, and death, but it is acceptable as a temporary intervention in hemodynamically unstable patients (while waiting for surgery) and in patients who cannot tolerate surgery.
Prognosis for aortic stenosis
Aortic stenosis can progress slowly or rapidly, so dynamic monitoring is necessary to detect changes in a timely manner, especially in sedentary elderly patients. In such patients, the flow can significantly decrease without clinical symptoms.
Overall, approximately 3% to 6% of asymptomatic patients with normal systolic function develop symptoms or decreased left ventricular EF within 1 year. Predictors of poor outcome (death or symptoms requiring surgery) include valve area < 0.5 cm2, peak aortic velocity > 4 m/s, rapid increase in peak aortic velocity (> 0.3 m/s per year), and moderate to severe valvular calcification. Median survival without treatment is approximately 5 years after the onset of angina, 4 years after the onset of syncope, and 3 years after the development of heart failure. Aortic valve replacement reduces symptoms and improves survival. The risk of surgery is increased in patients who also require coronary artery bypass grafting (CABG) and in those with decreased left ventricular systolic function.
Approximately 50% of deaths occur suddenly. For this reason, patients with a critical aortic valve gradient awaiting surgery should limit activity to avoid sudden death.
Aortic sclerosis probably increases the risk of myocardial infarction by 40% and can lead to angina, heart failure, and stroke. The cause may be progression to aortic stenosis or concomitant dyslipidemia, endothelial dysfunction, and underlying systemic or local inflammation causing valvular sclerosis and coronary artery disease.