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AV hole. Patients with significant mitral stenosis are characterized by the presence of a cardiac impulse and epigastric pulsation, which reflect right ventricular hypertrophy. Percussion reveals an expansion of the boundaries of relative cardiac dullness due to

an increase in the left atrium and right parts of the heart. In patients with severe dilatation right ventricle marked pulsation of the jugular veins.

The most characteristic auscultatory signs of mitral stenosis are

loud (clapping) I tone, mitral valve opening sound (mitral click) and diastolic murmur. Strengthening of the 1st heart sound is due to the fact that due to an increase in pressure in in the left atrium, the closure of the mitral valve occurs somewhat later than usual - in

the moment when the increase in systolic pressure in the left ventricle, reaching a maximum

low speed, causes a more abrupt movement of the valves. Loud I tone is heard

both in sinus rhythm and in AF. As the mobility of the mitral valve leaflets decreases or regurgitation increases, the intensity of the first tone decreases. Sound of opening of the mitral valve arises due to a sharp deflection of the leaflets of the mitral valve soldered along the edges in the direction of the ventricle and is heard immediately

after the II tone above the apex. This auscultatory phenomenon is considered as one of the earliest s mitral stenosis, since even a small fusion is enough for its occurrence

sashes. At the same time, the intensity of the sound of the opening of the mitral valve does not reflect

the severity of the defect, because the immobilization of the leaflets is accompanied by a weakening of the mitral valve clicks. Diastolic murmur occurs with significant mitral stenosis due to increased blood

flow through the valve. Noise begins at some distance after tone II,

immediately after the opening tone of the mitral valve and, gradually weakening,

continues throughout the diastole (mid-diastolic murmur). Patients with preserved sinus rhythm

often there is an increase in noise at the end of diastole due to increased blood flow through

mitral valve during atrial systole (presystolic murmur). diastolic

noise with mitral stenosis is heard over the valve projection, at the apex of the heart and in left axillary region.

Developing with mitral stenosis, pulmonary hypertension is manifested by accent II tone on the pulmonary artery. Severe pulmonary hypertension is accompanied by expansion trunk of the pulmonary artery and the development of pulmonary regurgitation, which causes the appearance of diastolic murmur of Graham Still. Unlike the mesodiastolic murmur, which is directly associated with mitral stenosis, the murmur of pulmonary

regurgitation is not separated from the second tone, i.e., it is protodiastolic. Best Graham Still Noise

auscultated in the II intercostal space to the left of the sternum.

If the dilatation of the right ventricle resulting from pulmonary hypertension leads to the formation of relative tricuspid insufficiency, a systolic murmur of tricuspid regurgitation appears, which is best heard over the sword

a prominent process of the sternum.

Instrumental diagnostics. ECG changes in mitral stenosis include

signs of left atrial hypertrophy in the form of an extended two-humped P wave in leads I, aVL, V4–V6 (P. mitrale), signs of right ventricular hypertrophy and in some

patients with AF.

X-ray examination of the heart reveals an increase in the left atrium, with

severe mitral stenosis - expansion of the pulmonary trunk, enlargement of the right ventricle

and right atrium, sometimes - calcifications in the valve area. When examining the lungs there are signs of pulmonary hypertension, and often interstitial pulmonary edema (Kerley lines).

The most valuable diagnostic information can be obtained using echocardiography. This method allows you to visualize the mitral valve and identify dia-

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gnostic signs of mitral stenosis, clarify the morphology of the altered valve,

determine the severity of calcification of the leaflets and assess the condition of the subvalvular structures,

calculate the area of the mitral orifice and pressure gradient, evaluate the blood flow through

the mitral valve, as well as obtain data on the size of the left atrium and the presence of blood clots in its cavity, calculate the pressure in the pulmonary artery, measure the volumes of the right

ventricle and right atrium.

Diagnosis of mitral stenosis does not require the use of invasive research methods.

vanity.

