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Physical examination

Palpation. The apex impulse in mitral stenosis is most often normal or reduced, which reflects normal LV function. In the left lateral position, diastolic tremor can be detected. With the development of pulmonary hypertension, a cardiac impulse is detected along the right border of the sternum.

Auscultation. There are auscultatory signs characteristic of mitral stenosis:

• intensified (popping) sound I, the intensity of which decreases as the stenosis progresses;
• mitral valve opening tone (disappears with valve calcification);
• diastolic murmur with a maximum at the apex (mesodiastolic, presystolic, pandiastolic), which must be listened to in the left lateral position.

With the development of severe decompensation of heart failure, dacies mitralis is determined (bluish-pink blush on the cheeks, caused by a decrease in ejection fraction, systemic vasoconstriction and right ventricular heart failure), epigastric pulsation and signs of right ventricular heart failure (swelling in the legs, enlarged liver, swelling of the veins of the neck, etc. .)

Laboratory research

Laboratory findings are nonspecific.

Instrumental studies

Electrocardiography. There are several signs characteristic of mitral stenosis:

• the appearance of P-mitrale (wide, jagged P wave in the second standard lead);
• deviation of the electrical axis of the heart to the right, especially with the development of pulmonary hypertension;
• myocardial hypertrophy of the right (with isolated mitral stenosis) and left (in combination with mitral insufficiency) ventricles.

Chest X-ray. An increase in the LA shadow and a posterior displacement of the esophagus are detected (on a lateral image with barium contrast). The method was considered the “gold standard” for diagnosing mitral stenosis before the advent of echocardiography, but is currently not used. The LV shadow with isolated mitral stenosis does not change; when combined with mitral insufficiency and progression of the defect, as well as in the presence of pulmonary hypertension, the trunk of the pulmonary artery is expanded, and the waist of the heart is smoothed.

Echocardiography

To diagnose mitral stenosis, two-dimensional, Doppler, stress and transesophageal echocardiography is performed.

• Two-dimensional echocardiography. This is the method of choice for diagnosing mitral stenosis. It allows you to assess the mobility of the leaflets, the severity of commissure fusion, fibrosis and calcification, and the presence of subvalvular adhesions (Fig. 1 and 2). EchoCG data is extremely important for the subsequent selection of timing and type of surgical treatment.
• Doppler echocardiography. The severity of stenosis is assessed using Doppler ultrasound. The average transmitral pressure gradient and mitral valve area can be determined quite accurately using the constant wave technique (Fig. 3). Assessing the degree of pulmonary hypertension, as well as concomitant mitral and aortic regurgitation, is of great importance.
• Stress EchoCG . Additional information can be obtained using this stress test by recording transmitral and tricuspid blood flow. With mitral valve area<1,5 см² и градиенте давления >50 mmHg (after loading), it is necessary to consider performing balloon mitral valvuloplasty.
• Transesophageal echocardiography. Spontaneous echo contrast during the study is an independent risk factor for embolic complications in patients with mitral stenosis. This method makes it possible to clarify the question of the presence or absence of an LA thrombus and to determine the degree of mitral regurgitation during planned balloon mitral valvuloplasty. In addition, it allows you to accurately assess the condition of the valve apparatus, the severity of changes in subvalvular structures and the likelihood of restenosis.

Rice. 1. Mitral stenosis: unidirectional diastolic movement of the mitral valve leaflets; in the four-chamber position, shortening of the posterior leaflet of the mitral valve, marginal thickening of both leaflets, dome-shaped deflection of the anterior leaflet of the mitral valve (patient S., 52 years old; M-modal study)

Rice. 2. Mitral stenosis: parasternal short axis of the LV at the level of the mitral valve, diastole; planimetric measurement of the area of ​​the mitral valve opening (patient P., 54 years old; A1 - area of ​​the mitral opening)

Rice. 3. Combined mitral disease with predominant stenosis: pulsed Doppler study of transmitral blood flow on the mitral valve from the apical four-chamber position; peak pressure gradient across the mitral valve 10.8 mm Hg, mean pressure gradient 5.0 mm Hg. (patient T., 43 years old).

Catheterization of the heart and great vessels. This research is carried out in cases where surgical intervention is planned, and the data from non-invasive tests do not give a clear result. To directly measure pressure in the LA and LV, transseptal catheterization is required, which is accompanied by an unjustified risk. An indirect method for measuring LA pressure is to determine the pulmonary artery wedge pressure.

Differential diagnosis

With a thorough examination, the diagnosis of mitral stenosis is usually beyond doubt. Differential diagnostic signs of mitral stenosis and other heart defects detected during physical examination are presented in Table. 1.

Mitral stenosis is also differentiated from the following diseases:

• LA myxoma;
• other valve defects (mitral regurgitation, tricuspid valve stenosis);
• ASD;
• pulmonary vein stenosis;
• congenital mitral stenosis.

Table 1

Differential diagnosis of heart defects according to physical examination

Vice	Noise	I tone	II tone	Other signs	Diagnostic tests
Aortic stenosis Mitral stenosis Aortic insufficiency Mitral regurgitation Mitral valve prolapse	Mid- or late-systolic; in case of severe stenosis may be silent or absent Diastolic, with pre-systolic amplification Blowing, diastolic Holo-systolic Medium or late systolic	Not changed Loud, "clapping" Weakened Weakened Not changed	Paradoxical split Not changed Not changed Not changed or split Not changed	Pulse on sleepy arteries slowed down and weakened; can be III and IV tone Click open mitral valve High pulse blood pressure, systolic hypertension There may be a III tone; The pulse in the carotid arteries is not changed Mid-systolic click	After execution Valsalva maneuver noise becomes quiet Noise intensifies after short-term physical activity Noise intensifies at squats Noise intensifies after the test Valsalva Noise intensifies in position standing

1). “Mitral” P wave – more than 0.12 s, double-humped in leads I, II, aVL, V 5, V 6. 2). Deep negative phase in lead V 1. 3). In pulmonary hypertension - deviation of the electrical axis of the heart to the right and signs of right ventricular hypertrophy (complexes like R, Rs, qR in the right chest leads and complexes like RS, rS in the left chest leads).

Signs of right ventricular hypertrophy ECG: high wave R in the right chest leads and deep S in left chest leads (ratio R:S in lead V1 more than 1); deviation of the electrical axis of the heart to the right; decreased ST segment; negative wave T in right chest leads.

1. deviation of the electrical axis of the heart to the right in combination with depression of the ST segment and a change in the T wave in II, III, avF in the form of biphasic (+-) or negativity

2. In the right chest leads, the R wave increases (R/S is greater than 1.0), and in the left chest leads the S wave increases (R/S is less than 1.0)

EXAMINATION CARD No. 4

1. Manifestations of exacerbation of chronic coronary heart disease.

Exacerbation of ischemic heart disease manifests itself as angina pectoris. Clinic: pain syndrome - substernal pain that occurs during exercise, stress, heavy food intake, lasting 1-15 minutes, squeezing, pressing in nature, radiating to the left arm, lower jaw; associated symptoms - nausea, vomiting, sweating, shortness of breath, fatigue, tachycardia, increased blood pressure. Pallor and immobility are noted. Laboratory data: ECG - ST segment depression, the appearance of ST depression at a heart rate of more than 120, ventricular tachycardia. Myocardial infarction: pain lasting more than 15-20 minutes, not relieved by nitroglycerin, shortness of breath (up to pulmonary edema), sweating, nausea, abdominal pain, dizziness, episodes of loss of consciousness, a sharp decrease in blood pressure, arrhythmias, a decrease in heart rate to 30-40. ECG signs: the appearance of new Q waves more than 30 ms wide and more than 2 mm deep, complete blockade of the left bundle branch. Serum markers: CK (MB-CK), LDH, myoglobin, troponins.

