Mitral stenosis

Mitral stenosis is a narrowing of the mitral orifice that prevents blood from flowing from the left atrium to the left ventricle. The most common cause is rheumatic fever. Symptoms are the same as in heart failure. Objectively determine the opening tone and diastolic murmur. The diagnosis is made by physical examination and echocardiography. The prognosis is favorable. Drug treatment of mitral stenosis includes diuretics, beta-blockers or heart rate-reducing calcium channel blockers and anticoagulants. Surgical treatment of mitral stenosis of more severe cases consists of balloon valvulotomy, commissurotomy or valve prosthetics.

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

Epidemiology

Almost always, mitral stenosis is a consequence of acute rheumatic fever. The incidence varies considerably: in developed countries, there are 1-2 cases per 100,000 population, while in developing countries (for example, India), rheumatic mitral defects are observed in 100-150 cases per 100,000 population.

[5], [6], [7], [8], [9], [10], [11], [12],

Causes of the mitral stenosis

Mitral stenosis is almost always the result of acute rheumatic fever (RL). Isolated, “clean” mitral stenosis occurs in 40% of cases among all patients with rheumatic heart disease; in other cases - a combination with failure and damage to other valves. Among the rare causes of mitral stenosis are rheumatic diseases (rheumatoid arthritis, systemic lupus erythematosus) and calcification of the mitral ring.

[13], [14]

Pathogenesis

In rheumatic mitral stenosis, seal, fibrosis and calcification of the valve leaflets, fusion of the commissures with frequent involvement of the chords are observed. Normally, the area of the mitral orifice is 4-6 cm ², and the pressure in the cavity of the left atrium does not exceed 5 mm Hg. When the left atrioventricular orifice narrows to 2.5 cm ², the normal blood flow from the left atrium to the left ventricle is obstructed and the valve pressure gradient begins to grow. As a result, pressure builds up in the cavity of the left atrium up to 20-25 mm Hg. The resulting pressure gradient between the left atrium and the left ventricle promotes blood flow through the narrowed opening.

As stenosis progresses, the transmitral pressure gradient increases, which allows maintaining diastolic blood flow through the valve. In accordance with the Gorlin formula, the area of the mitral valve (5 MK) is determined by the values of the transmitral gradient (DM) and the mitral blood flow (MC):

BMK - MK / 37.7 • ΔDM

The main hemodynamic consequence of mitral heart defects is stagnation in the pulmonary circulation (ICC). With a moderate increase in pressure in the left atrium (no more than 25–30 mm. Hg), blood flow to the ICC is hampered. The pressure in the pulmonary veins increases and is transmitted through the capillaries to the pulmonary artery, as a result of which venous (or passive) pulmonary hypertension develops. With increasing pressure in the left atrium more than 25-30 mm. Hg the risk of rupture of pulmonary capillaries and the development of alveolar pulmonary edema increases. To prevent these complications, a protective reflex spasm of the pulmonary arterioles arises. As a result, the blood flow to the cell capillaries from the right ventricle decreases, but the pressure in the pulmonary artery sharply increases (arterial or active pulmonary hypertension develops).

In the early stages of bleeding, pressure in the pulmonary artery increases only during physical or emotional stress, when the blood flow in the ICC should increase. The late stages of the disease are characterized by high values of pressure in the pulmonary artery even at rest and even greater pressure increases. The long existence of pulmonary hypertension is accompanied by the development of proliferative and sclerotic processes in the wall of arterioles of the ICC, which are gradually obliterated. Although the occurrence of pulmonary arterial hypertension can be viewed as a compensatory mechanism, the diffuse capacity of the lungs drops sharply due to a decrease in capillary blood flow, especially during exercise. The progression of pulmonary hypertension due to hypoxemia is activated. Alveolar hypoxia causes pulmonary vasoconstriction by direct and indirect mechanism. The direct effect of hypoxia is associated with depolarization of vascular smooth muscle cells (mediated by a change in the function of the potassium channels of cell membranes) and their contraction. The indirect mechanism is the effect on the vascular wall of the endogenous mediators (such as leukotrienes, histamine, serotonin, angiotensin II and catecholamines). Chronic hypoxemia leads to endothelial dysfunction, which is accompanied by a decrease in the production of endogenous relaxing factors, including prostacyclin, prostaglandin E2 and nitric oxide. Due to the long-term existence of endothelial dysfunction, obliteration of the pulmonary vessels and damage to the endothelium occur, which in turn leads to an increase in blood clotting, proliferation of smooth muscle cells with a tendency to thrombosis in situ and an increase in the risk of thrombotic complications with the development of subsequent chronic post-thrombotic pulmonary hypertension.