Diagnosis. The diagnosis must reflect the clinical variant of the underlying disease, which served as the cause of the formation of heart disease, the nature of the damage to the mitral valve, the type and severity of complications.

Examples of diagnoses:

1. Chronic rheumatic heart disease. mitral stenosis. Permanent form of atrial fibrillation. Chronic cardiac insufficiency IIA Art., III f. to.

2. Acute rheumatic fever. Combined mitral

heart disease with a predominance of stenosis. Pulmonary edema 20.12.2009.

differential diagnosis. Mitral stenosis must be differentiated from left atrial myxoma, atrial septal defect, primary pulmonary

hypertension. Left atrial myxoma is characterized by variability in diastolic

noise when changing body position, absence of mitral click and symptoms characteristic of a tumor disease (weight loss, anemia, increased ESR). With an atrial septal defect, signs of dilatation of the right ventricle are revealed, the left atrium

has normal dimensions, no Kerley lines, splitting of the II tone is wide and fixed (does not depend on the phases of respiration). Primary pulmonary hypertension has a number of similar with mitral stenosis of symptoms, but with this disease there is no coarse diastolic murmur, mitral click and left atrial dilatation.

Flow. In patients with mitral stenosis, the area of the left AV foramen steadily decreases. The rate of narrowing of the mitral orifice depends on the degree of deformation of the valvular apparatus and the characteristics of the course of rheumatic heart disease. The gradual worsening of the condition of patients is mainly due to the progression of chronic HF. Sudden worsening of the condition is usually associated with either pulmonary edema or

thromboembolic complications. The development of a permanent form of AF exacerbates the disorders systemic hemodynamics and contributes to the formation of blood clots in the left atrium. Due

with this, in patients with AF, the risk of embolism in the system of a large circle increases significantly circulation. Stagnation in the systemic circulation and reduced physical activity contribute to

the development of phlebothrombosis of the veins of the lower extremities, which

often become a source of thromboembolism in the pulmonary artery system. Patients with mitral stenosis have an increased risk of infective endocarditis, the development of which

significantly worsens the course and prognosis of the disease.

Forecast and outcomes. With a moderate degree of mitral stenosis, the absence of its rapid progression and the preserved contractility of the heart muscle, patients

for a long time retain their ability to work and good health. progressive

mitral stenosis and the development of complications contribute to the rapid worsening of

heart failure, which is the most common cause of death in patients with mitral steatosis. nose.

Treatment. Radical method of treatment of patients with mitral stenosis is

surgical correction of the defect. The operation is indicated for patients with severe ("clean" or

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predominant in combined defect) mitral stenosis in the presence of symptoms that significantly limit their physical activity and reduce their ability to work, especially in patients suffering from cardiac asthma and hemoptysis. absolute

The indication for surgery is a critical narrowing of the mitral orifice (area

less than 1 cm2 ). Patients whose mitral orifice area exceeds 2 cm2 no need for medical treatment. The least traumatic type of surgery is a closed commissurotomy by balloon valvuloplasty. If application

this method is impossible, perform an open commissurotomy. With pronounced morphological changes in the mitral valve to restore intracardiac hemodynamic

Miki apply his prosthetics.

In cases of impossibility of surgical treatment or the absence of such a need, symptomatic drug therapy is carried out aimed at stabilizing

sinus rhythm or heart rate control in AF, prevention of progression of heart failure, prevention of thromboembolism.

Prevention. Prevention of mitral stenosis is reduced to the prevention of diseases that cause the formation of this heart disease, mainly rheumatic

and infective endocarditis.

Mitral insufficiency

Definition. Mitral insufficiency is a heart disease in which

structural changes in the valvular apparatus as a whole or its individual components,

there is no phase of complete closure of the mitral valve and during left ventricular systole, part

blood from its cavity moves to the left atrium.

Prevalence. Isolated mitral valve insufficiency occurs in 2-3% of patients with heart defects. In most cases, mitral regurgitation

combined with mitral stenosis and aortic defects. In the population, the frequency of mitral insufficiency (including mitral valve prolapse) is about 10%. Prolapse

mitral valve in children and adolescents is much more common than in adults, in girls and girls more often than boys and boys. In men and women of middle and older age, mitral insufficiency is detected with the same frequency.