2. Stigma of alcoholism in liver cirrhosis.

Facies alcoholica – puffy face, dilated venous network on the skin of the face, mumps, injection of blood vessels of the sclera and conjunctiva; telangiectasia, spider veins, gynecomastia, palmar erythema. Dupietren's contracture, red nose.

3. Treatment of non-insulin-dependent diabetes mellitus.

Fat-restricted diet. Antihyperglycemic drugs (increasing tissue sensitivity to insulin: manninil, glyurinorm). It is necessary to compensate for diabetes: normal glycemia during the day, elimination of glucsuria, normalization of lipid levels in the blood. Diet. Isocaloric, 4-5 times, strictly distributed consumption of carbohydrates, exclusion of easily digestible carbohydrates, sufficient amount of fiber, 40-50% fats of vegetable origin. 60% carbon-24% fat-16% protein., vitamins A, C, B1, B2, PP . Sugar substitutes – sorbitol, xylitol, aspartame. + Herbal medicine: peas, beans, arfazetine. Physical activity is contraindicated for retinopathy and nephropathy. Sugar-lowering agents - sulfonamides. They increase the number of tissue insulin receptors, increase sensitivity to endogenous insulin, stimulate the activity of β-cells themselves, and inhibit α-cells. 1st generation. Chlorpropamide, butamide, cyclamide - no more than 2 g/day, 2nd generation. Glibenclamide, glipizide. 5-20 mg/day. Biguanides. Glybutide, metformin. 2-3 tablets/day, 0.5 g each. They act extrapancreatically, potentiate the effect at the receptor level, increase permeability to glucose, enhance anaerobic glycolysis, increasing its utilization by muscles, reduce the absorption of glucose by the intestine, reduce gluconeogenesis, increase glycogen, activate lipolysis .

4. Clinical and laboratory signs of nephritis activity.

Oliguria, proteinuria, renal hematuria, arterial hypertension (diastolic), edema. Muscle cramps, renal eclampsia, acute renal failure, nausea, vomiting.

5. ECG signs of atrioventricular block.

I degree: prolongation of the interval P-R (P-Q) more than 200 ms due to a slowdown in impulse conduction through the AV junction. Causes of first degree AV block: increased tone of the parasympathetic nervous system, taking drugs (cardiac glycosides, beta-blockers, verapamil, diltiazem), lesions of the conduction system (fibrosis, myocarditis).

II degree: 1st type (Mobitza I,) characterized by periodicity Wenckebach - interval extension P-R from cardiac cycle to cycle until the cessation of impulse conduction to the ventricles and loss of the complex QRS. The reasons are the same. 2nd type (Mobitsa II) characterized by sudden loss of the complex QRS without previous prolongation of the interval P-R. The block usually occurs below the AV junction. Causes: myocardial infarction of the lower wall of the left ventricle, fibrosis of the conduction system of the heart (disease Leva), surgical interventions on the heart. Usually tends to progress to third degree AV block.

Ill degree: absence of impulse conduction to the ventricles. The rhythm is set from the centers of automatism of the lower order - the ventricles. The ventricular contraction rate is usually 35-50 per minute. Dizziness and fainting are possible as a result of deterioration of cerebral circulation (attacks Morgagni-Adams-Stokes).

First degree blockade according to ECG in the form of interval prolongation PQ up to 0.21 s or more. In this case, the atrial impulses reach the ventricles, the rhythm remains correct. Second degree atrioventricular block is characterized by the loss of individual ventricular complexes due to the fact that the impulse from the atria is not conducted to the ventricles. There are 2 types of this blockade: type I - Wenckebach type, Mobitz type I, characterized by a progressive lengthening of the interval PQ in a series of 3-4 cycles. In this case, the interval PQ may lengthen from the normal 0.18 s to 0.21 s in the next cycle and then to 0.27 s, while the next impulse is not carried to the ventricles and their contraction falls out. Such an increase in the interval PQ before the loss of the ventricular complex may be natural (Wenckebach periods). With atrioventricular blockade type II - Mobitz type II, interval prolongation PQ before the prolapse, the ventricular complex is not observed, and the prolapse can be both regular and irregular. If atrioventricular blockade is recorded with 2"L, then attributing it to one type or another is impossible.

Atrioventricular block of the third degree (complete atrioventricular block) is characterized by the fact that atrial impulses are not conducted, and the activity of the ventricles is supported by the rhythm emanating from the conduction system. The atria and ventricles are excited in a rhythm independent of each other. ECG shows waves R at regular intervals and independently of them complexes QRST(usually occurring more rarely) in the correct rhythm.

6. Pulmonary hypertension. Reasons. Clinic. Instrumental research methods.

An increase in mean blood pressure in the pulmonary artery of more than 20 mm Hg. Art. at rest and more than 30 mm Hg. Art. under load. Causes: Mitral valve defects, left ventricular insufficiency, left atrial myxoma, compression of the pulmonary veins, patent ductus arteriosus, chronic alveolar hypoxia (chronic lung diseases, stay in high mountains), pulmonary emphysema, chronic destructive lung diseases. When the cause is not clear - primary pulmonary hypertension. Clinic: shortness of breath (present at rest, worsens with little physical activity, persists in a sitting position), fatigue, dry (non-productive) cough, chest pain (due to dilatation of the pulmonary artery trunk and right ventricular myocardial ischemia), swelling of the legs, pain in the right hypochondrium (due to liver enlargement), the appearance of hoarseness in patients with pulmonary hypertension due to compression of the recurrent laryngeal nerve by the dilated trunk of the pulmonary artery, syncope during physical activity, because the right ventricle is not able to increase cardiac output adequately to the demands increased during exercise. Examination: cyanosis (peripheral vasodilation as a result of hypercapnia, patients' hands are usually warm). Pulsations: in the epigastric region - the hypertrophied right ventricle, in the second intercostal space to the left of the sternum - the trunk of the pulmonary artery. Swelling of the neck veins both during inhalation and exhalation. Peripheral edema and hepatomegaly. Auscultation: systolic “click” and accent of the II tone over the pulmonary artery, fixed splitting of the II tone, systolic ejection murmur in the 11th intercostal space to the left of the sternum, soft diastolic murmur of pulmonary artery valve insufficiency, systolic murmur in the projection of the tricuspid valve. X-ray: dilation of the pulmonary artery trunk and roots of the lungs, dilation of the right descending branch of the pulmonary artery more than 16-20 mm. ECG: P-pulmonale(high prong R in leads II, III, aVF, Vi), deviation of the electrical axis of the heart to the right, signs of right ventricular hypertrophy (high teeth R in leads Vi-z and deep teeth S in leads Vs-e)" signs of blockade of the right leg of the Fox bundle. EchoCG: dilatation of the RA and RV, thickening of the RV wall (more than 5-6 mm). Catheterization of the cardiac cavities: increased pressure in the pulmonary artery, pulmonary artery wedge pressure is low or normal.