The causes of pulmonary hypertension in mitral malformations, including mitral stenosis, are:

• passive pressure transfer from the left atrium to the pulmonary vein system;
• pulmonary arteriole spasm in response to increased pressure in the pulmonary veins;
• swelling of the walls of small pulmonary vessels;
• obliteration of pulmonary vessels with endothelial damage.

To date, the mechanism of mitral stenosis progression remains unclear. A number of authors consider the main factor to be the current valvulitis (often subclinical), others assign the leading role of traumatizing valve structures to turbulent blood flow with thrombotic masses on the valves, which underlies the narrowing of the mitral orifice.

[15], [16], [17], [18], [19], [20]

Symptoms of the mitral stenosis

Symptoms of mitral stenosis correlate poorly with the severity of the disease, since in most cases the pathology progresses slowly, and patients decrease their activity without noticing it. Many patients have no clinical manifestations until pregnancy occurs or atrial fibrillation develops. The initial symptoms are usually signs of heart failure (shortness of breath on exertion, orthopnea, paroxysmal dyspnea at night, fatigue). They usually appear 15–40 years after an episode of rheumatic fever, but in developing countries even children may have symptoms. Paroxysmal or persistent atrial fibrillation increases existing diastolic dysfunction, causing pulmonary edema and acute shortness of breath if the rate of ventricular contractions is poorly controlled.

Atrial fibrillation can also manifest as palpitations; in 15% of patients not receiving anticoagulant drugs, it causes systemic embolism with limb ischemia or stroke.

More rare symptoms include hemoptysis due to rupture of small pulmonary vessels and pulmonary edema (especially during pregnancy, when blood volume increases); dysphonia due to compression of the left recurrent laryngeal nerve by the dilated left atrium or pulmonary artery (Ortner syndrome); symptoms of pulmonary arterial hypertension and failure of the right ventricle.

The first symptoms of mitral stenosis

When the area of the mitral orifice is> 1.5 cm ^2, symptoms may be absent, however, an increase in the transmitral blood flow or a decrease in the diastolic filling time lead to a sharp increase in pressure in the left atrium and the appearance of symptoms. Provocative (trigger) factors of decompensation: physical activity, emotional stress, atrial fibrillation (atrial fibrillation), pregnancy.

The first symptom of mitral stenosis (approximately 20% of cases) may be an embolic event, most often a stroke with the development of persistent neurological deficit in 30-40% of patients. One third of thromboembolism develops within 1 month after the development of atrial fibrillation, two thirds during the first year. The source of embolism are usually blood clots located in the left atrium, especially in its ear. In addition to strokes, possible embolism in the spleen, kidney, peripheral arteries.

With sinus rhythm, the risk of emboli is determined by:

• age;
• thrombosis of the left atrium;
• the area of the mitral orifice;
• concomitant aortic insufficiency.

With a constant form of atrial fibrillation, the risk of embolism increases significantly, especially if the patient has already had similar complications in history. Spontaneous contrasting of the left atrium during conduction of the stomach with esophageal echoCG is also considered a risk factor for systemic emboli.

With increasing pressure in the ICC (especially at the stage of passive pulmonary hypertension) there are complaints of shortness of breath during exercise. With the progression of stenosis, shortness of breath occurs at lower loads. It should be remembered that complaints of shortness of breath may be absent even with undoubted pulmonary hypertension, since the patient can lead a sedentary lifestyle or subconsciously restrict daily physical activity. Paroxysmal nocturnal dyspnea occurs as a result of stagnation of blood in the ICC when the patient is lying down as a manifestation of interstitial pulmonary edema and a sharp increase in blood pressure in the ICC vessels. Due to the increase in pressure in the pulmonary capillaries and the sweating of plasma and erythrocytes into the lumen of the alveoli, hemoptysis may develop.

Patients often complain also of pa increased fatigability, palpitations, interruptions in the work of the heart. Transient hoarseness (Ortner syndrome) may occur. This syndrome results from the compression of the recurrent nerve by the enlarged left atrium.