Etiology. In more than half of cases, mitral regurgitation is caused by rheumatism. Mitral insufficiency of rheumatic origin is almost always associated with mitral stenosis. The main cause of non-rheumatic mitral regurgitation is mitral valve prolapse due to dysplasia.

connective tissue. Connective tissue dysplasia is characterized by myxomatous degeneration (thickening and elongation) of the mitral valve leaflets, which prevents their normal closure. Infective endocarditis of the mitral valve in most cases

leads to insufficiency. Some patients develop mitral regurgitation

due to dysfunction or rupture of papillary muscles. The most common reasons for them damage are myocardial infarction and acute myocarditis. Chord breaks as a mechanism mitral insufficiency are observed in patients with connective tissue dysplasia and infective endocarditis, as well as with severe dilatation of the left ventricle, aortic stenosis, due to blunt chest trauma. The cause of dislocation of the mitral valve leaflets during systole, accompanied by regurgitation of blood through the left AV foramen, may be idiopathic calcification of the mitral annulus. Dilatation of the left ventricle of any nature contributes to the formation of relative mitral insufficiency, since in this case the length of the papillary muscles and chords is not enough to tightly close the mitral valve cusps.

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Pathogenesis. Incomplete closure of the mitral valve leaflets causes

that during ventricular systole, part of the blood returns to the left atrium. The same additional blood flow during diastole from the left atrium to the left

ventricle. Due to the increase in the volume of incoming blood, the atrium and ventricle gradually expand. With a small amount of regurgitation, dilatation of the left chambers of the heart

is insignificant. The force of contraction of the myocardium of the left ventricle increases in accordance with Starling'slaw, which provides a state of compensation of blood circulation. An increase in the volume of regurgitation causes an increase in diastolic overload, progressive dilatation and eccentric hypertrophy of the left ventricle. When increasing it

contractility reaches the limit, there is a breakdown of the compensation mechanism, which accompanies

given by a decrease in cardiac output and an increase in diastolic pressure in the cavity left ventricle. This prevents the flow of blood into the ventricle and leads to an increase in

pressure in the cavity of the left atrium, and then in the pulmonary veins and capillaries.

In cases of sudden development of mitral insufficiency, for example, due to

rupture of valve leaflets or subvalvular structures, pressure in the left atrium, pulmonary

veins and capillaries rises sharply, which often leads to the development of pulmonary edema.

Morphology. The nature of morphological changes in the mitral valve depends on

underlying disease. For damage to rheumatic etiology, compaction and

deformation of the valve leaflets, calcium deposition at the base of the leaflets and in the annulus fibrosus.

Mitral valve prolapse is associated with myxomatous degeneration of the valvular apparatus,

which is manifested by thickening and increasing the length of the valves, myxomatous change,

elongation and sometimes rupture of chords. When mitral regurgitation occurs

due to hemodynamic overload and dilatation of the left ventricular cavity, dysfunction of the papillary muscle, or rupture of the chords of ischemic origin, the valve leaflets usually do not

have morphological changes. In infective endocarditis, valvular changes apparatus are very diverse: vegetation of various sizes and densities,

erosions, tears and perforations of the valves, ruptures of the chords, abscesses of the fibrous ring, paravalvular fistulas, etc.

Classification. Allocate acute and chronic mitral insufficiency. Acute mitral insufficiency is classified according to the morphological principle into mitral insufficiency due to damage to the valve ring, damage to

valve leaflets, rupture of the tendon chords, damage or dysfunction of the papillary

muscles, prosthetic valve dysfunction. Chronic mitral insufficiency is classified according to etiology into mitral insufficiency caused by inflammatory changes, degenerative changes, infectious changes,

structural changes of a congenital nature.