Mitral stenosis is a heart defect in which the left atrioventricular orifice narrows, thereby impairing the function of the muscle. In the initial stages, the defect does not cause inconvenience to the patient, however, it can subsequently lead to serious complications.

Features of the disease

Most often, mitral stenosis is found in women 40-60 years old. In children, the congenital form of the defect is extremely rare: approximately 0.2% of all defects. Symptoms are the same for all ages.

Often the disease does not cause discomfort to the patient, however, you can become pregnant with it only if the opening of the mitral valve is larger than 1.6 cm 2 in area. Otherwise, the patient is advised to terminate the pregnancy.

Now let's talk about the types and degrees of mitral valve stenosis.

The following video will tell you in great detail about the features of mitral stenosis:

Forms and degrees

Mitral stenosis is distinguished by the anatomical shape of the affected valve, degree and stage. The form could be:

1. loop-shaped (doctors call it a “jacket loop”;
2. funnel-shaped (“fish mouth”);
3. in the form of a double narrowing;

In doctoral practice, there are 4 degrees of the disease, depending on the area of ​​narrowing of the atrioventricular opening:

• The first or minor, when the area is less than 3 cm 2.
• Second or moderate, when the area fluctuates between 2.3-2.9 cm 2.
• Third or pronounced, the area varies between 1.7-2.2 cm 2.
• Fourth, critical. The hole narrows to 1-1.6 cm2.

There are several classifications of the defect by stages, however, in Russia, the most popular is according to A. N. Bakulev, which distributes the defect into 5 stages:

• Full compensation of blood circulation. There are no symptoms, the disease is detected during examination. The mitral orifice area is 3-4 cm 2.
• Relative circulatory insufficiency. Symptoms are mild, the patient complains of shortness of breath, hypertension, and slightly increased venous pressure. The mitral orifice is 2 cm 2, and the left atrium increases in size to 5 cm.
• Severe deficiency. The symptoms are pronounced, the size of the heart and liver increases significantly. The mitral orifice is 1-1.5 cm 2, and the left atrium is > 5 cm in size.
• Severe insufficiency with stagnation in the large circle. It is expressed by a strong enlargement of the liver and heart, high venous pressure and other signs. The mitral orifice narrows, becomes less than 1 cm 2, the left atrium becomes even larger.
• The fifth stage corresponds to the third, terminal, stage of failure according to the classification of V. Kh. Vasilenko. The heart and liver are significantly enlarged, ascites and swelling appear. The mitral orifice becomes dangerously narrowed, and the left atrium enlarges.

Mitral stenosis diagram

Causes

The most common cause of mitral stenosis is rheumatism. In children, the defect appears due to congenital pathologies. Other causes of the disease include:

• blood clots;
• growths that partially narrow the mitral orifice;
• autoimmune diseases;

Rarely, the appearance of stenosis can be influenced by external factors, for example, uncontrolled medication use. Let's now look at the main signs and symptoms of mitral valve stenosis.

Symptoms

Symptoms of mitral stenosis do not appear in any way at the first stage. As the disease progresses, patients note:

1. shortness of breath, which in the later stages occurs even at rest;
2. cough streaked with blood;
3. tachycardia;
4. cardiac asthma;
5. pain in the heart area;
6. cyanosis of the lips, tip of the nose;
7. mitral flush;
8. cardiac hump (protrusion of the sternum on the left);

Signs of pathology depend on the stage and extent of the disease. Thus, compression of the recurrent nerve, angina pectoris, hepatomegaly, peripheral edema, and edema of the cavities may be observed. Patients often suffer from bronchopneumonia and lobar pneumonia.

Now let's look at methods for diagnosing mitral stenosis.

The following video will tell you in more detail about the symptoms of mitral valve stenosis:

Diagnostics

Primary diagnosis consists of collecting a history of complaints and palpation, which reveals presystolic tremor. This and auscultation help detect mitral stenosis in more than half of patients.

Auscultation usually reveals a weakening of the first sound at the apex and a systolic murmur behind the first sound, which has a decreasing or constant character. The localization of listening to this noise extends to the armpits and rarely to the subscapularis, sometimes it can be carried out towards the sternum. The volume of the noise can be different, for example, with severe insufficiency, it is soft.

After making a preliminary diagnosis, the doctor prescribes:

• Phonocardiography, which allows you to trace how the detected noise relates to the phase of the heart cycle.
• An ECG revealing hypertrophy of the heart, disturbances in its rhythm, blockade of the His bundle in the area of ​​the right leg.
• EchoGK, detecting the area of ​​the mitral orifice, an increase in the size of the left atrium. Transesophageal echocardiography helps to exclude vegetations and valve calcification and identify blood clots.
• X-ray is necessary to detect bulging of the pulmonary artery arch, atria and ventricles, expansion of the shadows of veins and other signs of the disease.
• Probing of the heart cavities, which is rarely used, helps to detect increased pressure in the right chambers of the heart.

If the patient is subsequently referred for valve replacement, he will need to undergo left ventriculography, atriography and coronary angiography. Additional consultation with specialists, for example, a therapist or rheumatologist, is also possible.

Mitral valve stenosis requires treatment, the methods of which we will discuss further.

Treatment

The main treatment for mitral stenosis is surgical, since other measures only help to stabilize the patient’s condition.

Surgery is not required for the first and fifth stages. In the first case, there is no need for it, because the disease does not interfere with the patient, but in the second, it can be dangerous for his life.

Therapeutic

This technique is based on monitoring the patient’s condition. Since the disease can develop, the patient should undergo a full examination and consultation with a cardiac surgeon every 6 months. Patients are also shown minimal stress on the heart, including avoiding stress and a low-cholesterol diet.

Medication

Drug therapy is aimed at preventing the causes of stenosis. The patient is prescribed:

• Antibiotics for the prevention of infective endocarditis.
• Diuretics and cardiac glycosides to relieve heart failure.
• Beta blocker to eliminate arrhythmia.

If the patient has experienced thromboembolism, he is prescribed antiplatelet agents and heparin subcutaneously.

Operation

If the heart is severely damaged, patients are prescribed its replacement using biological or artificial prostheses or open mitral commissurotomy. The last operation consists of dissecting the commissures and subvalvular adhesions, at which time the patient is connected to artificial circulation.

For young patients, it is especially important to perform this operation sparingly, which is called open mitral commissurotomy. During surgery, the mitral orifice is widened with a finger or instruments by dividing the adhesions.

Sometimes patients are prescribed percutaneous balloon dilatation. The operation is performed under X-ray or ultrasound. A balloon is inserted into the opening of the mitral valve, which is inflated, thereby separating the leaflets and eliminating the stenosis.

Disease prevention

Preventive measures are limited to treatment and prevention of relapses of rheumatism, focal sanitation of streptococcus. Patients should be observed by a cardiologist and rheumatologist every 6-12 months to exclude the progression of mitral stenosis.