Patients with mitral stenosis often have chest pains resembling angina of exertion. Their most likely causes are pulmonary hypertension and right ventricular hypertrophy.

With severe decompensation, facies mitralis can be observed (bluish pink blush on the cheeks, which is associated with a decrease in the ejection fraction, systemic vasoconstriction and right-sided heart failure), epigastric pulsation and signs of right ventricular heart failure.

[21],

Inspection and auscultation

On examination and palpation, cardiac tones determined by I (S1) and II (S2) can be detected. S1 is best palpable at the apex, and S2 - at the left upper edge of the sternum. The pulmonary component S3 (P) is responsible for the impulse and is the result of pulmonary arterial hypertension. The visible pulsation of the pancreas, palpable at the left edge of the sternum, may accompany the swelling of the jugular veins if there is pulmonary arterial hypertension and diastolic dysfunction of the right ventricle develops.

The apical impulse in mitral stenosis is most often normal or reduced, which reflects the normal function of the left ventricle and a decrease in its volume. The palpated I tone in the precordial region indicates the preserved mobility of the anterior mitral valve. In the position of the fawn side, diastolic tremor can be felt. With the development of pulmonary hypertension along the right border of the sternum, cardiac impulse is noted.

Auscultation picture with mitral stenosis is quite characteristic and includes the following signs:

• amplified (clapping) I tone, the intensity of which decreases with the progression of stenosis;
• the tone of opening of the mitral valve following the II tone, disappearing at valve calcification;
• diastolic noise with a maximum at the apex (mesodiastolic, presystolic, pandiastolic), which must be heard in the position on the left side.

Auscultatively determine the loud S 1 caused by the flaps of the stenotic mitral valve, closing abruptly, like a "inflating" sail; This phenomenon is best heard at the top. Usually, a split S with increased P due to pulmonary arterial hypertension is also heard. The most striking is the early diastolic click of the opening of the valves in the left ventricle (LV), which is loudest at the left lower edge of the sternum. It is accompanied by a low, decreasing rumbling diastolic noise, which is best heard through a stethoscope with a funnel at the apex of the heart (or above the palpable apical impulse) at the end of the exhale, when the patient lies on his left side. The opening tone may be soft or absent if the mitral valve is sclerosed, fibrosed or compacted. The click shifts closer to P (increasing the duration of the noise) as the severity of mitral stenosis increases and the pressure in the left atrium increases. Diastolic noise increases with the Valsalva maneuver (when blood flows into the left atrium), after exercise and with squatting and handshaking. This may be less pronounced if the enlarged right ventricle displaces the left ventricle posteriorly and when other disorders (pulmonary arterial hypertension, valvular lesions of the right sections, atrial fibrillation with frequent ventricular rhythm) reduce blood flow through the mitral valve. Presystolic amplification is associated with a narrowing of the opening of the mitral valve during the contraction of the left ventricle, which also occurs during atrial fibrillation, but only at the end of the short diastole, when the pressure in the left atrium is still high.

The following diastolic murmurs can be combined with mitral stenosis:

• Graham Still's noise (a mild, decreasing diastolic murmur, heard best of all along the left edge of the sternum and caused by regurgitation on the pulmonary artery valve due to severe pulmonary hypertension);
• Austin Flint's noise (middle or late diastolic murmur, heard at the apex of the heart and caused by the influence of aortic regurgitation flow on the mitral valve leaflets) in the case when rheumatic carditis affects the mitral and aortic valves.

Disorders that cause diastolic murmurs that mimic the noise of mitral stenosis include mitral regurgitation (due to a large flow through the mitral opening), aortic regurgitation (causing Austin Flint noise), and atrial myxoma (which causes a noise that varies in volume and depending on position with each heartbeat).

Mitral stenosis can cause pulmonary heart symptoms. The classic sign of facies mitralis (hyperemia of the skin with a plum shade in the zygomatic bone) occurs only in the case when the functional state of the heart is low and pulmonary hypertension is expressed. The causes of facies mitralis are the dilatation of the skin vessels and chronic hypoxemia.

Sometimes the first symptoms of mitral stenosis are manifestations of embolic stroke or endocarditis. The latter rarely occurs in mitral stenosis, which is not accompanied by mitral regurgitation.

[22], [23], [24], [25], [26], [27], [28]

Clinical manifestations of pulmonary hypertension in mitral stenosis

The first symptoms of pulmonary hypertension are not specific, and this greatly complicates its early diagnosis.

Dyspnea is caused both by the presence of pulmonary hypertension and by the inability of the heart to increase cardiac output during exercise. Shortness of breath is usually inspiratory in nature, at the onset of the disease is intermittent, occurring only with moderate exertion, then, as pressure increases in the pulmonary artery, appears with minimal exertion, it may be present at rest. With high pulmonary hypertension, dry cough may occur. It should be remembered that patients can subconsciously limit physical activity, adapting to a certain lifestyle, so complaints of shortness of breath are sometimes absent even with undoubted pulmonary hypertension.

Weakness, increased fatigue - the causes of these complaints may be fixed cardiac output (the amount of blood ejected into the aorta does not increase in response to physical exertion), increased resistance of pulmonary vessels, as well as a decrease in perfusion of peripheral organs and skeletal muscles, caused by impaired peripheral blood circulation.

Dizziness and fainting caused by hypoxic encephalopathy, as a rule, provoked by exercise.

Persistent pain behind the sternum and to the left of it are caused by overstretching of the pulmonary artery, as well as insufficient blood supply to hypertrophied myocardium (relative coronary insufficiency).

Interruptions in the work of the heart and heartbeat. These symptoms are associated with frequent atrial fibrillation.

Hemoptysis occurs due to rupture of the pulmonary-bronchial anastomoses under the action of high venous pulmonary hypertension, may also be due to increased pressure in the pulmonary capillaries and sweating of the plasma and erythrocytes into the lumen of the alveoli. Hemoptysis can also be a symptom of pulmonary embolism and pulmonary infarction.

To characterize the severity of pulmonary hypertension, the functional classification proposed by WHO for patients with blood supply insufficiency is used:

• class I - patients with pulmonary hypertension, but without limiting physical activity. Normal physical activity does not cause shortness of breath, weakness, pain in the chest, dizziness;
• class II - patients with pulmonary hypertension, leading to some decrease in physical activity. At rest, they feel comfortable, but normal physical activity is accompanied by the appearance of shortness of breath, weakness, chest pain, dizziness;
• class III - patients with pulmonary hypertension, leading to a pronounced limitation of physical activity. At rest, they feel comfortable, but little physical activity causes the appearance of shortness of breath, weakness, chest pain, dizziness;
• class IV - patients with pulmonary hypertension who cannot perform any physical activity without the listed symptoms. Dyspnea or weakness are sometimes present even at rest, discomfort increases with minimal exertion.

[29], [30], [31], [32], [33], [34]

Forms

Mitral stenosis is classified according to severity (ACC / AHA / ASE 2003 guideline update for the clinical application of echocardiography).

Classification of mitral stenosis by degree

Degree of stenosis	The area of the mitral orifice, cm 2	Transmitral gradient, mm Hg Art.	Systolic pressure in the pulmonary artery, mm. Hg Art.
Light	>1.5	<5	<30
Moderate	1.0-1.5	5-10	30-50
Heavy	<1 0	>10	>50

In mitral stenosis, the mitral valve leaflets become thickened and immobile, and the mitral orifice narrows due to the fusion of the commissures. The most common cause is rheumatic fever, although most patients do not remember the disease. More rare causes include congenital mitral stenosis, septic endocarditis, systemic lupus erythematosus, atrial myxoma, rheumatoid arthritis, malignant carcinoid syndrome with atrial bypass from right to left. If the valve cannot close completely, mitral regurgitation (MP) may exist simultaneously with mitral stenosis. Many patients with mitral stenosis resulting from rheumatic fever also have aortic regurgitation.

The normal orifice area of the mitral valve is 4-6 cm ². The area of 1-2 cm ² indicates moderate or severe mitral stenosis and often causes clinical symptoms during exercise. An area of <1 cm ² is a critical stenosis and may cause symptoms at rest. The size of the left atrium and the pressure in it is progressively increased to compensate for mitral stenosis. Pulmonary venous and capillary pressure also increases and can cause secondary pulmonary hypertension, leading to right ventricular heart failure and regurgitation on the tricuspid valve and the pulmonary artery valve. The rate of progression of pathology varies.

Valve pathology with left atrial enlargement predisposes to the development of atrial fibrillation (AH) and thromboembolism.

[35], [36], [37], [38], [39]

Complications and consequences

Common complications are pulmonary arterial hypertension, atrial fibrillation and thromboembolism.

[40], [41], [42], [43], [44], [45], [46]

Diagnostics of the mitral stenosis

A preliminary diagnosis is made clinically and confirmed by echocardiography. Two-dimensional echocardiography provides information on the degree of valvular calcification, the size of the left atrium and stenosis. Doppler echocardiography provides information on the pressure gradient and pressure of the pulmonary artery. A transesophageal echocardiography can be used to detect or exclude small blood clots in the left atrium, especially in its ear, which can often not be detected by transthoracic examination.

A chest x-ray usually shows a smoothing of the left border of the heart due to the dilated abalone of the left atrium. The main trunk of the pulmonary artery can be seen; the diameter of the descending right pulmonary artery exceeds 16 mm if pulmonary hypertension is expressed. The pulmonary veins of the upper lobes may be dilated, since the veins of the lower lobes are constricted, which causes the upper parts to become full. A double shadow of the enlarged left atrium along the right contour of the heart may be detected. Horizontal lines in the lower posterior lung fields (Curly lines) indicate interstitial edema associated with high pressure in the left atrium.

Cardiac catheterization is prescribed only for preoperative detection of coronary artery disease: an increase in the left atrium, pressure in the pulmonary arteries and valve area can be estimated.

The patient's ECG is characterized by the appearance of P-mitrale (wide, with PQ notch), deviation of the electrical axis of the heart to the right, especially with the development of pulmonary hypertension, as well as right hypertrophy (with isolated mitral stenosis) and left ventricle (when combined with mitral insufficiency).

The severity of stenosis is assessed using Doppler studies. The average transmitter pressure gradient and the area of the mitral valve can be determined quite accurately using continuous-wave technology. Of great importance is the assessment of the degree of pulmonary hypertension, as well as concomitant mitral and aortic regurgitation.

Additional information can be obtained using the stress test (stress echocardiography) with the registration of transmitral and tricuspid blood flow. When the area of the mitral valve <1.5 cm ² and a pressure gradient of> 50 mm. Hg Art. (after exercise) it is necessary to consider the issue of balloon mitral valvuloplasty.

In addition, spontaneous echo contrast during transesophageal echocardiography is an independent predictor of embolic complications in patients with mitral stenosis.

Transesophageal echocardiography allows to clarify the presence or absence of a thrombus of the left atrium, to clarify the degree of mitral regurgitation with a planned balloon mitral valvuloplasty. In addition, a transversal research allows an accurate assessment of the state of the valve apparatus and the severity of changes in the subvalvular structures, as well as the likelihood of restenosis.

Catheterization of the heart and great vessels is carried out in cases where surgery is planned, and the data of non-invasive tests do not give an unambiguous result. For direct measurement of pressure in the left atrium and the left ventricle, transseptal catheterization is necessary, associated with undue risk. The indirect method of measuring pressure in the left atrium is the determination of the pressure of the pulmonary artery wedging.

[47], [48], [49], [50], [51], [52],

Differential diagnosis

With careful examination, the diagnosis of mitral disease is usually not in doubt.

Mitral stenosis is also differentiated with left atrial myxoma, other valve defects (mitral insufficiency, tricuspid valve stenosis), atrial septal defect, pulmonary stenosis, congenital mitral stenosis.

[53], [54], [55], [56], [57], [58], [59]

Examples of the wording of the diagnosis

• Rheumatic heart disease. The combined mitral defect with prevalence of a stenosis of the left atrioventricular opening of the III degree. Atrial fibrillation, permanent form, tachysystole. Pulmonary hypertension moderate. NC PB stage III FC.
• Rheumatic heart disease. The combined mitral defect. Prosthetic mitral valve (Medineh - 23) from DD / MM / GG. NC IIA stage II FC.

[60], [61], [62]

Treatment of the mitral stenosis

The main goals of treatment of patients with mitral stenosis are to improve the prognosis and increase life expectancy, alleviate the symptoms of the disease.

Asymptomatic patients are advised to limit intense physical exertion. With decompensation and symptoms of chronic heart failure, it is recommended to limit sodium in food.

Drug treatment of mitral stenosis

Drug treatment can be used to control the symptoms of mitral stenosis, for example, when preparing for surgery, Diuretics reduce pressure in the left atrium and relieve symptoms associated with congestion in the ICC. At the same time, diuretics should be used with caution, since cardiac output may be reduced, beta-blockers and rhythm-reducing blockers of slow calcium channels (verapamil and diltiazem) reduce heart rate at rest and under load, improving the filling of the left ventricle due to lengthening diastole. These drugs can alleviate the symptoms associated with physical activity, their use is especially indicated in sinus tachycardia and atrial fibrillation.

Atrial fibrillation is a frequent complication of mitral stenosis, especially in older individuals. The risk of thromboembolism in the presence of atrial fibrillation increases significantly (10-year survival rate - 25% of patients compared with 46% in patients with sinus rhythm).

Indirect anticoagulants (warfarin, starting dose 2.5-5.0 mg, under the control of INR) are indicated;

• all patients with mitral stenosis complicated by atrial fibrillation (paroxysmal, persistent or permanent form);
• a patient with a history of embolic events, even with a preserved sinus rhythm;
• patients with a blood clot in the left atrium;
• in patients with severe mitral stenosis and in patients with a left atrial size of> 55 mm.

Treatment is carried out under the supervision of the INR, the target levels of which are from 2 to 3. If the patient has embolic complications, despite ongoing anticoagulant treatment, it is recommended to add acetylsalicylic acid at a dose of 75-100 mg / day (alternatively dipyridamole or clopidogrel). It should be noted that randomized controlled studies on the use of anticoagulants in patients with mitral stenosis were not conducted, recommendations were based on extrapolation of data obtained in the cohorts of patients with atrial fibrillation.

Since the appearance of atrial fibrillation in a patient with mitral stenosis is accompanied by decompensation, primary treatment aimed at slowing the ventricular rhythm. As already mentioned, beta-adrenoblokagora, verapamil or diltiazem can be drugs of choice. It is also possible to use digoxin, however, the narrow therapeutic interval and the worst compared with beta-blockers the ability to prevent an increase in rhythm during exercise limit its use. Electrical cardioversion is also of limited use in persistent atrial fibrillation, since without the surgical treatment of atrial fibrillation the likelihood of a relapse is very high.

[63], [64], [65],

Surgical treatment of mitral stenosis

The main method of treating mitral stenosis is surgical, as there is currently no medical treatment that can slow the progression of stenosis.

Patients with more severe symptoms or signs of pulmonary arterial hypertension need valvulotomy, commissurotomy, or valve replacement.

The selection procedure is percutaneous balloon mitral valvuloplasty. This is the main method of surgical treatment of mitral stenosis. In addition, open commissurotomy and mitral valve replacement are used.

Percutaneous balloon valvulotomy is the preferred method for young patients; older patients who cannot undergo more invasive operations, and patients without pronounced valve calcification, subvalvular deformity, blood clots in the left atrium or significant mitral regurgitation. In this procedure, under echocardiographic control, the balloon is passed through the interatrial septum from the right to the left atrium and inflated to separate the connected mitral valve. Results are comparable to the effectiveness of more invasive operations. Complications are rare and include mitral regurgitation, embolism, left ventricular perforation, and atrial septal defect, which is likely to persist if the pressure difference between the atria is large.

Percutaneous balloon mitral valvuloplasty is shown to the following groups of patients with a mitral orifice of less than 1.5 cm ² :

• decompensated patients with favorable characteristics for percutaneous mitral valvuloplasty (class I, level of evidence B);
• decompensated patients with contraindications to surgical treatment or high operational risk (class I, level of evidence! And C);
• in case of planned primary surgical correction of the defect in patients with inappropriate valve morphology, but with satisfactory clinical characteristics (class IIa, level of evidence C);
• “Asymptomatic” patients with suitable morphological and clinical characteristics, high risk of thromboembolic complications or high risk of decompensation of hemodynamic parameters;
• with embolic complications in history (class IIa, level of evidence C);
• with the phenomenon of spontaneous echo contrast in the left atrium (class IIa, level of evidence C);
• with persistent or paroxysmal atrial fibrillation (class IIa, level of evidence C);
• with a systolic pressure in the pulmonary artery of more than 50 mm Hg. (class IIa, level of evidence C);
• if necessary, large non-cardiac surgery (class IIa, level of evidence C);
• in the case of pregnancy planning (class IIa, level of evidence C).

Suitable characteristics for percutaneous mitral valvuloplasty - no signs listed below:

• clinical: advanced age, history of comissurotomy, IV functional class of heart failure, atrial fibrillation, severe pulmonary hypertension;
• morphological: calcification of the mitral valve of any degree, assessed by fluorography, a very small area of the mitral valve, severe tricuspid regurgitation.

Patients with severe damage to the subvalvular apparatus, valve calcification or blood clots in the left atrium may be candidates for a commissurotomy, in which the connected mitral valve leaves are separated using an expander through the left atrium and the left ventricle (closed commissurotomy), or manually (an open commissure) Both operations require thoracotomy. The choice depends on the surgical situation, the degree of fibrosis and calcification.

Plastic surgery (open commissurotomy) or mitral valve replacement is performed according to the following indications of class I.

In the presence of heart failure III-IVFC and moderate or severe mitral stenosis in cases where:

• it is impossible to perform mitral balloon valvuloplasty;
• mitral balloon valvuloplasty is contraindicated in connection with a thrombus in the left atrium, despite the use of anticoagulants, or in connection with concomitant moderate or severe mitral regurgitation;
• valve morphology is not suitable for mitral balloon valvuloplasty.

With moderate or severe mitral stenosis and concomitant moderate or severe mitral regurgitation (valve prosthesis is indicated, if plasty is not possible).

Prosthetic valve - an extreme measure. It is prescribed to patients with mitral valve area <1.5 cm ², moderate or severe symptomatology and valve pathology (for example, fibrosis), which prevents the use of other methods.

Mitral valve replacement is advisable (class IIa indications) in severe mitral stenosis and severe pulmonary hypertension (systolic pressure in the pulmonary artery is more than 60 mmHg), symptoms of heart failure I-II FC, if mitral balloon valvuloplasty or mitral valve plasty are not expected Patients with mitral stenosis who do not have symptoms of decompensation should be examined annually. Examination includes the collection of complaints, anamnesis, examination, chest X-ray and ECG. If the patient's condition has changed in the previous period or according to the results of the previous examination there is severe mitral stenosis, echoCG is indicated. In all other cases, the annual echocardiogram is optional. If the patient complains of palpitations, it is recommended to conduct daily (Holter) ECG monitoring to detect paroxysms of atrial fibrillation.

In pregnancy, patients with mild and moderate stenosis can only receive medication. The use of diuretics and beta-blockers is safe. If anticoagulant treatment is necessary, patients are prescribed heparin injections, as warfarin is contraindicated.

[66], [67], [68], [69], [70], [71],

Prevention

The most important question of tactics for further management of patients with mitral stenosis - prevention of recurrence of rheumatic fever with penicillin drugs of prolonged action is prescribed for life, as well as all patients after surgical correction of the defect (including for the prevention of infective endocarditis). Benzathine benzylpenicillin is prescribed in a dose of 2.4 million IU to adults and 1.2 million IU to children intramuscularly 1 time per month.

For all patients with mitral stenosis, secondary prevention of recurrence of rheumatic fever is indicated. In addition, prevention of infective endocarditis is shown to all patients.

Patients without clinical manifestations need only prevention of recurrent rheumatic fever [for example, intramuscular injections of benzylpenicillin (penicillin G sodium sterile) 1.2 million IU every 3 or 4 weeks] until the age of 25-30 years and prevention of endocarditis before risky procedures.

[72], [73], [74], [75]

Forecast

The natural course of mitral stenosis may be different, but the time interval between the onset of symptoms and severe disability is approximately 7-9 years. The result of treatment depends on the patient's age, functional status, pulmonary arterial hypertension and the degree of atrial fibrillation. Valvulotomy and commissurotomy results are equivalent, both methods allow to restore the functioning of the valve in 95% of patients. However, over time, the functions deteriorate in most patients, and many need to be repeated. The risk factors for death are atrial fibrillation and pulmonary hypertension. The cause of death is usually heart failure or pulmonary or cerebrovascular embolism.

Mitral stenosis usually progresses slowly and proceeds with a long period of compensation. More than 80% of patients survive for 10 years in the absence of symptoms or moderately severe signs of CHF (I-II FC by NUNA). The 10-year survival rate of decompensated and non-operated patients is significantly worse and does not exceed 15%. In the formation of severe pulmonary hypertension, the average survival period does not exceed 3 years.

[76]