The severity of mitral insufficiency can be determined by the magnitude of transvalvular regurgitation, which is assessed using echocardiography. There are 4 degrees of regurgitation:

I degree - the reverse flow of blood into the systole of the ventricles is determined only at the valve, the left atrium is not dilated.

II degree - the reverse blood flow is determined in the middle part of the left atrium, marked its moderate expansion is expected.

III degree - reverse blood flow is recorded in the distant parts of the left atrial diya, its pronounced expansion is noted.

IV degree - the reverse blood flow is determined in the pulmonary veins, there is a significant dilatation of the left atrium.

clinical picture. Clinical manifestations of mitral insufficiency occur with a decrease in the contractile function of the left ventricle. The main factors

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affecting the timing of the onset of symptoms of mitral insufficiency are the nature

the underlying disease, the degree of regurgitation and the state of the myocardium of the left ventricle. At in rheumatic heart disease, the development of clinically significant mitral regurgitation may

take several years, in patients with anatomical damage to the subvalvular structures (for example, with avulsion of the head of the papillary muscle) after a few minutes

after the onset of mitral insufficiency, pulmonary edema may develop.

In chronic mitral insufficiency, the first complaints of the patient are usually

are general weakness and fatigue. Then shortness of breath and palpitations appear, which at first they disturb the patient only during physical exertion, and later they begin to appear and at rest. Palpitations can be caused not only by heart failure, but

and FP. These complaints, as hemodynamic disorders progress, are accompanied by a cough (dry or with a small amount of sputum, sometimes stained with blood),

attacks of cardiac asthma, and with the development of right ventricular failure - severity in right hypochondrium due to stretching of the liver capsule due to its increase,

and peripheral edema.

In patients with hypertrophy and dilatation of the left ventricle, palpation reveals diffuse and enhanced apex beat in the fifth intercostal space outward from the left midclavicular line, with percussion - an increase in the size of relative cardiac dullness

up and to the left due to dilatation of the left chambers of the heart. Auscultation reveals weakness I tone (sometimes very significant, up to disappearance) due to the absence of a period

closed valves. In patients with a small defect in the mitral valve, tone II does not change. With severe mitral insufficiency, splitting of the II tone occurs due to

accelerated emptying of the left ventricle and earlier closure of the aortic valve, and

with the development of pulmonary hypertension, an accent of the II tone appears over the pulmonary artery. Often

a pathological third tone is heard at the apex (protodiastolic gallop rhythm), caused by fluctuations in the wall of the left ventricle due to an increase in the amount of blood, coming into it from the left atrium. The leading auscultatory sign of the mitral insufficiency is a systolic murmur, which is caused by regurgitation of blood from

left ventricle to the left atrium. The murmur may be pansystolic or occupy

only part of the systole. With maximum intensity, the murmur is heard in the region of the apex of the heart, it intensifies on expiration, in the position of the patient on the left side and during isometric exercise. The noise has a different timbre - from soft blowing to rough, is carried out in axillary region and under the left shoulder blade. The intensity and duration of the noise depends

on the severity of regurgitation, but do not accurately reflect the severity of the valvular defect. Many patients noise is followed by systolic trembling at a top.

As HF intensifies, patients develop congestive rales in the lungs, peripheral

edema, hepatomegaly, ascites.

Instrumental diagnostics. With moderate mitral regurgitation ECG

often remains normal. The progression of the defect is accompanied by the appearance of signs of hypertrophy of the left atrium and left ventricle. In cases of severe pulmonary Hypertension on the ECG may show signs of right ventricular hypertrophy. Some patients with an electrocardiographic study revealed AF.

X-ray examination of the chest with compensated defect is not

reveals pronounced changes in the shape and size of the shadow of the heart. As hemodynamic disturbances intensify, expansion of the left chambers of the heart is observed, and

subsequently, the appearance of signs of pulmonary hypertension and expansion of the right ventricle. The main method of instrumental diagnosis of mitral insufficiency is echocardiography,

which can be used to conduct a qualitative and quantitative assessment of the anatomical features of the valvular apparatus, disorders of the intracardiac

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and central hemodynamics. Based on the results of ultrasound examination of the leaflets, valvular ring, chords and papillary muscles, an idea can be formed about the cause of mitral insufficiency. Measuring the dimensions of the cavities of the left atrium and left ventricle makes it possible to determine the severity of their volume overload and

assess the state of the contractile function of the left ventricle, and the use of the Doppler mode - to determine the degree and calculate the volume of mitral regurgitation.