It would be useful to follow the principles of a healthy lifestyle. Moderate and proper nutrition will help improve the body's immune abilities and the condition of the heart muscle.

Mitral stenosis and mitral regurgitation

According to statistics, it appears less frequently than mitral stenosis. The ratio of these pathologies in adults is approximately 1:10. According to Jonash's research in 1960, the ratio reached 1:20. Children suffer from mitral stenosis more often than adults.

A study of mitral regurgitation in patients who underwent commissurotomy showed that the defect occurs in approximately 35% of cases. Let's look at the possible complications of mitral stenosis.

Complications

If mitral stenosis is left untreated or diagnosed too late, the disease can lead to:

• . With this disease, the heart cannot pump blood normally.
• Expansion of the heart muscle. The condition develops due to the fact that with mitral stenosis, the left atrium is filled with blood. Over time, this leads to overflow of the right compartments.
• Atrial fibrillation. Due to the disease, the heart contracts chaotically.
• Thrombosis. Fibrillation leads to the formation of blood clots in the right atrium.
• Pulmonary edema, when plasma accumulates in the alveoli.

Since mitral stenosis affects hemodynamics, blood does not flow to the organs in a normal volume, which can affect their function.

The following video will tell you more about hemodynamics with mitral stenosis:

Forecast

Mitral stenosis tends to progress, so the five-year survival rate is 50%. If the patient undergoes surgery, his five-year survival rate increases to 90-95%. The probability of developing postoperative stenosis is 30%, so patients should be constantly monitored by a cardiac surgeon.

MITRAL STENOSIS

Stenosis of the left atrioventricular orifice

(Stenosis ostii atrioventricularis sinistra)

Mitral stenosis - common acquired heart defect. It can be isolated or combined with mitral valve insufficiency and damage to other valves.

Etiology. Almost always, mitral stenosis is a consequence of rheumatism and usually forms at a young age and more often in women.

Pathogenesis and changes in hemodynamics. In humans, the area of ​​the left atrioventricular opening fluctuates between 4-6 cm 2 and only when its area decreases to 1.5-1 cm 2 (critical area) do clear disturbances in intracardiac hemodynamics appear.

In most patients requiring surgical treatment, this value is 0.5-1 cm 2.

The narrowing of the mitral orifice serves as an obstacle to the expulsion of blood from the left atrium. Therefore, in order to ensure normal blood flow to the left ventricle, a number of compensatory mechanisms are activated. The pressure in the atrium cavity increases (from normal 5 mm to 20-25 mm Hg). This increase in pressure leads to an increase in the pressure gradient from the left atrium to the left ventricle, resulting in easier passage of blood through the narrowed mitral orifice. Left atrial systole lengthens and blood enters the left ventricle for a longer time. The increase in pressure in the left atrium and the lengthening of the systole of the left atrium initially compensate for the negative effect of the narrowed mitral orifice on intracardiac hemodynamics.

The progressive decrease in orifice area causes a further increase in pressure in the left atrium cavity, and this in turn leads to a retrograde increase in pressure in the pulmonary veins and capillaries. The pressure in the pulmonary artery also increases. The degree of its increase is proportional to the increase in pressure in the left atrium, and the normal gradient between them (20 mm Hg) usually remains unchanged. This method of increasing pressure in the pulmonary artery is passive, and the resulting pulmonary hypertension is called passive (retrograde, venous, postcapillary), since the pressure in the pulmonary vascular system increases first in the venous segment, and then in the arterial segment. Passive pulmonary hypertension is not high; the pressure in the pulmonary artery usually does not exceed 60 mmHg. Art. Nevertheless, already at this stage of development of mitral stenosis, hypertrophy of the right ventricle joins hypertrophy of the left atrium.

In 30% of patients, mostly young, an increase in pressure in the left atrium and pulmonary veins, due to irritation of baroreceptors, causes a reflex constriction of arterioles (Kitaev reflex). Functional narrowing of the pulmonary arterioles leads to a significant increase in pulmonary artery pressure, which can exceed 60 mmHg. Art. and reach 180-200 mm Hg. Art. Such pulmonary hypertension is called active (arterial, precapillary). With the development of active pulmonary hypertension, the pressure gradient between the pulmonary artery and the left atrium increases sharply. Under these conditions, the Kitaev reflex protects the pulmonary capillaries from excessive increases in pressure and sweating of the liquid part of the blood into the cavity of the alveoli. However, prolonged spasm of arterioles leads to proliferation of smooth muscles, thickening of the tunica media, narrowing of their lumen, and diffuse sclerotic changes in the branches of the pulmonary artery. Functional and then anatomical changes in the arterioles of the small circle create a so-called second barrier to blood flow. Activation of the second barrier increases the load on the right ventricle. A significant increase in pressure in the pulmonary artery and right ventricle makes it difficult to empty the right atrium. This is facilitated by a decrease in the ventricular cavity due to its hypertrophy (rigid walls of the ventricle, poorly relaxed in diastole). The difficulty of expelling blood from the right atrium causes an increase in pressure in its cavity and the development of hypertrophy of its myocardium.

Subsequently, weakening of the right ventricle occurs not only due to significant resistance in the pulmonary artery, but also as a result of the development of dystrophic and sclerotic changes in its myocardium. Incomplete emptying of the right ventricle during systole leads to an increase in diastolic pressure in its cavity. The developing dilatation of the right ventricle, causing relative tricuspid valve insufficiency, slightly reduces the pressure in the pulmonary artery, but the load on the right atrium increases. As a result, decompensation develops in the systemic circulation.

Clinical picture. On Stages of passive pulmonary hypertension include complaints of shortness of breath during exercise.

Increased blood flow to the heart during physical exertion causes capillary overflow (mitral stenosis prevents its normal outflow from the pulmonary circle) and impedes normal gas exchange. With a sharp rise in pressure in the capillaries, an attack of cardiac asthma may occur. Another complaint of patients at this stage is a cough, dry or with the release of a small amount of mucous sputum, often mixed with blood.

With high pulmonary hypertension, patients complain of rapidly occurring weakness, increased fatigue and palpitations. Much less often there are pains in the heart area that are aching or stabbing in nature, without a clear connection with physical activity. Only some patients experience typical angina attacks.

The appearance of patients with moderately severe circulatory disorders in the pulmonary circulation does not present any peculiarities.

However, with an increase in the degree of stenosis and an increase in symptoms of pulmonary hypertension, typical facies mitralis is observed; Against the background of pale skin, there is a sharply defined blush of the cheeks with a somewhat cyanotic tint, cyanosis of the lips and the tip of the nose. In patients with high pulmonary hypertension, cyanosis increases during physical activity and a grayish discoloration of the skin appears (“ashy” cyanosis).

At In a pronounced defect, there is a bulging of the heart area ("heart hump"), involving the lower region of the sternum, and pulsation in the epigastrium. These symptoms are associated with hypertrophy and dilatation of the right ventricle and with increased impacts on the anterior chest wall.

There is no apical impulse because the left ventricle is displaced by the hypertrophied right ventricle.

If, after preliminary physical exercise, the patient is placed on his left side, then by holding the breath at the height of exhalation at the apex of the heart or slightly lateral from it, by palpation with the palm of the hand, diastolic tremor (“cat purring”) can be determined, caused by low-frequency vibrations of the blood as it passes through the narrowed mitral hole.

