Aortic stenosis: general information

Aortic stenosis is a narrowing of the aortic valve that limits the flow of blood from the left ventricle to the ascending part of the aorta during systole. The causes of aortic stenosis include a congenital bicuspid aortic valve, idiopathic degenerative sclerosis with calcification, and rheumatic fever.

Progressive aortic stenosis without treatment ultimately leads to a classical triad - syncope, stenocardia and dyspnoea with physical exertion; possible heart failure and arrhythmias. A pulse in the carotid arteries with a small amplitude and a delayed peak is characteristic, as well as an increasing-decreasing noise of ejection. Diagnosis is established by physical examination and echocardiography. Asymptomatic aortic stenosis often does not require treatment. With progressive severe aortic stenosis or the appearance of clinical symptoms in children, balloon valvulotomy is used; an adult is shown replacing the valve.

[1], [2], [3], [4], [5]

Statistics

The prevalence of aortic stenosis, according to different authors, ranges from 3-4 to 7%. With age, the frequency of this defect increases, accounting for 15-20% of streets older than 80 years, and with an increase in the duration of the life of the population, the occurrence of this defect in the population will increase. The predominant sex of the male (2.4: 1), but in the older age group women predominate. Aortic stenosis is divided by origin into congenital and acquired, in terms of lesion - in isolated and combined, in localization - in valvular, supra-valued, poddklapanniy or caused by hypertrophic cardiomyopathy.

Causes of aortic stenosis

Aortic sclerosis, thickening of valvular structures in fibrosis and calcification (initially without stenosis) are the most frequent causes of aortic stenosis in the elderly; over the years, 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 arteriosclerosis, with the deposition of lipoproteins, active inflammation and calcification of the valves; risk factors are the same.

The most common cause of aortic stenosis in patients younger than 70 is the congenital bicuspid aortic valve. Congenital aortic stenosis is detected in 3-5 per 1,000 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 is caused by the presence of a congenital membrane or a hypoplastic narrowing above the sinuses of Valsalva, but is rare. The sporadic variant of the supravalvular aortic stenosis is combined with the characteristic features of the face (high and broad forehead, hypertelorism, strabismus, snub nose, long groove under the nose, wide mouth, dysplastic growth, chubby cheeks, micrognathia, low set ears). In the event that this anomaly is associated with idiopathic hypercalcemia at an early stage of development, this form is known as Williams syndrome. Subvalvular aortic stenosis is caused by the presence of a congenital membrane or fibrous ring located below the aortic valve; is also rare.

Aortic regurgitation can be combined with aortic stenosis. Approximately 60% of patients older than 60 with significant aortic stenosis also have calcification of the mitral ring, which can lead to significant mitral regurgitation.

As a consequence of aortic stenosis, hypertrophy of the left ventricle gradually develops. Significant hypertrophy of the left ventricle causes diastolic dysfunction and, with progression, can lead to a decrease in contractility, ischemia or fibrosis, either of which can cause systolic dysfunction and heart failure (CH). Expansion of the cavity of the left ventricle occurs only with damage to the myocardium (for example, with myocardial infarction). Patients with aortic stenosis are more likely to suffer from bleeding from the gastrointestinal tract or other localizations (Heid's syndrome, hepatorenal syndrome), since a high degree of trauma in the area of stenotic valves increases the sensitivity of von Willebrand factor to the activation of plasma metalloprotease and can increase the clearance of platelets. Gastrointestinal bleeding can also be a consequence of angiodysplasia. Hemolysis and aortic dissection in such patients occur more often.

What causes aortic stenosis?

[6], [7],

Symptoms of aortic stenosis

Congenital aortic stenosis usually proceeds asymptomatically, at least up to 10-20 years, after which the symptoms of aortic stenosis may begin to progress rapidly. In all forms, progressive aortic stenosis without treatment ultimately leads to fainting during exercise, angina and dyspnea (the so-called SAD triad). Other symptoms of aortic stenosis may include heart failure and arrhythmias, including ventricular fibrillation, leading to sudden death.

Fainting with exercise is developing, because the functional state of the heart can not provide the necessary level of blood supply for physical activity. Fainting without physical activity develops due to altered reactions of baroreceptors or ventricular fibrillation. Stenocardia tension appears in about two-thirds of patients. About a third have significant atherosclerosis of the coronary arteries, half of the coronary arteries are intact, but ischemia due to left ventricular hypertrophy is present.

There are no visible signs of aortic stenosis. Palpatory symptoms include changes in the pulse on the carotid and peripheral arteries: the amplitude is reduced, there is a discrepancy with the contractions of the left ventricle (pulsus parvus et tardus) and increased left ventricular contractions (a push instead of the I heart tone and a weakening of the heart's tone II) due to its hypertrophy. The area of palpation of contraction of the left ventricle palpation does not change until the development of systolic dysfunction in heart failure. Palpable IV heart tone, which is easier to identify at the tip, and systolic jitter, coinciding with the noise of aortic stenosis and determined better at the left upper edge of the sternum, can sometimes be determined in severe cases. Systolic blood pressure may be high with minimal or moderate aortic stenosis, but it decreases with increasing severity of aortic stenosis.

With auscultation, S1 is normal, and S2 is single, because the closure of the aortic valve is stretched due to the fusion of the aortic (A) and pulmonary (P) components of S or (in severe cases) A is absent. As the gravity increases, S1 weakens and can eventually disappear. Sometimes S ₄ is heard . The click of exile may sound right after in patients with aortic stenosis due to congenital bivalve AK, when valve flaps are rigid, but not completely fixed. The click does not change during load tests.

Auscultatory findings include an increasing-decreasing ejection noise, which is heard best by a stethoscope with a diaphragm at the left upper edge of the sternum, when the patient sits, leaning forward. Noise is usually carried to the right collarbone and to both carotid arteries (the left is often louder than the right) and has a hard or abrasive timbre. In elderly patients, the vibration of the unchanging tops of the valves of the calcified aortic valve may produce a louder high-frequency "cooing" or musical noise at the apex of the heart, with a softening or lack of noise in the parasternal region (the Gallavarden phenomenon), thus simulating mitral regurgitation. The noise is milder when the stenosis is less pronounced, however, as the progression of the stenosis becomes louder, longer and reaches a maximum in late systole (i.e., the phase of build-up becomes longer and the decrease is shorter). As the contractility of the left ventricle decreases with critical aortic stenosis, the noise decreases and may disappear before dying.

Aortic stenosis is usually worsened by a test that increases the volume of the left ventricle (for example, a leg lift, squat, after the ventricular extrasystole), and decreases with actions that reduce the volume of the left ventricle (Valsalva test) or increase afterload (isometric handshake). These dynamic actions have the opposite effect in the noise associated with hypertrophic cardiomyopathy, which in other circumstances can recall the noise of aortic stenosis.

Symptoms of aortic stenosis

Diagnosis of aortic stenosis

Presumptive diagnosis of aortic stenosis is put clinically and confirmed by echocardiography. Two-dimensional transthoracic echocardiography is used to detect the stenosis of the aortaptic valve and its possible causes. This study allows quantifying left ventricular hypertrophy and the degree of diastolic or systolic dysfunction, as well as concomitant valvular disorders (aortic regurgitation, mitral valve pathology) and complications (eg, endocarditis). Doppler echocardiography is used to quantify the degree of stenosis by measuring the area of the aortic valve, the flow rate and the supra-valued gradient of systolic pressure.

Valve area 0.5-1.0 cm or gradient> 45-50 mm Hg. Art. Evidence of severe stenosis; area <0.5 cm and gradient> 50 mm Hg. Art. - about critical stenosis. The gradient may be overestimated in aortic regurgitation and underestimated in systolic dysfunction of the left ventricle. The flow rate through the aortic valve <2-2.5 m / s in the presence of valvular calcification may be more indicative of sclerosis of the aorta than in moderate aortic stenosis. Sclerosis of the aortic valve 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 pectoris, or when there is a discrepancy between the clinical and echocardiographic results of the study.

Perform ECG and chest X-ray. The ECG demonstrates changes that are characteristic of left ventricular hypertrophy, with or without ischemic changes in the STv segment of the T wave. With chest radiography, calcification of the aortic valve and signs of heart failure can be detected. The dimensions of the left ventricle are usually normal, if there is no terminal systolic dysfunction.

Diagnosis of aortic stenosis

[8], [9], [10]

Treatment of aortic stenosis

Patients without clinical manifestations with a peak systolic gradient <25 mm Hg. Art. And a valve area> 1.0 cm have a low mortality and a small overall risk of surgical intervention for the next 2 years. The annual control of the progression of the symptoms is carried out by echocardiography (to estimate the gradient and the valve area).

Symptomatic patients with a gradient of 25-50 mm Hg. Art. Or valve area <1.0 cm have a higher risk of developing clinical manifestations in the next 2 years. Approaches to the management of such patients are controversial, but most of them show replacement of the valve. This operation is mandatory for patients with severe asymptomatic aortic stenosis, requiring CABG. Surgical treatment can be prescribed in the following cases:

• the development of arterial hypotension during the stress test-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 severe hypertrophy of the LV are also often subjected to surgical treatment, but the effectiveness is less clear. Recommendations for patients who do not have any of these conditions include more frequent monitoring of symptom progression, left ventricular hypertrophy, gradients, valve areas and drug treatment if necessary. Drug therapy is mainly limited to b-adrenoblockers, which slow down the heart rate and thus improve coronary blood flow and diastolic filling in patients with angina or diastolic dysfunction. Older patients are also prescribed statins, which stop the progression of aortic stenosis caused by aortic sclerosis. Other drugs may be harmful. The use of drugs that reduce preload (for example, diuretics) can reduce the filling of the left ventricle and reduce the functional state of the heart. Means that reduce afterload (for example, ACE inhibitors), can cause arterial hypotension and reduce coronary blood supply. Nitrates are the drugs of choice for angina pectoris, but high-speed nitrates can provoke orthostatic hypotension and (sometimes) faint, since a ventricle with a significantly limited ejection can not compensate for the sudden drop in blood pressure. Sodium nitroprusside was used as a means of reducing afterload in patients with decompensated heart failure for several hours before changing the valve, but since this drug can have the same effect as high-speed nitrates, it must be used carefully, under control.

Patients with clinical manifestations need to replace the valve or balloon valvulotomy. The replacement of the valve is indicated to almost everyone who can tolerate surgical intervention. Sometimes you can use your own pulmonary valve, which ensures optimal functioning and durability; In this case, the pulmonary artery valve is replaced by a bioprosthesis (Ross operation). Sometimes, in patients with concomitant severe aortic regurgitation against the background of the bicuspid valve, the aortic valve can be restored (valve plastic) rather than replaced. Preoperative assessment of IHD is necessary so that if necessary, CABG and valve replacement can be performed during one operation.

Balloon valvulotomy is used primarily in children and young people with congenital aortic stenosis. In older patients, balloon valvuloplasty leads to 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 can not tolerate a surgical operation.

Treatment of aortic stenosis

Prognosis for aortic stenosis

Aortic stenosis can progress slowly or rapidly, so dynamic monitoring is needed to detect changes in time, especially in sedentary elderly patients. In such patients, the flow can be significantly reduced without clinical symptoms.

In general, approximately 3-6% of patients with no symptomatic symptomatology with a normal systolic function develop clinical signs or a decrease in left ventricular ejection for 1 year. Indicators of adverse outcome (death or symptoms requiring surgery) include a valve area <0.5 cm2, aortic valve peak velocity> 4 m / s, a rapid increase in peak aortic velocity (> 0.3 m / s per year) and moderate or severe valvular calcification. The 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 onset of heart failure. Replacement of the aortic valve reduces symptoms and improves survival. The risk of surgical treatment is increased in patients who simultaneously require aortocoronary shunting (CABG), and patients with reduced systolic function of the left ventricle.

Approximately 50% of deaths occur suddenly. For this reason, patients with a critical gradient of the aortic valve waiting for surgery should limit their activity in order to avoid sudden death.

Aortic sclerosis, probably, increases the risk of myocardial infarction by 40% and can lead to the emergence of angina pectoris, heart failure and stroke. The cause is the progression of pathology to the development of aortic stenosis or concomitant dyslipidemia, endothelial dysfunction, as well as the underlying systemic or local inflammation that causes valvular sclerosis and ischemic heart disease.