Confirmation of the diagnosis of mitral regurgitation does not require the use of invasive research methods.

Diagnosis. The diagnosis indicates the disease that caused the formation of of heart disease, the degree of mitral insufficiency and complications.

Examples of diagnoses:

1. Chronic rheumatic heart disease. Mitral failure. Mitral regurgitation III stage. permanent form atrial fibrillation. Chronic heart failure IIA stage, III

f. to.

2. Primary myxomatous mitral valve prolapse. Myxomatous degeneration of the mitral valve leaflets. Mitral regurgitation stage II Supraventricular extrasystole.

differential diagnosis. Systolic murmur at the apex of the heart, not associated with mitral insufficiency, is often detected in healthy young people and

teenagers. The causes of systolic murmur of non-valvular origin may be anemia, thyrotoxicosis, autonomic dystonia. In these cases, the noise is usually not loud.

and short, has a soft timbre and is not combined with a change in heart sounds. At relative mitral insufficiency due to diseases leading to

dilatation of the left ventricle, an increase in this chamber of the heart prevails over an increase

left atrium, while with organic mitral insufficiency it increases

predominantly the left atrium. Mitral insufficiency should be differentiated

vat with other heart defects, which are characterized by the appearance of systolic murmur:

tricuspid valve insufficiency, aortic orifice stenosis, and pulmonary artery stenosis. In addition to diagnosing mitral insufficiency as such, it is necessary to analyze its possible causes in order to establish the etiology of heart disease.

Flow. Chronic mitral insufficiency with moderate regurgitation flows favorable: in patients for a long time (years and even decades) a good well-being and no signs of heart failure. As pulmonary hypertension develops,

shortness of breath on exertion, and then at rest, attacks of cardiac asthma. to stagnation in In the pulmonary circulation, symptoms of right ventricular failure quickly join. In acute mitral regurgitation, heart failure is

pump manifests itself and progresses much faster. Development of AF (probability of this complications are especially high when mitral insufficiency is combined with mitral stenosis)

accelerates the process of circulatory decompensation and increases the risk of thromboembolic complications.

Forecast and outcomes. The prognosis of patients with mitral insufficiency depends mainly way from the severity of violations of intracardiac hemodynamics and the state of the myocardium.

With moderate mitral insufficiency, patients remain able to work for a long time. Severe mitral insufficiency, especially developed acutely, quickly

leads to circulatory decompensation. Progressive heart failure is the leading cause of death in patients with mitral regurgitation.

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Treatment. Elimination of mitral insufficiency is possible only surgically.

way. The main type of surgical treatment is mitral valve replacement. However, mitral valve repair is considered preferable, since the reconstructive operation provides greater synchrony of the left ventricular contraction,

reduces the risk of infective endocarditis and makes permanent anticoagulant therapy unnecessary. Indications for surgical treatment are decompensation

blood circulation in combination with severe mitral regurgitation and acute mitral insufficiency. When determining the indications for surgery, the patient'sage, the

contractility of the left ventricle, and the etiology of mitral insufficiency are taken into account. As a quantitative criterion for predicting the recovery of left ventricular function

after the operation, the value of its end-systolic size is used. If this indicator does not exceed 40 mm, the prognosis for recovery of function is considered good, but urgent surgical intervention is not mandatory. With a value of more than 50 mm

the need to eliminate the valvular defect becomes obvious, but the likelihood of restoring left ventricular function after surgery is significantly reduced. Optimal

considered surgical treatment of patients in whom the end-systolic size of the left ventricle is 40 to 50 mm. Medical treatment of patients includes drugs,

used to reduce symptoms and prevent the progression of HF.

Prevention. Taking into account the etiology of the defect, the main direction of prevention mitral insufficiency is to reduce the risk of rheumatism and infectious myocarditis.

aortic stenosis

Definition. Aortic stenosis (stenosis of the aortic mouth) is a narrowing of the efferent

tract of the left ventricle in the region of the aortic valve, which impedes the outflow of blood from

left ventricle, resulting in an increase in pressure gradient between the left ventricle and

aorta.

Prevalence. Aortic stenosis is detected in 20-25% of patients with defects hearts. In men, this defect is diagnosed 3-4 times more often than in women.

Etiology. The most common causes of aortic stenosis are idiopathic (primary degenerative) leaflet disease with annular calcification, bicuspid aortic valve fibrosis, and rheumatism. A defect due to degeneration and

calcification of the aortic valve, usually diagnosed at the age of 55 - 65 years. Bicuspid aortic valve is a developmental anomaly that, as a rule, begins to manifest itself clinically due to fibrosis and calcification of the valve leaflets by the age of 45–50 years.

Aortic stenosis of rheumatic origin in most patients is formed in the young

age. Among the causes of aortic stenosis is atherosclerosis of the aorta. However, aortic stenosis of atherosclerotic origin in its pure form is considered to be a rather rare phenomenon. In most cases, atherosclerosis is an additional etiological factor in aortic stenosis. In the later stages of the disease, many patients with aortic

stenosis of any origin, calcification, deformation of the aortic

valve and signs of atherosclerosis of the aorta, which makes the determination of the etiology of the defect very

difficult.

Pathogenesis. Normally, the area of the aortic orifice is 2.5 - 3.5 cm2 . A significant obstruction to blood flow occurs only when it is narrowed by more than half. In aortic stenosis, an increase in systolic pressure in the left ventricle is necessary to move blood into the aorta. As a result, the pressure gradient between the left

stomach and aorta. Normally, its value does not exceed 12 mm Hg. Art., but with aortic

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stenosis transaortic pressure gradient is more than 20 mm Hg. Art., and in some

cases reaches 100 mm Hg. Art. and more. The mechanism that provides an increase in systolic pressure in the left ventricle is its concentric hypertrophy, i.e. thickening of the walls with a relative decrease in the cavity. As myocardial hypertrophy develops, its extensibility decreases, filling of the left ventricle becomes more difficult and increases

load on the left atrium. This leads to a moderate increase in pressure in the pulmonary veins and the gradual development of left atrial hypertrophy, the work of which should

provide diastolic filling of the left ventricle, sufficient for the formation of cardiac output adequate to the metabolic needs of the body. With moderate stenosis, the state of compensation persists for a long time (up to 15-20 years). Minute

the volume of blood circulation is maintained at a level sufficient to ensure even significant physical exertion. With the progression of aortic stenosis, the increase in minute volume during physical activity decreases markedly and the phenomenon of a “fixed minute volume” is formed, i.e., limiting its increase when a certain

level of physical activity. The subsequent decrease in the contractility of the hypertrophied left ventricle is accompanied by its dilatation and increase

end-diastolic pressure in its cavity. As a result, the pressure in

left atrium and pulmonary veins, stagnation develops in the pulmonary circulation. At

in some patients with severe left ventricular failure, with a significant expansion of the left ventricle, the annulus of the bicuspid valve is stretched

and relative insufficiency of the mitral valve develops - the so-called "mitralization" of the aortic defect, which further exacerbates blood stasis in the lungs. Subsequently, the pressure in the right chambers of the heart rises and the right ventricular

failure.

Morphology. Aortic stenosis of rheumatic origin is characterized by

commissural stenoses that limit the movement of the aortic valve cusps, thickening, compaction and deformation of the cusps. With the passage of time from the onset of rheumatic valvulitis, calcification of the affected valve intensifies. At

primary degenerative aortic stenosis is dominated by calcification of valvular structures. Calcium deposition begins at the annulus fibrosus and at the base of the valve leaflets. Progressively, the degenerative-calcifying process spreads to the free edges of the leaflets, causing commissural fusion and a decrease in the functional area of the valve.

Classification. By origin, aortic stenosis is divided into congenital and acquired. According to the level of obstruction, valvular, subvalvular and

supravalvular aortic stenosis. According to ethology, rheumatic, idiopathic (primary degenerative or senile) aortic stenosis and bicuspid calcification

valve. According to the degree of circulatory disorders, aortic stenosis is divided into compensated and decompensated.

The severity of aortic stenosis is determined by the systolic pressure gradient between the left ventricle and the aorta and the area of the aortic orifice:

1)minor stenosis (gradient < 30 mm Hg, aortic orifice area 1.3

–2 cm2 );

2)moderate stenosis (pressure gradient 30–50 mm Hg, aortic orifice area 0.75–1.3 cm2 );

3)severe stenosis (pressure gradient > 50 mm Hg, area of the aortic

stia < 0.75 cm2 ).

clinical picture. Stenosis of the aortic mouth for a long time proceeds

asymptomatic. The first complaints in the compensation stage reflect the phenomenon of “fixed

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minute volume": dizziness, nausea, fainting during physical

load or a rapid change in body position due to short-term insufficiency of cerebral circulation. With the development of HF, rapid fatigue appears

and shortness of breath on exertion. In some patients with aortic stenosis, attacks of angina pectoris of exertion and rest occur, associated with relative coronary insufficiency, the causes of which are: increased metabolic needs of hypertrophied myocardium; decrease in blood flow to the coronary arteries due to low

pressure in the aorta and acceleration of blood flow through the narrowed aortic opening; high dove

Lesion in the cavity of the left ventricle, which causes compression of the subendocardial arteries. When a decrease in myocardial contractility is added to the diastolic dysfunction of the left ventricle and severe pulmonary hypertension develops, shortness of breath becomes constant, and a number of patients develop attacks of cardiac asthma. Signs of right ventricular insufficiency (peripheral edema, heaviness in the right hypochondrium, liver enlargement)

rare in isolated aortic stenosis. Their presence indicates

significant pulmonary hypertension, which usually develops with a combination of aortic stenosis with mitral valve defects.

Severe aortic stenosis is characterized by a decrease in systolic and pulse

HELL. In the stage of decompensation of aortic stenosis, on palpation, an enhanced apical

impulse is determined in the 5th - 6th intercostal space to the left of the midclavicular line. In patients with

significant narrowing of the aortic opening is often determined by systolic trembling

based on the heart. Percussion reveals a shift of the left border of relative cardiac dullness to the left. Auscultation reveals the most characteristic sign of aortic stenosis - a rough and loud (scraping, cutting) systolic murmur with a maximum in the middle of systole. Noise is localized in the III intercostal space to the left of the sternum (respectively

projection of the aortic valve) and in the II intercostal space to the right of the sternum (above the region of the ascending aorta), has a wide irradiation (neck vessels, interscapular space, area apex of the heart). Aortic stenosis is characterized by the absence of changes or weakening

I tone, expressed to varying degrees (depending on the severity of the stenosis), weakening of the II tone above the aorta, sometimes splitting of the II tone, the appearance of IV pathological tone due to increased contraction of the left atrium and pathological III tone - with the development of systolic dysfunction and volume overload of the left ventricle.

Instrumental diagnostics. ECG in patients with aortic stenosis in most cases reveals signs of severe left ventricular hypertrophy. Signs of systolic overload of the left ventricle in the form of segment depression are often recorded.

ST and biphasic T waves in leads I, aVL, V5–V6. In some patients, there is an increase in the amplitude and duration of the P waves in leads I, aVL, V4–V6, which is associated

with overload and hypertrophy of the left atrium.