Percussion of the heart reveals increased dullness upward due to the left atrial appendage and to the right due to the right atrium. There is no enlargement of the heart to the left.

Auscultation of the heart provides the most significant signs for diagnosis, since the detected phenomena are directly related to impaired blood flow through the mitral orifice and changes in the functioning of the mitral valve leaflets. Changes in tones with this defect come down to the following.

The first tone is strengthened (clapping). This depends on the fact that in the preceding diastole the left ventricle is not completely filled with blood and therefore contracts faster than usual, and the mitral valve leaflets at the time of contraction of the left ventricle are at a greater distance from the left venous opening and their movement with a greater amplitude produces a stronger jerky sound. The first flapping sound is heard only in the absence of gross deformations of the valves.

At the apex, and sometimes in the IV intercostal space to the left of the sternum, the opening tone of the mitral valve ("opening click") is heard, which is formed by the slight movement of the mitral valve leaflets at the beginning of diastole (protodiastole).

The opening tone of the mitral valve appears 0.03-0.11 s after the second sound. The shorter the interval between the second sound and the opening sound of the mitral valve, the greater the atrioventricular pressure gradient and the more pronounced the stenosis. The opening tone of the mitral valve does not disappear with atrial fibrillation.

The flapping 1st sound in combination with the 2nd tone and the opening tone of the mitral valve creates at the apex of the heart a three-part melody characteristic of this defect - the “quail rhythm”.

As a result of increased pressure in the pulmonary artery in the second intercostal space to the left of the sternum, an accent of the second tone is heard, often in combination with its bifurcation, due to the non-simultaneous closure of the pulmonary artery and aortic valves. The most characteristic auscultatory symptoms of mitral stenosis include diastolic murmur. Diastolic murmur can occur during various periods of diastole. At the beginning of diastole, following the opening tone (protodiastolic murmur), in the middle of diastole (mesodiastolic murmur), at the end of diastole (presystolic murmur).

Diastolic murmur is heard at the apex of the heart and, depending on the time of its appearance, has a different duration and different timbre.

Blood pressure usually does not change. In severe cases of mitral stenosis, atrial fibrillation occurs as a consequence of dilatation of the left atrium, dystrophic and sclerotic changes in its muscles.

X-ray examination. The purpose of an X-ray examination is to more accurately determine the enlargement of individual chambers of the heart and determine the condition of the small circle vessels.

When examining a patient in the anteroposterior projection, a smoothing of the “waist” of the heart is observed, sometimes a bulging of the third arch of the left contour of the heart due to an increase in the left atrium in the first oblique or left lateral projection. This part of the heart displaces the contrasted esophagus to the right and back. With mitral stenosis, the esophagus deviates along an arc of small radius (no more than 6 cm).

Tomography is used to determine the degree of left atrium enlargement.

In some cases (with high pulmonary hypertension), an increase in the second arch of the left contour is observed - bulging of the pulmonary artery arch. The right ventricle first enlarges upward due to hypertrophy of the outflow tract, then hypertrophy and dilatation of the inflow tract occurs. This leads to bulging to the right of the lower arch of the right contour of the heart, formed by the right atrium. Enlargement of the right ventricle is also manifested by a narrowing of the retrosternal space when examining the patient in oblique projections.

Changes in the pulmonary vessels are expressed by the expansion of the roots, which give a homogeneous shadow with blurred boundaries. Sometimes, with passive pulmonary hypertension, linear shadows extend from the roots in different directions from the periphery of the pulmonary fields.

With active (arterial) pulmonary hypertension, there is an expansion of the shadow of the roots of the lungs with clear contours due to bulging of the pulmonary artery arch and expansion of its branches. Since the small branches of the pulmonary artery are narrowed, a sudden break of the expanded branches is observed instead of their gradual transition into smaller branches - a symptom of “amputation” of the roots.

Electrocardiogram(ECG). The purpose of the electrocardiographic study is to identify hypertrophy of the left atrium and right ventricle, and to assess emerging heart rhythm disturbances.

Signs of left atrial hypertrophy are as follows:

1) the appearance of a two-apex P wave in leads I, aVL, V 4-6. In these leads, the second peak, caused by the excitation of the left atrium, exceeds the first, caused by the excitation of the right atrium;

2) in lead V 1 there is a sharp increase in amplitude and duration of the second phase of the P wave;

3) an increase in the time of internal deviation of the P wave by more than 0.06 s (the interval from the beginning of the P wave to its apex).

As the degree of hypertrophy of the left atrium increases, the amplitude of the P wave (especially its second part) increases, the P wave exceeds the normal duration - 0.10 s, and the time of internal deviation of the P wave increases to an even greater extent. With severe dilatation of the left atrium, the amplitude of the P wave can be significantly reduced.

There is no clear relationship between changes in the P wave and the degree of stenosis of the mitral orifice.

Signs of right ventricular hypertrophy:

1) deviation of the electrical axis of the heart to the right in combination with a shift in the S-T interval and a change in the T wave in leads aVF, III (less often II);

2) in the right chest leads the R wave increases, and in the left - S;

3) in the right precordial leads with right ventricular hypertrophy, the S-T interval shifts downward and a negative T wave appears.

ECG changes in the right precordial leads correlate with the severity of pulmonary hypertension. Sometimes an ECG reveals a complete block of the right bundle branch.

Phonocardiogram(FKG). At the apex of the heart, the first sound has a large amplitude of vibrations. The duration of the interval from the beginning of the second sound to the opening tone of the mitral valve (II -QS) ranges from 0.03 to 0.12 s, depending on the degree of stenosis. The Q-I sound interval lengthens as the pressure in the left atrium increases and reaches 0.08-0.12 s.

As a rule, various diastolic murmurs are recorded (presystolic, meso- and protodiastolic).

Diastolic (protodiastolic) murmur begins immediately after the “opening tone” or at some interval after this tone.

Presystolic murmur (presystolic component) usually turns into the first sound.

The value of PCG increases with atrial fibrillation, since auscultation does not allow the auscultated murmur to be attributed to one or another phase of the cardiac cycle.

Echocardiogram. Signs of mitral stenosis will be: a) unidirectional diastolic movement of the mitral valve leaflets; b) a pronounced decrease in the rate of early diastolic closure of the anterior mitral leaflet; c) reduction in the general excursion of the mitral valve movement; d) an increase in the size of the left atrium cavity.

Two-dimensional echocardiography can reveal: 1) a decrease in the area of ​​the mitral orifice (less than 3 cm 2); 2) an increase in the size of the left atrium with a normal left ventricle; 3) friendly movement of the mitral valve leaflets towards the IVS; 4) compaction (to the point of calcification) of the structures of the valve and fibrous ring.

Diagnostics. Among patient complaints and objective symptoms, one should distinguish between a group of signs caused by the presence of mitral stenosis itself ("direct" signs) and a group of signs caused by hemodynamic disorder in the systemic and pulmonary circulation ("indirect" signs).

If a defect is diagnosed based on “direct” signs, then the presence and severity of “indirect” signs characterize the severity of the disease.