X-ray examination during the period of compensation for changes in size hearts are usually not found. In decompensated patients, cardiomegaly with

significant displacement of the apex to the left and the formation of an "aortic" configuration heart shadow. Severe aortic stenosis is often accompanied by post-stenotic dilatation of the aorta, which is explained by increased pressure of the blood stream on the wall of the ascending aorta. Patients with pulmonary hypertension usually have x-ray

signs of stagnation in the pulmonary circulation.

Two-dimensional echocardiography in combination with Doppler echocardiographic

examination makes it possible to assess morphological changes in the valve and, in some cases, to judge possible etiology of the defect, determine the size of the left atrium, left ventricle and

thickness of the myocardium, measure the maximum blood flow velocity on the valve, calculate the trans-saortic pressure gradient and the area of the aortic orifice.

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Invasive methods for the diagnosis of aortic stenosis are not used. Catheterization of the left chambers of the heart is performed only in the process of preoperative preparation in order to

verification of the diagnosis and quantitative assessment of the degree of narrowing of the aortic orifice. At in persons over 50 years of age, an invasive examination in the preoperative period includes

coronary angiography.

Diagnosis. The diagnosis specifies the etiology of aortic stenosis and complications.

Examples of diagnoses:

1.Chronic rheumatic heart disease. aortic stenosis.

2.Fibrosis of the bicuspid aortic valve. aortic stenosis. Permanent form of atrial fibrillation. Chronic cardiac insufficiency IIA Art., III f. to.

differential diagnosis. The main diagnostic sign of aortic stenosis - systolic murmur over the base of the heart - is also detected in some other heart defects. Unlike pulmonary stenosis, aortic stenosis weakens II

tone is noted over the aorta, and not over the pulmonary artery and on x-ray

a predominant increase in the left rather than the right ventricle is found. In case of defect interventricular septum, there is no conduction of the murmur to the vessels of the neck and weakening of the II tone over the aorta, which is characteristic of aortic stenosis. In cases where the maximum systolic murmur is determined at the left edge of the sternum and at the apex, it is necessary to differentiate aortic stenosis from mitral insufficiency. murmur in aortic stenosis

has a rougher timbre, the 1st tone at the top is preserved, and the 2nd tone over the aorta is weakened. Reception

Nitroglycerin often causes a decrease in systolic murmur due to mitral insufficiency. Systolic murmur over the aorta in elderly patients may be due to fibrosis of the aortic valve cusps without stenosis, atherosclerosis, and dilatation.

ascending aorta. The cause of systolic murmur over the aorta may be conditions

which are characterized by an acceleration of blood flow (thyrotoxicosis, anemia). In these cases, the noise has a more gentle timbre and does not increase towards the middle of systole, as with aortic stenosis.

By the nature of the systolic murmur and other clinical signs, it can be difficult to distinguish valvular aortic stenosis from subaortic stenosis in obstructive cardiomyopathy. Here, how and in other cases, echocardiography helps to make the correct diagnosis.

Flow. Aortic stenosis is characterized by a favorable course. Even in patients with a high transaortic pressure gradient, a hypertrophied left ventricle

for a long time provides cardiac output adequate to metabolic needs

organism. A noticeable deterioration in the condition of patients occurs after the development of systolic left ventricular dysfunction due to rapid progression of heart failure. Additional

factors aggravating the course of the defect are episodes of acute coronary insufficiency and the development of AF.

Forecast and outcomes. Moderate aortic stenosis does not have a significant negative impact on the ability to work and well-being of patients. The prognosis significantly worsens after

decompensation of the defect and the development of HF. Other factors contribute to poor prognosis complications of the disease - MI, rhythm and conduction disturbances. Main reasons

deaths in patients with aortic stenosis are progression of HF and life-threatening

arrhythmias.

Treatment. Correction of aortic stenosis is possible only surgically. At

In determining the indications for surgery, the magnitude of the transaortic pressure gradient and the area of the aortic orifice are taken into account. An equally important factor is the occurrence of clinical signs of decompensation. With critical stenosis (the area of the aortic

holes less than 0.75 cm2 ), increase in transaortic pressure gradient to values

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