“Direct” signs include valvular symptoms: a) flapping 1st sound; b) the tone of the mitral valve opening (“opening click”); c) diastolic murmur (during auscultation); d) diastolic tremor (palpation).

“Indirect” signs include three groups of symptoms.

1. Left atrial: a) radiological signs of left atrium enlargement; b) electrocardiographic syndrome of left atrial hypertrophy.

2. Pulmonary(as a consequence of stagnation in the small circle):

a) shortness of breath on exertion; b) cardiac asthma; c) bulging of the pulmonary artery trunk; d) expansion of the branches of the pulmonary artery.

3. Right ventricular(changes in the right heart due to pulmonary hypertension): a) pulsation in the epigastrium due to the right ventricle; b) radiological signs of enlargement of the right ventricle and right atrium; c) electrocardiographic syndrome of right ventricular hypertrophy (in some cases, right atrium); d) circulatory disorders in the systemic circle (right ventricular failure).

Flow. According to the evolution of hemodynamic disorders during mitral stenosis, 5 stages are distinguished (classification by A. N. Bakulev and E. A. Damir, 1955).

Stage I - complete compensation of the valve defect by the left atrium. Patients give the impression of completely healthy people and do not show any complaints. However, upon objective examination, direct signs of the defect are revealed, primarily auscultatory ones.

There are no “indirect” symptoms.

Stage II - signs of circulatory disorders in the pulmonary circle are detected only during physical activity.

Stage III - in the small circle there are pronounced signs of stagnation, in the large circle there are initial signs.

Stage IV - pronounced signs of stagnation in the systemic and pulmonary circulation, atrial fibrillation.

Stage V - “dystrophic”, corresponds to stage III of circulatory disorders according to the classification of N. D. Strazhesko and V. X. Vasilenko.

With the development of right ventricular failure, a decrease in the contractile function of the right ventricle can reduce the pressure in the pulmonary artery, which leads to some change in subjective sensations. Shortness of breath, hemoptysis, cough decrease, but complaints associated with stagnation in the systemic circulation appear: heaviness and dull pain in the right hypochondrium, swelling in the legs, oliguria, and later ascites. Significant expansion of the right ventricle causes the development of relative tricuspid valve insufficiency. In such patients, expansion of the heart to the right is observed (due to hypertrophy and dilatation of the right atrium), swelling and pulsation of the neck veins, sometimes a positive venous pulse, and a systolic murmur is heard at the base of the xiphoid process, increasing at the height of inspiration (Rivero-Corvallo symptom). With significant tricuspid regurgitation, there may be liver pulsation.

Complications of mitral stenosis caused by: 1) stagnation of blood in the small circle; 2) dilatation of the heart.

To the first group of complications include hemoptysis, cardiac asthma, high pulmonary hypertension (arterial), pulmonary aneurysm.

In patients with pulmonary hypertension, the ostium of the pulmonary artery may be distended, as a result of which the valve leaflets do not close and a diastolic murmur of relative pulmonary valve insufficiency appears (Graham-Still murmur). This gentle timbre, blowing protodiastolic noise is best heard along the left edge of the sternum with the epicenter of sound in the second intercostal space on the left.

To the second group of complications include heart rhythm disturbances in the form of atrial fibrillation or flutter, thromboembolic complications, symptoms of compression of the mediastinal organs (mediastinal syndrome).

With the development of atrial fibrillation, their active systole disappears. This can change the auscultatory symptoms of mitral stenosis: the presystolic murmur disappears, which is precisely due to the increased passage of blood through the narrowed mitral orifice under the influence of active atrial contraction.

Atrial fibrillation contributes to the formation of blood clots in the left atrium. Broken blood clots can be a source of embolism in the vessels of the extremities, kidneys, brain, and abdominal cavity. The source of thromboembolism of the vessels of the pulmonary circulation is phlebothrombosis of the veins of the lower extremities, developing in connection with congestion in the systemic circulation and low physical activity of patients. In the vessels of the small circle there may also be local thrombus formation, which is facilitated by local congestion.

A significant increase in the size of the left atrium sometimes leads to compression of the recurrent nerve located nearby and, as a result, the development of paralysis of the vocal cords and hoarseness (Horner's symptom).

Compression of the subclavian artery by the enlarged left atrium causes a decrease in pulse filling in the left radial artery (Popov's symptom).

Pressure on the sympathetic nerve can cause anisocoria.

Prognosis for mitral stenosis depends on the severity of the defect, the condition of the heart muscle, its contractility, the frequency of rheumatic attacks, and the magnitude of pulmonary hypertension.

With moderate degrees of stenosis and rare rheumatic attacks, patients can remain able to work for a long time.

Progressive stenosis of the mitral orifice and repeated attacks of rheumatic carditis lead to circulatory disorders. High pulmonary hypertension, thromboembolism, and atrial fibrillation aggravate circulatory disorders; in these conditions, the prognosis worsens, the ability to work is significantly reduced, up to complete loss.

Treatment. There are no specific methods of conservative treatment of patients with mitral stenosis. Circulatory failure is treated according to generally accepted symptoms: cardiac glycosides, diuretics, drugs that correct water-salt balance disorders and eliminate metabolic disorders in the myocardium, peripheral vasodilators, inhibitors are prescribed APF. With an active rheumatic process - antirheumatic drugs. The radical treatment method for this heart defect is mitral commissurotomy.

The operation is indicated for patients with severe mitral stenosis ("pure" or predominant) in the presence of symptoms that significantly limit the patient's physical activity and reduce ability to work. These are patients with stages II, III, IV according to A. N. Bakulev and E. A. Damir. At stage I of mitral stenosis, surgery is not indicated, since patients can lead an active lifestyle.

The operation is especially indicated for patients suffering from cardiac asthma and hemoptysis. The presence of thromboembolic complications in the systemic circle suggests thrombus formation in the left atrial appendage. Timely commissurotomy relieves such patients from repeated embolisms.

Atrial fibrillation is not a contraindication to surgery. Exacerbation of the rheumatic process serves as a relative contraindication: surgery should be postponed until the symptoms of exacerbation subside. It is possible only 2-3 months after normalization of activity indicators. It is impossible to delay sending patients with mitral stenosis for surgery, since wear of the myocardium, repeated rheumatic attacks, and the formation of an organic second barrier worsen the results of commissurotomy

Commissurotomy can be performed according to vital indications if the patient has severe pulmonary hypertension with attacks of cardiac asthma, hemoptysis and the development of pulmonary edema.

Concomitant mitral regurgitation, expressed to a slight degree, is not a contraindication to surgery, just like minor aortic valve insufficiency or aortic stenosis.

When mitral stenosis is combined with severe mitral insufficiency, aortic insufficiency, or organic insufficiency of the tricuspid valve, commissurotomy is contraindicated.

In some of these patients, implantation of an artificial mitral valve is possible.

One of the main conditions for the proper functioning of the human heart is the flow of blood through the heart chambers and vessels in one direction. This is ensured due to the anatomical structure of the heart itself and the presence of valves in it, which act as a kind of “door” that opens only in one direction.

If one or another heart valve ceases to perform its function as a “regulator” of blood flow, a heart defect called “valvular stenosis” occurs. Among such defects, the most common is mitral valve stenosis, which can be acquired, therefore we will consider the pathogenesis of this syndrome, what is the insufficiency of the heart valve in such a pathology.

The mechanism of pathology is as follows:

ICD-10 code

According to the International Classification of Diseases, pathology has the following codes:

• Mitral stenosis of rheumatic etiology - I05.0;
• Non-rheumatic stenosis - I34.2.

Statistics

Mitral stenosis is a commonly diagnosed acquired defect of the mitral heart valve.:

• the disease is detected in approximately 90% of all patients with;
• 1 person out of 50-80 thousand suffers from this disease;
• in 40% of cases this is an isolated pathology, in the rest it is combined with other anatomical defects in the structure of the heart;
• the risk of clinical manifestations of the disease increases with age: the most “dangerous” age is 40-60 years;
• women are more predisposed to this disease than men: among patients with this defect, 75% of the fairer sex.

Classification of types and degrees

The disease is classified according to 2 bases. As the area of ​​the mitral orifice decreases There are 5 successively worsening degrees of the disease:

Depending on the type of anatomical narrowing of the valve opening, the following forms of mitral stenosis are distinguished:

• "jacket loop" type– the valve leaflets are thickened and partially fused to each other, easily separated during surgery;
• fish mouth type– as a result of the proliferation of connective tissue, the valve opening becomes narrow and funnel-shaped, such a defect is more difficult to surgically correct.

Stages of the disease (according to A.N. Bakulev):

• compensatory– the degree of narrowing is moderate, the defect is compensated by hypertrophy of the heart, there are practically no complaints;
• subcompensatory– the narrowing of the hole progresses, compensatory mechanisms begin to exhaust themselves, the first symptoms of trouble appear;
• decompensation– severe right ventricular failure and pulmonary hypertension, which quickly worsen;
• terminal– stage of irreversible changes with fatal outcome.

Valve Disease Clinic

The clinical picture depends on the stage and degree of narrowing of the bicuspid valve. With a narrowing of up to 3-4 sq.cm, there are no complaints for a long time; with critical stenosis (less than 1 sq.cm), complaints are always present.

The appearance of a patient with mitral stenosis is characterized by:

1. Forced position - sitting with emphasis on the palms.
2. "Mitral butterfly" on the face.
3. Noisy heavy breathing.
4. Marked weakness.

Due to pulmonary hypertension, patients complain of shortness of breath, which gradually becomes constant. A decrease in cardiac output leads to cardialgia (non-anginal pain in the heart). As a rule, the pain is localized at the apex, accompanied by a feeling of interruptions, freezing or uneven heartbeat.

In the lying position, the patient's condition worsens. A characteristic symptom of “night apnea” is sudden suffocation during sleep.. Patients sleep on a high headboard and suffer from insomnia.

In the stage of decompensation (right ventricular dilatation), cardiogenic edema develops. Swelling increases in the evening, is localized in the lower extremities and has an ascending nature. In the right hypochondrium, nagging pain appears due to stretching of the liver capsule, which protrudes from under the edge of the costal arch. Fluid accumulates in the abdominal cavity (ascites), and the subcutaneous veins of the abdomen dilate (symptom of the “head of the jellyfish”).

With dilatation of the right ventricle, visible pulsation develops in the area of ​​the costal angle(heartbeat), hemoptysis and pulmonary edema.

Auscultatory signs

When listening to the heart, a complex of specific symptoms that make up the auscultatory picture is revealed for mitral stenosis:

• The opening tone of the bicuspid valve is heard before the first sound; with mitral stenosis, it is caused by the splitting of the 2nd tone into two components.
• Clapping first tone.
• At the second point of auscultation there is an accentuated second tone.
• At the apex of the heart there is a diastolic murmur, which intensifies after test physical exercise in the presence of mitral valve stenosis.
• Extrasystoles and tachycardia may be heard.

Three audible tones form a specific symptom, detected only in this disease - “quail rhythm”. With developing pulmonary edema, moist fine bubbling rales are heard in the lower parts of the pulmonary fields.

Auscultation with mitral valve stenosis can show disorders as they arise.

More about the auscultatory picture of mitral valve stenosis in this video:

Description of hemodynamics

The disease refers to defects with enrichment of pulmonary circulation. The narrowing of the valve opening causes an increase in pressure first in the left atrium, then in the pulmonary veins. The atrium enlarges and dilates, its contractility decreases.

Develops, which causes contraction of the muscle cells of the capillaries of the lungs. In response to microvascular spasm, the pressure in the pulmonary trunk system and the right (venous) ventricle increases. The right ventricle expands and gradually dilates. Venous stagnation develops in the systemic circulation.

Hypoxia caused by a lack of arterial blood first manifests itself as acrocyanosis. Subsequently, cyanosis becomes universal (affects all skin and mucous membranes).

This video describes the hemodynamics that are characteristic of mitral valve stenosis:

Etiology and risk factors

The causes of the disease in most cases are:

• rheumatic diseases (rheumatism, systemic lupus erythematosus, scleroderma) – 80-90% of cases;
• – 6%;
• infectious diseases (angina, syphilis and other sexually transmitted diseases, sepsis, tick-borne diseases) – 6%;
• heart muscle injuries;
• valve calcification of non-rheumatic nature;
• heart tumors.

Thus, it can be seen that there is rheumatic and non-rheumatic mitral valve stenosis.

Risk factors are the frequency and severity of infectious diseases, inadequate treatment of autoimmune and other provoking diseases, genetic predisposition (pathology is transmitted through the maternal line in 25% of cases).

Symptoms of pathology

Manifestations of the defect are divided into pulmonary, cardiac and general.

General symptoms:

1. Decreased performance.
2. Insomnia.
3. Weakness.
4. Forced sitting position.
5. Pale skin combined with cyanosis.

Pulmonary symptoms:

• Dyspnea.
• Difficulty noisy exhalation.
• Cough for no apparent reason.
• Tendency to respiratory diseases.
• In later stages - hemoptysis.

Heart symptoms:

• Frequent heartbeat.
• Cardialgia.
• Reduced blood pressure.
• Ascending edema of the lower extremities.

Features of the skin

The first manifestation of the defect is pale skin. As hypoxia progresses, acrocyanosis develops—blue discoloration of the lips, earlobes, and fingertips. In the stage of decompensation, cyanosis becomes widespread, and bluish discoloration of the mucous membranes occurs.

A specific symptom is characteristic - “mitral face” - pronounced pallor of the face combined with a crimson blush on the cheeks and cyanosis of the lips. Despite the presence of these symptoms, a diagnosis is not made based on skin changes.

Causes of hemoptysis

The appearance of blood streaks in the sputum is due to cardiogenic pulmonary edema.

Developing pulmonary hypertension underlies spasm of microvasculature vessels - capillaries, arterioles and venules.

Microvascular spasm further aggravates hypertension, resulting in damage to the vascular walls. Through damaged vessels, blood begins to flow into the lung tissue. During the process of self-cleansing of the lungs, blood mixes with mucus and is coughed up by the patient (hemoptysis).

Heart rhythm disturbance

The disease is characterized by early onset of arrhythmia. Rhythm disturbances are caused by hypertrophy of the venous ventricle and left atrium, as a result of which the heart chambers cannot contract simultaneously. The following types of arrhythmias are distinguished:

1. Atrial fibrillation.
2. Ventricular tachycardia and fibrillation.
3. Atrial flutter.
4. Atrioventricular blockade.
5. Extrasystole.

Pressure gradient

The pressure gradient is the difference in pressure between the left chambers of the heart. Normally, the pressure in the left ventricle is 33-45 mmHg, in the atrium - 3-6 mmHg.

With bicuspid valve stenosis, the pressure initially becomes equal in both chambers. As it progresses, the pressure in the atrium becomes greater than in the ventricle, on the basis of which the following classification of the defect is made:

• Slight stenosis (gradient is 7-11 mmHg).
• Moderate (12-20 mmHg).
• Significant (more than 20 mmHg).

The magnitude of the gradient also reflects the degree of pulmonary hypertension.

Patients' complaints

Symptoms of mitral stenosis appear gradually: at first they bother the patient only after physical activity, then they are observed even at rest. It is typical for the clinic of mitral valve stenosis that patients complain of:

• shortness of breath or cardiac asthma;
• cough, which may be dry at first, and then becomes wet - with an increased content of sputum, foamy and even mixed with blood;
• increased fatigue and weakness;
• frequent dizziness and fainting;
• thermoregulation disorders;
• hoarseness of voice;
• frequent bronchitis and pneumonia;
• pain in the heart area - most often from the back between the shoulder blades;
• tachycardia.

The patient's appearance is characteristic: he is pale, and a feverish blush is noticeable on his cheeks, the tip of the nose, lips and fingers are bluish, the veins in the neck are swollen, swelling on the body and a swollen abdomen may be noticeable.

When to see a doctor and which one?

You should contact a cardiologist or primary care physician immediately If the former are detected, shortness of breath and fatigue with frequent dizziness.

The patient should not be misled by the fact that these symptoms disappear quickly at first - as the disease progresses, they may become irreversible.

Diagnostics

The doctor makes a diagnosis of mitral stenosis, relying not only on the history and examination, but also on the results of such instrumental studies:

Type of diagnostic test	Characteristic signs of mitral stenosis
Electrocardiogram (ECG)	Enlargement of the left atrium and right ventricle. Tachyarrhythmia.
Phonocardiogram	Characteristic murmur of mitral stenosis. Valve clicking sound.
X-ray of the heart	Enlargement of the left atrium and right ventricle. Expansion of the shadow of the vena cava and pulmonary artery. Change in lung pattern. Valve calcification.
Heart ultrasound with Doppler (EchoCG - echocardiography) or transesophageal ultrasound	Changes in blood flow to the heart. Reduction in the area of ​​the mitral orifice. Enlargement of individual chambers of the heart.
Invasive research methods with cardiac catheterization	Increased pressure in the left atrium and right ventricle.

To clarify the diagnosis and determine treatment tactics for mitral valve stenosis sometimes a CT scan and diagnostic bypass may be required. As a rule, the diagnostic methods given in the table are sufficient to make the correct diagnosis and carry out a differential diagnosis of mitral stenosis with the following pathologies:

• or ;
• heart tumor;
• thyrotoxicosis.

This video describes the features of echocardiography for mitral stenosis, which will be shown by this diagnostic method:

Features in children

The causes of mitral stenosis in children may be systemic autoimmune diseases:

• Rheumatism.
• Dermatomyositis.
• Systemic lupus erythematosus.
• Polymyositis.

In the vast majority of cases, the etiology of the defect in a child is untreated sore throat. and lack of bicillin prophylaxis after streptococcal infection.

The disease is characterized by the same hemodynamic changes as in adults, but the clinic has some features:

1. Retarded physical development.
2. “Mitral face” rarely develops.
3. The disease is not complicated by atrial fibrillation.
4. The “quail rhythm” is rarely heard; protodiastolic and prediastolic murmurs at the apex of the heart are more typical.

Special symptoms:

• Frequent fainting.
• Pronounced epigastric pulsation (up to the development of a “heart hump”).

Treatment methods:

1. Conservative (preparation for surgery)
2. Surgical (valve replacement).

The prognosis without treatment is poor. The operation is performed in the first month after diagnosis and is successful in more than 90% of cases. The life expectancy of treated patients is 55-65 years.

Treatment methods

Medication

Conservative drug therapy for this defect is of secondary importance. Its main purpose:

• Treatment of diseases that provoked pathology (autoimmune, infectious).
• Neutralization of disease symptoms when surgical intervention is impossible or in the preoperative period. For this purpose, diuretics (Furosemide, Veroshpiron), cardiac glycosides (Digoxin, Celanide), adrenoblockers (Atenolol), anticoagulants (Warfarin, Heparin), vitamins and minerals are prescribed.

Drug therapy, along with diet and minimizing physical activity, is the leading method of treating patients with the disease in the compensation stage.

Conservative therapy is carried out:

1. Into the compensation stage.
2. If the general condition of the patient is satisfactory.
3. With a slight degree of valve narrowing.

Drugs used:

• Diuretics – for the development of cough and hemoptysis (veroshpiron).
• Cardioprotectors – trimetazidine, riboxin.
• Anticoagulants - if there is a threat of thrombosis (atrial fibrillation): heparin, warfarin.
• In patients without arrhythmia with mitral stenosis, beta blockers (bisoprolol, metaprolol), calcium channel blockers (nifedipine) are used.
• In patients with arrhythmia, antiarrhythmics (amiodarone) are used.
• Bronchodilators (ipratropium bromide).
• Mucolytics (expectorants - mucaltin).

Surgical

But More often, patients consult a doctor when the symptoms of the disease are already severe– in this case, the classic treatment is surgical intervention. The operation is also performed in situations where drug treatment cannot compensate for a heart defect in the form of mitral stenosis, and the indications for surgical treatment are as follows:

1. Pulmonary artery pressure is more than 60 mmHg.
2. Thrombosis of the left atrium.
3. Narrowing of the valve to 1 sq.cm.
4. Decompensation of the defect (heart failure).

In this case, the following types of operations can be performed:

In the case of a stage of severe decompensation of the pathology (grade 4-5), any corrective surgery is contraindicated, and patients are prescribed only palliative drug treatment.

Danger and complications

If the pathology is not detected in time and not treated, complications in the form of progression of heart failure and pulmonary hypertension are inevitable.

Adequate treatment can significantly reduce the risk of all these complications. and reduce the likelihood of tragic events by 90-95%.

In rare cases, the following postoperative complications occur:

• – 1-4%;
• thromboembolism – 1%;
• restenosis or repeated narrowing after surgical correction – in 20% of patients within 10 years after surgery.

Forecasts and preventive measures

The prognosis is unfavorable only in the absence of proper treatment– over the next 10 years, 65% of such patients will die. After appropriate surgery for mitral valve stenosis, this figure drops to 8-13%.

Prevention of pathology and its relapses is timely treatment of rheumatic and infectious diseases, adherence to a healthy lifestyle and careful attention to one’s own health.

If these conditions are met, the risk of mitral stenosis, if not completely disappearing, is significantly reduced, and the likelihood of a fatal outcome of an early detected defect is reduced to almost zero.

Find out more useful information on the topic from the video: