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What are heart defects?

Heart defects- These are congenital or acquired lesions of the heart valves. Humans and mammals have 4 heart valves: tricuspid, bicuspid, or mitral, and 2 semilunar. The bicuspid (mitral) valve is formed by two leaflets that are attached to the edges of the left atrioventricular orifice. Blood passes through it from the atrium to the ventricle, but the valve prevents its reverse flow.

Aortic valve - located between the left ventricle and the aorta, consists of 3 semilunar valves, they prevent blood from returning from the aorta to the ventricle.

The tricuspid valve consists of three leaflets that separate the right atrium and the right ventricle. It prevents blood from returning from the ventricle to the atrium. The semilunar valve is one of the two heart valves, located at the exit of the aorta and pulmonary artery. Each valve has three leaflets that ensure blood flow in one direction - from the ventricles to the pulmonary trunk and aorta.

Due to various reasons The function of the heart valves may be impaired. These defects can be congenital or acquired.

Symptoms of heart defects

  • Dyspnea.
  • Edema.
  • Catarrhal bronchitis.
  • Decreased performance.
  • Irregular pulse.
  • Dizziness and fainting.

Stenosis

One of heart defects- stenosis - narrowing of the valve opening. Due to stenosis of the tricuspid or bicuspid valve, blood flow in the affected half of the atrium slows down. In case of stenosis of the aortic or pulmonary valves, due to the large overload of the heart, the corresponding ventricles are also affected. When the closure is incomplete, the heart works under overload. At the same time, blood flows through the openings of the valves not only in the desired direction, but also in the opposite direction, so the heart has to pump out blood again. If the damaged valves do not close enough during contraction of the heart muscle, then acquired heart defects develop - bicuspid or tricuspid valve insufficiency. If the edges of the valves become scarred, their openings narrow and the movement of blood through them becomes difficult, then stenosis develops. The most common manifestation is stenosis of the valves of the left half of the heart (bicuspid and aortic).

Mitral valve stenosis

The disease progresses quite slowly. Symptoms: shortness of breath on exertion, cold extremities, irregular pulse. In addition, the disease is usually accompanied by cough, fatigue, and rapid heartbeat. pain on the right side, swelling of the lower extremities. The skin of the patient's lips and cheeks acquires a bluish tint. X-rays and other research methods show an enlarged left ventricle, which is caused by a large overload of the heart.

Aortic valve stenosis

The valve does not open completely due to the narrowing of the gap between the movable valve flaps. For some time, the left ventricle is able to compensate for the disruption of blood flow. However, if malfunctions of the ventricle begin, the following symptoms appear: shortness of breath, dizziness, fainting, pain in the heart. When performing heavy physical work this heart disease especially dangerous due to the threat of sudden death.

Causes of valve stenosis

More often heart defects are congenital. They can be caused by rheumatic inflammation, bacterial endocarditis, septic endocarditis. Stenosis can occur with scarlet fever, less often as a result of trauma, atherosclerosis, or syphilis. In all cases, the valve flaps are soldered and narrowed. At the same time, the hole through which blood flows narrows. Of course, valve stenosis is possible due to scarring of the valve leaflets or tendon cords that remain after endocarditis - inflammation of the inner lining of the heart and its valves.

Stenosis of the right atrioventricular orifice

With stenosis of the right atrioventricular orifice due to damage to the tricuspid valve, blood flow in the vena cava slows down, while less blood. The heart tries to compensate for this defect by stronger contraction of the right atrium. However, blood quickly begins to accumulate even in the neck veins and liver. Severe swelling appears and the patient begins to choke.

What is heart valve insufficiency?

Incomplete closure of the heart valve causes the direction of blood flow to change during heart contractions. This dysfunction of the valve is called heart valve regurgitation. Failure of any valve can occur, but the left heart valves are most commonly affected. An increase in load leads to the fact that the heart cannot cope with its task, as a result of which the heart muscle thickens, the patient experiences heart failure and shortness of breath.

Sometimes the doctor diagnoses insufficiency of one or another heart valve in a newborn. In many cases, small holes are found in the valve flaps or pockets semilunar valves or damage to these formations. However, among congenital heart defects, valve stenosis is the most common. Holes in the valves or damage to them can also occur in adults. Valve insufficiency often manifests itself in them due to shortening of the ligaments that fix the valve in the cavity of the heart. Usually these changes are caused by rheumatism, bacterial infection, are less commonly associated with atherosclerosis.

Another specific case is the so-called heart valve aneurysm, characterized by protrusion of the valve leaflets due to inflammation, congenital anomalies or degeneration. Sometimes a heart valve aneurysm leads to valve failure.

Treatment of heart defects

Treatment of heart disease begin immediately after its identification. If a heart defect is a complication of rheumatism or any other disease, then these diseases are treated first.

It is almost impossible to cure heart valve damage with medications; surgery is necessary. There are two types of operations. The first type includes operations during which they only try to cure the heart valve, the second includes operations to replace the natural heart valve with an artificial one. In some cases, expansion of the affected valve can remove or reduce stenosis. The holes located on the walls of the valves are often sutured.

Sometimes the only way out one of the situations is the implantation of an artificial heart valve. Artificial valves are divided into: autologous, homologous and heterologous. Autologous prostheses are made from a person’s own tissue, homologous ones are made from another person’s tissue, heterologous ones are made from other materials, e.g. animal tissue or plastic. Artificial heart valves are devices equipped with a locking element.

Are heart defects dangerous?

The danger is associated primarily with the fact that the patient’s heart is subjected to greater stress than the heart healthy person. To cope with this load, the heart muscle increases in size. However, subsequently, despite hypertrophy, the work of the heart weakens and it does not pump blood well. As a result, the patient experiences total heart failure, characterized by impaired activity of the left and right hearts. Thus, heart defects need urgent treatment.

Due to the fact that the heart does not push out an insufficient amount of blood, the blood supply to the tissues is disrupted, they receive less nutrients and oxygen. With the accumulation of blood in the heart and blood vessels the danger increases: edema occurs, the functions of the lungs and other vital organs are disrupted (venous pressure increases, the liver, abdominal cavity liquid collects). With absence treatment of heart defects lead to heart failure. which can cause the death of the patient.

Etiology of aortic insufficiency

The most common causes of organic aortic valve insufficiency are:

  • Rheumatism (about 70% of cases);
  • Infective endocarditis;
  • More rare causes of this defect include atherosclerosis, syphilis, systemic lupus erythematosus (Libman-Sachs lupus endocarditis), rheumatoid arthritis, etc.

With rheumatic endocarditis, thickening, deformation and shrinkage of the semilunar valve leaflets occurs. As a result, their tight closure during diastole becomes impossible, and a valve defect is formed.

Infectious endocarditis most often affects previously altered valves (rheumatic lesions, atherosclerosis, congenital anomalies, etc.), causing deformation, erosion or perforation of the leaflets.

It should be borne in mind the possibility of relative insufficiency of the aortic valve as a result of a sharp expansion of the aorta and the fibrous annulus of the valve in the following diseases:

  • arterial hypertension;
  • aortic aneurysms of any origin;
  • ankylosing rheumatoid spondylitis.

In these cases, as a result of the expansion of the aorta, divergence (separation) of the aortic valve leaflets occurs and they also do not close during diastole.

Finally, one should be aware of the possibility of a congenital defect of the aortic valve, for example, the formation of a congenital bicuspid aortic valve or dilatation of the aorta in Marfan syndrome, etc.

Aortic valve insufficiency with congenital defects is rare and is more often combined with other congenital defects.

Aortic valve insufficiency causes a significant portion of the blood thrown into the aorta (regurgitation) to return back into the left ventricle during diastole. The volume of blood returning to the left ventricle can exceed half of the total cardiac output.

Thus, with aortic valve insufficiency, during diastole the left ventricle fills as a result of both blood flow from the left atrium and aortic reflux, which leads to an increase in end-diastolic volume and diastolic pressure in the left ventricular cavity.

As a result, the left ventricle enlarges and significantly hypertrophies (the end-diastolic volume of the left ventricle can reach 440 ml, while the norm is 60-130 ml).

Hemodynamic changes

Loose closure of the aortic valve leaflets leads to regurgitation of blood from the aorta to the LV during diastole. The reverse flow of blood begins immediately after the closure of the semilunar valves, i.e. immediately after the second sound, and can continue throughout diastole.

Its intensity is determined by the changing pressure gradient between the aorta and the LV cavity, as well as the size of the valve defect.

Mitralization of the defect- the possibility of “mitralization” of aortic insufficiency, i.e. occurrence of relative deficiency mitral valve with significant dilatation of the LV, dysfunction of the papillary muscles and expansion of the fibrous ring of the mitral valve.

In this case, the valve leaflets are not changed, but do not completely close during ventricular systole. Typically, these changes develop in the late stages of the disease, with the occurrence of LV systolic dysfunction and pronounced myogenic dilatation of the ventricle.

“Mitralization” of aortic valve insufficiency leads to regurgitation of blood from the LV to the left atrium, expansion of the latter and a significant worsening of stagnation in the pulmonary circulation.

The main hemodynamic consequences of aortic valve insufficiency are:

Compensatory eccentric hypertrophy of the LV (hypertrophy + dilatation), which occurs at the very beginning of the formation of the defect. Signs of left ventricular systolic failure, blood stagnation in the pulmonary circulation and pulmonary hypertension developing during decompensation of the defect. Some features of blood supply in the arterial vascular system great circle blood circulation:

- increased systolic blood pressure;

- decreased diastolic blood pressure;

- increased pulsation of the aorta, large arterial vessels, and in severe cases- arteries of the muscular type (arterioles), caused by an increase in arterial filling in systole and a rapid decrease in filling in diastole;

- impaired perfusion of peripheral organs and tissues due to a relative decrease in effective cardiac output and a tendency to peripheral vasoconstriction.

Relative insufficiency of coronary blood flow.

1. Eccentric left ventricular hypertrophy

An increase in diastolic filling of the LV with blood leads to volume overload of this part of the heart and an increase in ventricular EDV.

As a result, pronounced eccentric LV hypertrophy develops (myocardial hypertrophy + dilatation of the ventricular cavity) - the main mechanism for compensating for this defect. Over a long period of time, an increase in the force of LV contraction, which is caused by increased muscle mass of the ventricle and the activation of the Starling mechanism, ensures the expulsion of an increased volume of blood.

Another peculiar compensatory mechanism is a tachycardia characteristic of aortic insufficiency, leading to shortening of diastole and some limitation of regurgitation of blood from the aorta.

2. Cardiac decompensation

Over time, LV systolic function decreases and, despite the continued increase in ventricular EDV, its stroke volume no longer increases or even decreases. As a result, EDP in the LV, filling pressure and, accordingly, pressure in the LA and veins of the pulmonary circulation increase. Thus, stagnation of blood in the lungs when systolic dysfunction of the left ventricle occurs (left ventricular failure) is the second hemodynamic consequence of aortic valve insufficiency.

Subsequently, with the progression of LV contractility disorders, persistent pulmonary hypertension and hypertrophy develop, and in rare cases, RV failure. In this regard, it should be noted that with decompensation of aortic valve insufficiency, as well as with decompensation aortic stenosis, clinical manifestations of left ventricular failure and blood stagnation in the pulmonary circulation always predominate, while signs of right ventricular failure are weakly expressed or (more often) completely absent.

The third hemodynamic consequence of aortic valve insufficiency is the significant features of filling the arterial bed of the systemic circulation with blood, which are often detected even at the stage of compensation of the defect, i.e. even before the development of left ventricular failure. The most significant of them are:

- decrease in diastolic pressure in the aorta, which is explained by regurgitation of part of the blood (sometimes significant) in the LV

- a pronounced increase in pulse pressure in the aorta, large arterial vessels, and in severe aortic valve insufficiency - even in muscular arteries (arterioles). This diagnostically important phenomenon occurs as a result of a significant increase in LV SV (increased systolic blood pressure) and the rapid return of part of the blood to the LV (“emptying” of the arterial system), accompanied by a drop in diastolic blood pressure. It should be noted that an increase in pulse fluctuations of the aorta and large arteries and the appearance of arteriole pulsations unusual for resistive vessels underlie numerous clinical symptoms detected in aortic valve insufficiency.

4. “Fixed” cardiac output

It was shown above that with aortic insufficiency at rest for a long time, the LV can provide ejection of an increased systolic blood volume into the aorta, which completely compensates for the excess diastolic filling of the LV.

However, when physical activity, i.e. under conditions of even greater intensification of blood circulation, the compensatory increased pumping function of the LV is not enough to “cope” with the even more increased volume overload of the ventricle, and a relative decrease in cardiac output occurs.

5. Impaired perfusion of peripheral organs and tissues

With the long-term existence of aortic valve insufficiency, a peculiar paradoxical situation arises: despite a sharp increase in cardiac output (more precisely, its absolute values), a decrease in the perfusion of peripheral organs and tissues is observed.

This is primarily due to the inability of the LV to further increase stroke volume during physical and other types of exercise (fixed stroke volume). In case of decompensation of the defect great importance also acquires a decrease in LV systolic function (both at rest and during exercise). Finally, activation of the SAS, RAAS, and tissue neurohormonal systems, including endothelial vasoconstrictor factors, also plays a certain role in peripheral blood flow disorders.

With severe aortic regurgitation, disturbances in the perfusion of peripheral organs and tissues can also be caused by the described features of blood supply to the arterial vascular system, namely: rapid outflow of blood from the arterial system or, at least, stopping or slowing down the movement of blood through peripheral vessels during diastole.

6. Coronary circulatory insufficiency

Particularly worth explaining is another important consequence of aortic valve insufficiency - the occurrence of coronary circulatory insufficiency, which is explained by two main reasons related to the peculiarities of intracardiac hemodynamics in this defect:

- low diastolic pressure in the aorta.

As is known, filling of the coronary vascular bed of the LV occurs during diastole, when intramyocardial tension and diastolic pressure in the LV cavity drop and, accordingly, the pressure gradient between the aorta (about 70–80 mm Hg) and the LV cavity rapidly increases (5– 10 mm Hg), which determines coronary blood flow. It is clear that a decrease in aortic diastolic pressure leads to a decrease in the aortic-left ventricular gradient, and coronary blood flow drops significantly.

- the second factor leading to the occurrence of relative coronary insufficiency is the high intramyocardial tension of the LV wall during ventricular systole, which, according to Laplace’s law, depends on the level of intracavitary systolic pressure and the radius of the LV. Pronounced dilatation of the ventricle is naturally accompanied by an increase in the intramyocardial tension of its wall. As a result, LV work and myocardial oxygen demand sharply increase, which is not fully provided by coronary vessels operating in unfavorable conditions from a hemodynamic point of view.

Clinical manifestations

Formed aortic valve insufficiency for a long time (10–15 years) may not be accompanied by subjective clinical manifestations and may not attract the attention of the patient and the doctor. The exception is cases of acutely developed aortic valve insufficiency in patients with infective endocarditis, dissecting aortic aneurysm, etc.

One of the first clinical manifestations of the disease is unpleasant sensation of increased pulsation in the neck, in the head, as well as increased heart beats (patients “feel their heart”), especially in a lying position. These symptoms are associated with high cardiac output and pulse pressure in arterial system described above.

These sensations are often accompanied by cardiopalmus. associated with sinus tachycardia characteristic of aortic valve insufficiency.

If there is a significant defect in the aortic valve, the patient may experience dizziness. a sudden feeling of lightheadedness and even a tendency to faint, especially with exertion or a rapid change in body position. This indicates insufficiency cerebral circulation, caused by the inability of the LV to adequately change cardiac output (fixed stroke volume) and impaired cerebral perfusion.

Heartache(angina) - can also occur in patients with a severe aortic valve defect, long before the onset of signs of LV decompensation. The pain is usually localized behind the sternum, but often differs in nature from typical angina.

They are less often associated with certain external triggers (for example, physical activity or emotional stress), as attacks of angina in patients with coronary artery disease. The pain often occurs at rest and is of a pressing or squeezing nature, usually lasts quite a long time and is not always well relieved with nitroglycerin. Seizures are particularly difficult for patients nocturnal angina accompanied by profuse sweating.

Typical anginal attacks in patients with aortic valve insufficiency, as a rule, indicate the presence of concomitant ischemic heart disease and atherosclerotic narrowing of the coronary vessels.

The period of decompensation is characterized by the appearance of signs of left ventricular failure.

Dyspnea first appears during physical activity, and then at rest. With a progressive decline in LV systolic function, shortness of breath becomes orthopnea.

Then it is joined by attacks of suffocation (cardiac asthma and pulmonary edema). Characteristic is the appearance of rapid fatigue during exercise and general weakness. For obvious reasons, all symptoms associated with cerebral and coronary circulatory insufficiency are aggravated when left ventricular failure occurs. Finally, in more rare cases, when it persists and progresses over a long period of time pulmonary hypertension. and patients do not die from left ventricular failure, individual signs of blood stagnation in the venous bed of the systemic circulation (edema, heaviness in the right hypochondrium, dyspeptic disorders) associated with a decrease in the systolic function of the hypertrophied RV may be detected.

However, more often this does not happen and the clinical picture is dominated by the symptoms described above, caused by damage to the left side of the heart, the peculiarities of blood supply to the arterial vascular system of the systemic circulation and signs of blood stagnation in the veins of the pulmonary circulation.

Inspection

At general examination patients with aortic insufficiency First of all, attention is drawn to the pallor of the skin, indicating insufficient perfusion of peripheral organs and tissues.

With a pronounced defect of the aortic valve, one can identify numerous external signs of systolic-diastolic pressure drops in the arterial system, as well as increased pulsation of large and smaller arteries:

  • increased pulsation of the carotid arteries(“carotid dance”), as well as visible pulsation in the area of ​​all superficially located large arteries (brachial, radial, temporal, femoral, artery of the dorsum of the foot, etc.);
  • de Musset's sign- rhythmic rocking of the head back and forth in accordance with the phases of the cardiac cycle (systole and diastole);
  • Quincke's symptom(“capillary pulse”, “precapillary pulse”) - alternating redness (in systole) and blanching (in diastole) of the nail bed at the base of the nail with sufficiently intense pressure on its tip. In a healthy person, with such pressure both in systole and diastole, the pale color of the nail bed remains. A similar version of Quincke’s “precapillary pulse” is detected by pressing on the lips with a glass slide;
  • Landolfi's sign- pulsation of the pupils in the form of their narrowing and dilation;
  • Müller's sign- pulsation of the soft palate.

Palpation and percussion of the heart

The apical impulse is significantly enhanced due to LV hypertrophy, diffuse (“dome-shaped”) and shifted to the left and down (LV dilatation). With a pronounced defect of the aortic valve, the apical impulse can be detected in the VI intercostal space along the anterior axillary line.

Systolic tremors are often detected at the base of the heart - along the left and right edge of the sternum, in the jugular notch and even on carotid arteries. In most cases, it does not indicate aortic stenosis accompanying aortic insufficiency, but is associated with the rapid expulsion of an increased volume of blood through the aortic valve. In this case, the opening of the aortic valve becomes relatively “narrow” for the sharply increased volume of blood ejected into the aorta during expulsion. This contributes to the occurrence of turbulence in the area of ​​the aortic valve, clinical manifestation which are low-frequency systolic tremor, detected by palpation, and functional systolic murmur at the base of the heart, determined by auscultation.

Diastolic tremors in the precordial region with aortic valve insufficiency are detected extremely rarely.

Percussion in all patients with aortic insufficiency reveals a sharp shift of the left border of the relative dullness of the heart to the left. The so-called aortic configuration with an emphasized “waist” of the heart is characteristic.

Only when LA dilatation occurs, caused by “mitralization” of the defect, can the “waist” of the heart be smoothed out.

Auscultation of the heart

Typical auscultatory signs of aortic insufficiency are diastolic murmur on the aorta and at Botkin’s point, weakening of the 2nd and 1st heart sounds, as well as the so-called “accompanying” systolic murmur on the aorta of a functional nature.

Changes in the first tone. Typically, the first sound at the apex is weakened as a result of a sharp volume overload of the LV and a slowdown in isovolumic contraction of the ventricle. Sometimes the first tone is split.

Changes in tone II. Depending on the etiology of the defect, tone II can either intensify or weaken until it disappears. Deformation and shortening of the valve leaflets due to rheumatism or infective endocarditis contributes to the weakening of the second tone in the aorta or its disappearance. Syphilitic damage to the aorta is characterized by an increased II tone with a metallic tint (“ringing” II tone).

Pathological III tone heard in aortic insufficiency quite often. The appearance of the third tone indicates a pronounced volume overload of the LV, as well as a decrease in its contractility and diastolic tone.

Diastolic murmur on the aorta is the most characteristic auscultatory sign of aortic insufficiency. The murmur is best heard in the 2nd intercostal space to the right of the sternum and in the 3rd–4th intercostal space at the left edge of the sternum and is carried to the apex of the heart.

Diastolic murmur in aortic insufficiency begins in the protodiastolic period, i.e. immediately after the second sound, gradually weakening throughout diastole. Depending on the degree of regurgitation, the frequency characteristic of the diastolic murmur changes: slight regurgitation is accompanied by a soft blowing, predominantly high-frequency murmur; with severe regurgitation, a mixed frequency composition of noise is determined; severe regurgitation leads to the appearance of coarser low- and mid-frequency noise. This type of noise is observed, for example, with syphilitic lesions of the aorta.

It should be remembered that with decompensation of the defect, tachycardia, as well as with combined aortic heart disease, the intensity of the diastolic murmur of aortic insufficiency decreases.

Functional noise

Flint's functional diastolic murmur is a presystolic murmur of relative (functional) stenosis of the left atrioventricular orifice, which is occasionally heard in patients with organic insufficiency of the aortic valve.

It occurs as a result of displacement of the anterior leaflet of the mitral valve by a stream of blood regurgitating from the aorta, which creates an obstacle to the diastolic blood flow from the LA to the LV during active atrial systole.

In the genesis of this noise, vibration of the leaflets and chords of the mitral valve, which occurs as a result of the “collision” of turbulent blood flows entering the LV cavity from the aorta and left atrium, is probably also important.

At the same time, at the apex of the heart, in addition to the wired organic diastolic murmur of aortic insufficiency, presystolic amplification of the murmur is also heard - Flint's murmur.

Functional systolic murmur relative stenosis of the aortic mouth is often heard in patients with organic aortic valve insufficiency.

The murmur occurs due to a significant increase in the systolic volume of blood ejected into the LV aorta during the ejection period, for which the normal unchanged opening of the aortic valve becomes relatively narrow - a relative (functional) stenosis of the aortic mouth is formed with turbulent blood flow from the LV to the aorta.

At the same time, on the aorta and at Botkin’s point, in addition to the organic diastolic noise of aortic insufficiency, during the expulsion of blood, a functional systolic murmur is heard, which can be heard throughout the sternum, apex of the heart and spread to the area of ​​the jugular notch and along the carotid arteries.

When examining the vascular system in patients with aortic valve insufficiency, it is necessary to pay attention to the existence of two more vascular auscultatory phenomena:

1. Durosier's sign (double Durosier murmur). This unusual auscultatory phenomenon is heard over the femoral artery in groin area, directly below the ligament of Poupart.

By simply applying a stethoscope to this area (without pressure), the tone of the femoral artery can be determined - a sound synchronous with the local arterial pulse. With gradual pressure with the head of the stethoscope in this area, an artificial occlusion of the femoral artery is created and a quiet and short systolic murmur begins to be heard, and then a more intense systolic murmur.

Subsequent compression of the femoral artery sometimes leads to the appearance of diastolic murmur. This second murmur is quieter and shorter than the systolic murmur. The phenomenon of Durosier's double murmur is usually explained by a higher than normal volumetric blood flow velocity or retrograde (toward the heart) blood flow in large arteries.

2. Traube double tone- a rather rare sound phenomenon when two tones are heard on a large artery (for example, the femoral) (without compression of the vessel). The second tone is usually associated with reverse blood flow in the arterial system, caused by pronounced regurgitation of blood from the aorta to the LV.

Arterial pressure

With aortic insufficiency, systolic blood pressure increases and diastolic blood pressure decreases, resulting in an increase in pulse blood pressure.

A decrease in diastolic pressure with aortic valve insufficiency requires comment. With direct invasive measurement of aortic blood pressure, diastolic pressure never falls below 30 mmHg. Art. However, when measuring blood pressure using the Korotkoff method in patients with severe aortic valve insufficiency, diastolic pressure is often reduced to zero. This means that during blood pressure measurements, when the pressure in the cuff decreases below the true diastolic pressure, Korotkoff sounds continue to be heard in the aorta above the artery.

The reason for this discrepancy between direct and indirect blood pressure measurements lies in the mechanisms of the appearance of Korotkoff sounds when measuring blood pressure. One way or another, Korotkoff sounds are detected by auscultation as long as intermittent blood flow remains in a large artery. In a healthy person, such a “pulsating” blood flow is artificially created by compressing the brachial artery with a cuff. When the pressure in the cuff reaches diastolic blood pressure, the difference between the speed of blood flow in the brachial artery in systole and diastole decreases, and Korotkoff sounds sharply weaken (phase IV Korotkoff sounds) and disappear completely (phase V).

Severe aortic valve insufficiency is characterized by the constant existence of a large circle of “pulsating” blood flow in the arterial system. Therefore, if you listen to the area of ​​a large artery (even without compressing it with a cuff), sometimes (with severe aortic insufficiency) you can listen to sounds reminiscent of Korotkoff sounds. It should be remembered that an “endless tone” in a large artery (or diastolic blood pressure = 0) can also be determined with a pronounced decrease in tone arterial wall, for example, in patients with neurocirculatory dystonia.

In most cases, the radial pulse is characteristics: a rapid rise (increase) of the pulse wave and an equally sharp and rapid decline are determined.

The arterial pulse becomes fast, high, large and fast (pulsus celer, altus, magnus et frequens). Such a pulse, creating an alternation of rapid and strong tension in the walls of the arteries, can lead to the fact that tones begin to be detected in the arteries, where sounds are not normally heard. Moreover, the severity of pulsus celer et magnus may be reflected in the appearance of the so-called “palmar tone”, determined on the inner surface of the patient’s hand, applied to the doctor’s ear.

Instrumental diagnostics

ECG

An electrocardiographic study reveals a rotation of the electrical axis of the heart to the left, an increase in the R wave in the left chest leads, and, subsequently, a downward displacement of the ST segment and inversion of the T wave in the standard and left chest leads.

In case of aortic valve insufficiency, the ECG shows:

    In case of aortic valve insufficiency, in most cases, signs of pronounced LV hypertrophy are revealed without its systolic overload, i.e. without changing the terminal part of the ventricular complex. Depression of the RS-T segment and smoothness or inversion of T wave are observed only during the period of decompensation of the defect and the development of heart failure. With “mitralization” of aortic insufficiency, in addition to signs of LV hypertrophy, signs of left atrial hypertrophy (R-mitrale) may appear on the ECG.

X-ray examination

In case of aortic valve insufficiency, as a rule, distinct radiological signs LV expansion. In the direct projection, already at the very early stages of the development of the disease, a significant lengthening of the lower arch of the left contour of the heart and a displacement of the apex of the heart to the left and down are determined.

In this case, the angle between the vascular bundle and the LV contour becomes less obtuse, and the “waist” of the heart becomes more emphasized (“aortic” configuration of the heart). In the left anterior oblique projection, a narrowing of the retrocardial space occurs.

Echocardiography

Echocardiographic examination reveals a number of characteristic symptoms. The end-diastolic size of the left ventricle is increased. Hyperkinesia of the posterior wall of the left ventricle and the interventricular septum is determined. High-frequency flutter (tremor) of the anterior mitral valve leaflet, interventricular septum, and sometimes the posterior leaflet is recorded during diastole. The mitral valve closes prematurely, and during its opening the amplitude of movement of the leaflets is reduced.

Cardiac catheterization

During cardiac catheterization and appropriate invasive studies in patients with aortic insufficiency, an increase in cardiac output, LV EDP and the volume of regurgitation are determined. The latter indicator is calculated as a percentage relative to the stroke volume. The volume of regurgitation fairly well characterizes the degree of aortic valve insufficiency.

Diagnosis and differential diagnosis

Recognition of aortic valve insufficiency usually does not cause difficulties with diastolic murmur at Botkin's point or on the aorta, enlargement of the left ventricle and certain peripheral symptoms of this defect (high pulse pressure, increase in the pressure difference between the femoral and brachial arteries to 60-100 mm Hg . characteristic changes pulse).

However, diastolic murmur in the aorta and at the V point can also be functional, for example, with uremia. With combined heart defects and small aortic insufficiency, recognition of the defect can be difficult. In these cases, echocardiographic examination helps, especially in combination with Doppler cardiography.

The greatest difficulties arise in establishing the etiology of this defect. Others are possible rare causes: myxomatous valve disease, mucopolysaccharidosis, osteogenesis imperfecta.

Rheumatic origin heart disease can be confirmed by anamnesis: approximately half of these patients have indications of typical rheumatic arthritis. Convincing signs of mitral or aortic stenosis also speak in favor of a rheumatic etiology of the defect. Detection of aortic stenosis can be difficult. Systolic murmur over the aorta, as already mentioned above, is also heard in cases of pure aortic insufficiency, and systolic trembling over the aorta occurs only with its severe stenosis. In this regard, echocardiographic examination is of great importance.

The appearance of aortic insufficiency in a patient with rheumatic mitral heart disease is always suspicious for the development infective endocarditis. although it may also be due to a relapse of rheumatism. In this regard, in such cases it is always necessary to conduct a thorough examination of the patient with repeated blood cultures. Aortic valve insufficiency of syphilitic origin has become much less common in recent years. Diagnosis is facilitated by identifying signs of late syphilis in other organs, such as damage to the central nervous system. In this case, the diastolic murmur is better heard not at the Botkin-Erb point, but above the aorta - in the second intercostal space on the right and widely spreads down, on both sides of the sternum. The ascending aorta is dilated. In a significant number of cases positive serological reactions, the immobilization reaction of Treponema pallidum is of particular importance.

Aortic insufficiency may be due to atherosclerosis. With atheromatosis of the aortic arch, the valve ring expands with the appearance of slight regurgitation; atheromatous damage to the leaflets of the valve itself is less common. At rheumatoid arthritis(seropositive) aortic insufficiency is observed in approximately 2-3% of cases, and with a long course (25 years) of ankylosing spondylitis, even in 10% of patients. Cases of rheumatoid aortic insufficiency have been described long before the appearance of signs of damage to the spine or joints. Even less often, this defect is observed in systemic lupus erythematosus (according to V.S. Moiseev, I.E. Tareeva, 1980, in 0.5% of cases).

Prevalence Marfan syndrome in expressed form, according to various sources, from 1 to 4-6 per 100,000 population.

Cardiovascular pathology, along with typical changes in the skeleton and eyes, is part of this syndrome, but is difficult to detect in almost half of these patients only with the help of echocardiography. In addition to typical damage to the aorta with the development of its aneurysm and aortic insufficiency, damage to the aortic and mitral valves is possible. With a clear family predisposition and pronounced extracardiac signs of cardiovascular pathology, the syndrome is detected in childhood. If skeletal anomalies are mild, as in the patient described above, then heart damage can be detected at any age, however, usually in the third, fourth and even sixth decades of life. Changes in the aorta concern primarily the muscle layer; Necrosis with cysts are found in the wall, and fibromyc-somatous changes in the valves are possible. Aortic regurgitation often progresses gradually, but it can appear or worsen suddenly.

Cystic necrosis, without other signs of Marfan syndrome, is called Erdheim syndrome. It is believed that similar changes can simultaneously or independently occur in the pulmonary arteries, causing them the so-called congenital idiopathic dilatation. An important differential diagnostic feature that allows distinguishing aortic lesions in Marfan syndrome from syphilitic ones is the absence of its calcification. Damage to the mitral valve and chordae with their breakage occurs only in some patients, usually accompanies damage to the aorta and leads to prolapse of the mitral valve leaflets with mitral insufficiency.

A rare cause of aortic regurgitation may be Takayasu disease- nonspecific aortoarteritis, which occurs mainly in young women in the second - third decade of life and is associated with immune disorders. The disease usually begins with common symptoms: fever, weight loss, joint pain. Subsequently, the clinical picture is dominated by signs of damage to large arteries arising from the aorta, often from its arch. Due to impaired patency of the arteries, the pulse often disappears, sometimes only in one arm. Damage to the large arteries of the aortic arch can lead to cerebrovascular insufficiency and visual impairment. Defeat renal arteries accompanied by development arterial hypertension. Valvular insufficiency of the aorta may be due to dilatation of the aortic arch in patients with gangan cell arteritis. This disease develops in older people, manifesting itself as damage to the temporal arteries, which, in typical cases, are palpated in the form of a dense, painful, nodular cord. Intracardiac arteries may also be affected.

Aortic insufficiency is often combined with a variety of extracardiac manifestations, a careful analysis of which allows us to establish the nature of the heart defect.

Forecast

The life expectancy of patients, even with severe aortic insufficiency, is usually more than 5 years from the moment of diagnosis, and in half - even more than 10 years.

The prognosis worsens with the addition of coronary insufficiency (angina attacks) and heart failure. Drug therapy in these cases it is usually ineffective. The life expectancy of patients after the onset of heart failure is about 2 years. Timely surgical treatment significantly improves the prognosis.

Heart valve insufficiency

Incomplete closure of the heart valves leads to the flow of part of the blood back, from the cavity with high pressure to the cavity with lower pressure.

This is heart valve insufficiency, which leads to additional stress on the heart and an increase in direct blood flow through the valve.

Fatigue of the heart occurs, stretching of the cavities of the heart and large vessels near the valve.

Valve insufficiency and causes

When there is heart valve insufficiency, the ventricle adjacent to it must increase in size in proportion to the flowing volume of blood. The left ventricle has a conical shape and experiences higher pressure, and therefore is more often affected as a result of valve insufficiency, compared to the sickle-shaped right ventricle, which experiences noticeably less pressure. That is why heart failure is more often observed with valve insufficiency of the left chambers of the heart.

Diagnostics

Valve insufficiency is diagnosed in three stages. At the first stage, the very fact of insufficiency is established, which is determined by the characteristic regurgitation noise, and it is also recognized which specific valve is affected. The murmur of regurgitation always captures the relaxation phase. Auscultation (listening) is carried out over the aorta at the upper right edge of the sternum, the pulmonary trunk located at the upper left edge of the sternum, the mitral valve, and the tricuspid valve at the lower left edge of the sternum. In these places, noises characteristic of valve insufficiency are best heard. Listening is often enough to make a diagnosis.

The second stage should show the severity of valve insufficiency. Clarification is carried out using:

  • physical examination,
  • radiography,
  • The patient's complaints are also taken into account.

The third stage is to determine the origin of this pathology, since such knowledge determines the treatment regimen.

Venous heart insufficiency

Physical inactivity characteristic of modern life, which manifests itself in prolonged sitting or standing in one place and sometimes existing congenital features hormonal status and the vascular system often result in problems with venous blood outflow.

Venous insufficiency is determined by insufficiency of the deep vein valves. This is a very common pathology, which, unfortunately, is often not paid due attention. Scientists claim that this is man's payment to nature for walking upright.

Venous valves There are both deep and superficial veins. With thrombosis of the deep veins of the lower extremities, their lumen is blocked, and when it is restored, the valves remain affected. The veins lose and fibrosis begins, causing the vein valves to collapse and preventing normal blood flow.

The body needs valves to counteract the reverse flow of blood through the veins of the legs and when they are insufficient, venous insufficiency occurs. Pain and heaviness in the legs begin, swelling is observed in the evenings, disappearing by morning, night cramps occur, a noticeable change in the color of the skin in the lower part of the leg, loss of skin elasticity, and the appearance of varicose veins. In more late stage possible dermatitis, eczema and trophic ulcers, mostly in the ankle area

Treatment of valve insufficiency

Insufficiency of deep vein valves is treated with compression therapy, for which elastic bandages are used, but it is better to use special compression hosiery.

Sclerotherapy treatment involves injecting certain substances into the vein that irritate the inner wall of the vein, causing a chemical burn. In this case, the walls of the veins stick together and their fusion occurs. These drugs include:

ethoxysclerol, fibrowein and thrombovar. Compression of the veins is continued for three months.

Apply and surgical methods treatment, for example, removal of a conglomerate of varicose veins or ligation of the confluence saphenous vein thighs into the femoral vein.

Aortic valve stenosis is most often associated with a congenital bicuspid valve. Less commonly, the tricuspid aortic valve may degenerate and may be a consequence of rheumatic valvulitis. Mild to moderate aortic stenosis causes left ventricular hypertrophy. X-rays may reveal valve calcification. In typical cases Right side the ascending aorta protrudes due to poststenotic dilatation.

The border of the left ventricle may be rounded or there may be elevation of the apex of the heart due to concentric hypertrophy of the left ventricle. More severe valve narrowing may result in left ventricular and left atrium enlargement proportional to the degree of stenosis and severity of associated mitral regurgitation. Patients with severe aortic stenosis may also develop pulmonary venous hypertension and pulmonary edema.

Aortic regurgitation may occur with a stenotic bicuspid aortic valve. It may also result from rheumatic valvulitis, infective endocarditis, or annular dilatation resulting from enlargement of the ascending aorta in conditions such as annuloaortic ectasia. Aortic regurgitation can also be caused by aortic dissection. In mild aortic regurgitation, the heart size usually remains normal and the ascending aorta is normal sizes or slightly dilated. Left atrial enlargement suggests coexisting mitral regurgitation. In patients with moderate severity or severe aortic regurgitation, the left ventricle and aorta are enlarged. In contrast to aortic stenosis, patients with aortic regurgitation may experience diffuse dilatation of the aorta. If aortic regurgitation is secondary to annuloaortic ectasia, the aortic root is disproportionately enlarged. Valve calcification often occurs in patients with aortic regurgitation caused by congenital bicuspid valve or rheumatic aortic valve disease. In chronic aortic regurgitation, the left ventricle becomes enlarged, but the lungs appear normal. In acute aortic regurgitation, such as due to trauma or aortic dissection, a chest x-ray reveals pulmonary venous hypertension and pulmonary edema without left ventricular enlargement.

Mitral stenosis is most often secondary to rheumatic heart disease. One of the first radiological manifestations of mitral stenosis is a slight enlargement of the left atrium. With more severe stenosis, the left atrium dilates further, and its appendage may enlarge disproportionately. Pulmonary venous hypertension and cephalization may develop, as well as enlargement of the central pulmonary arteries. The mitral valve often becomes calcified. In most patients with mitral stenosis, the left ventricle appears normal.

Chronic mitral regurgitation can result from a variety of causes, such as ischemic cardiomyopathy, rheumatic heart disease, mitral valve prolapse due to myxomatous degeneration, and mitral annulus calcification. X-rays of the OGK reveal enlargement of both the left atrium and the left ventricle. Due to volume overload, a pronounced increase in chambers is possible. Acute mitral regurgitation can be caused by rupture of the chordae tendineus or papillary muscle, ischemic dysfunction, and bacterial endocarditis. Although the heart size may remain normal, these patients have left-sided heart failure causing severe alveolar pulmonary edema. Sometimes asymmetric pulmonary edema occurs, more severe in the right upper lobe. It results from selective retrograde blood flow from the mitral valve into the pulmonary veins of the right upper lobe. Valve assessment and quantitative measurement of the degree of regurgitation are carried out using echocardiography or MRI.

Tricuspid valve regurgitation may be due to ischemic cardiomyopathy, rheumatic heart disease, Ebstein's anomaly and other causes. In typical cases, the right chambers of the heart are enlarged, and the right atrium may be disproportionately dilated. Patients with tricuspid regurgitation experience massive enlargement of the heart, known as a “wall-to-wall heart.”

Why does the heart need valves?

The human heart is a hollow muscular organ, which is also called the “pump” in the human body. After all, this is how it is, the heart has to pump blood every minute, thereby providing our body with nutrients and oxygen. Moreover, the entire cardiovascular system is also involved in the removal (elimination) harmful substances and metabolic products from our body, thereby ensuring its full development.

The formation of the valve apparatus begins at the stage of formation of a two-chamber heart. Even then, a tubercle is formed, which will later become the site of development of the heart valves. At the same time that the four-chambered heart is being formed, valves are also being formed. In the final version, the heart acquires four chambers, which form the right venous and left arterial heart. In fact, a person has one heart, but due to the fact that blood with different gas compositions moves through the right and left sections, it is customary to divide it in this way.

The heart has four chambers, and the exit of each of them is equipped with a kind of “passage” - a valve apparatus. If a portion of blood has flowed from one chamber to another, the valve prevents it from flowing back to its original location. Thus, the correct direction of blood flow and the functioning of two circles of blood circulation are ensured - the small and large circles of blood circulation, working simultaneously.

Such names accurately reflect their characteristics. The small circle ensures blood flow in the vessels of the lungs, enriching the blood with oxygen. The systemic circulation, starting from the left ventricle, ensures the enrichment of all other organs and tissues with oxygen. If the heart valves did not work correctly, not performing the role of a “pass-through” at all, the work of the pulmonary and systemic circulation would not be possible.

2 Where are the valves located?

Each of these “passers” appeared in its own time and place. And such wonderful harmony allows the cardiovascular system to work clearly and correctly. Moreover, each of them has already received its own name. The exit from the left atrium is equipped with the left atrioventricular valve. Another name for it is bicuspid or mitral. It is called mitral because it resembles the Greek headdress - miter. The exit from the left ventricle, the ancestor of the systemic circulation, is the location of the aortic valve.

It is also called crescentic in another way, because its three doors resemble crescents. The opening between the right atrium and the right ventricle is the location of the right atrioventricular valve. Its other name is tricuspid or tricuspid. The exit from the right ventricle into the pulmonary trunk is controlled by the pulmonary valve, also called the pulmonary valve. The pulmonary valve or pulmonary valve also has three leaflets, which also resemble crescents.

3 How valves work

Heart valves work differently. The mitral and tricuspid operate in active mode. The aortic and pulmonary are passive, since their opening and closing is not supported by the chordae, as in the two above, but depends on the pressure and blood flow. Therefore, the mechanism of operation of leaflet and semilunar valves is different. When the blood pressure in the atrium becomes equal to that in the ventricles or exceeds it, the valve leaflets open into the cavity of the ventricles.

Being in a relaxed state, they do not interfere with the filling of the ventricles. Then the pressure in the ventricles begins to increase. Their walls tense, and the contraction of the papillary muscles present in the wall of the ventricles pulls the tendon threads - the chords. Thus, stretching like sails, the valves are protected from sagging into the cavity of the atria, and blood is not thrown back. The semilunar valves are closed at this moment, as they need to perform an important function - to prevent blood from returning back from large vessels to the ventricles.

When the increasing pressure in the ventricle begins to exceed that in the efferent vessels, they open, and blood from the ventricles is expelled into the aorta and pulmonary trunk. In this case, the blood, trying to get back into the chambers of the heart, first enters the pockets of the semilunar valves, which entails the slamming of the valves and obstruction of the retrograde flow of blood. This is how the human “pump” works thanks to the valve apparatus in response to received impulses from the conduction system. When filled with blood, the atria contract and push blood into the ventricles, and the latter into large vessels. And such work goes on twenty-four hours a day.

In the literature you can find interesting data that the human heart is capable of maximum load with its high activity, pump 40 liters of blood in one minute. Despite the fact that the human body consists of several tens of trillions of cells, the entire cardiac cycle takes only 23 seconds. That is, the large and small circles of blood circulation do their work in less than half a minute.

An amazing organ is our heart. Each component is important and necessary, including the valve apparatus. Without their proper functioning, the body's cells would not be able to receive oxygen and nutrients. Therefore, it is worth protecting your heart and taking care of it.

The four heart valves act as gates to prevent blood from flowing in the wrong direction.

If the valves are dilated, narrowed, do not close tightly or are torn, then they no longer close, and with each contraction of the heart, blood flows back into the ventricles or atria, respectively.

In this case, the heart constantly experiences heavy load and over time loses its effectiveness. In the worst case, this can lead to rhythm disturbances or even heart failure.

  • Aortic valve (outlet valve): Prevents blood from flowing from the aorta into the left ventricle of the heart.
  • Mitral valve (inlet valve): prevents blood from flowing from the left ventricle of the heart into the left atrium when contraction of the heart muscle forces blood into the circulatory vessels.
  • Pulmonary valve (outlet valve): Prevents blood from flowing from the pulmonary artery into the right ventricle of the heart.
  • Tricuspid valve (inlet valve): the valve between the right ventricle of the heart and the right atrium.

Heart defects may affect right And left half a heart.

  • Valves left ventricle: damage to the mitral and aortic valves: left heart failure
  • Valves in the right half: damage to the pulmonary and tricuspid valves, right heart failure

Forms of heart defects

A distinction is made between narrowing or calcification of the valves (stenosis and, accordingly, valvular sclerosis) and improper closure of the valve (heart valve insufficiency).

  • Narrowing (stenosis) and calcification (sclerosis) of the valves: insufficient blood flows.
  • Valve insufficiency (insufficient closure): blood leaks back even though the valve is closed.

Causes

There are many causes of valve defects. Acquired heart valve defects most often occur in the left half (mitral and aortic valves). The percentage of congenital heart defects is only 1%.

Specific reasons:

  • Calcification (sclerosis): can be compared in terms of the mechanism of formation with arteriosclerosis. The aortic valve is most often affected. Causes: age, poor diet, lack of exercise
  • Inflammation of the valves and lining of the heart (endocarditis): often due to the rheumatic process with mitral valve stenosis.
  • Heart attack: death of a certain area of ​​the heart muscle, the valves become weak or their function is impaired.
  • Bacterial and viral infections of the heart (myocarditis): lead to enlargement of the heart muscle and the inability of the valves to close tightly.
  • Congenital malformations (usually pulmonary stenosis)

Symptoms (complaints)

Complaints and symptoms depend on the severity of the disease. Often, heart valve defects do not cause any complaints for a long time. In this case, heart failure is in the stage of compensation, but over time the process decompensates, which can lead to heart failure.

Left heart defects (mitral and aortic valves)

Lead to the development of left heart failure

  • Stagnation of blood in the lungs, their swelling, which leads to difficulty breathing and shortness of breath
  • Dizziness and fainting during exercise and stress (primarily with aortic stenosis)
  • Complaints similar to a sore throat (feeling of pressure, chest pain, fear, squeezing and lack of air)
  • Heart rhythm disturbances (atrial fibrillation)

Heart defects in the right half (pulmonary and tricuspid valves)

Lead to the development of right heart failure

  • Swelling of the body (liver, ankle area), so-called edema, fatigue, decreased performance, shortness of breath on exertion.

Diagnostics (examination)

  • Studying the medical history and all symptoms
  • Examination of physical status (palpation, auscultation)
  • ECG: indicates valve damage.
  • Radiography chest: shows an increase in heart volume and the presence of edema.
  • Echocardiography (ultrasound of the heart) with or without contrast (this is The best way diagnostics of diseases of the valve apparatus): contractions of the heart and the function of its individual parts are presented in color.
  • Cardiac catheterization

Therapy (treatment)

Treatment is aimed at the cause of the disease and is different for different heart defects. Mild heart defects do not always need to be operated on. However, constant monitoring by specialists (cardiologists) is very important.

  • Therapy for heart failure
  • Therapy for atrial fibrillation
  • Treatment for stenosis (narrowing of the valves): surgery. A balloon of a certain size is inserted and the existing stenosis is expanded
  • Severe defects: surgical treatment with valve replacement with artificial grafts. In this case, blood-thinning drug therapy is used throughout life.
  • Infections: a combination of antibiotic therapy and surgical treatment.

Protection against infection due to valve defects

Before surgery, patients need to be given antibiotics to protect against infection. This is the only way to prevent inflammatory damage to the valves. This is called endocarditis prevention.

Possible complications

Without proper treatment, heart defects sometimes lead to death. Treatment depends on the type heart defect and the severity of damage to the heart muscle. Prevention of inflammation is necessary in any case. Inflammation may spread to neighboring organs and lead to the formation of abscesses and fistulas. When sections of tissue tear off and enter the bloodstream, thromboembolism can develop.

Preventive actions

The whole range of measures aimed at protecting heart function - healthy eating, normalizing weight, maintaining normal blood pressure - is a prevention of the development of heart defects.

  • Valve disease
  • Surgical methods of treatment
  • Valve replacement surgery
  • Mechanical and allografts

Heart valves ensure that blood moves in the right direction, preventing it from flowing back. Therefore, it is very important to maintain the correct rhythm of their work and, if it is disrupted, to carry out strengthening procedures.

Valve disease

Most often, heart valves begin to hurt when a person’s age exceeds 60-70 years. At this age, wear and tear on the body increases, as a result of which the work of the heart apparatus will become more difficult. But they can also arise as a result of infectious diseases affecting the cardiovascular system. In this case, the spread of infectious bacteria occurs quite rapidly and takes from 2 to 5 days.

The human heart muscle has 4 cavities, which include 2 atria and 2 ventricles. It is into them that blood enters from the veins, and from there it is distributed through the arteries of the body. The heart valves are located at the junction of the atria and the ventricles. Their structure helps maintain the direction of blood flow.

The heart valve has character traits, determining changes in its work, which are divided into 2 main groups. In the first case, the valve apparatus of the heart does not close completely, which leads to the return of blood mass (regurgitation). The second group of disorders includes incomplete opening of the valves (stenosis). This greatly impedes the flow of blood fluid, which puts a lot of strain on the heart and causes it to fatigue prematurely.

Valve defects are a fairly common disease. They make up 25-30% of all ailments of cardio-vascular system. In this case, mitral and mitral defects most often occur. Similar diagnoses can be established in children, since they may have viral nature origin. Infectious diseases that impair the functioning of the heart muscle include endocarditis, myocarditis and cardiomyopathy.

Most often, doctors make a diagnosis in which the work of the heart will be accompanied by extraneous noises or clicks. A similar violation occurs due to the fact that at the moment of ventricular contraction its opening does not close tightly. This causes the atrium to sag, causing blood to flow in the opposite direction.

Prolapse can be primary or secondary. Primary is congenital disease, which develops due to a genetic defect in connective tissues. Secondary prolapse may occur due to mechanical damage chest, myocardial infarction or rheumatism.

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Symptoms of the disease and its treatment

If a person has a malfunctioning heart valve, he will experience the following symptoms of the disease:

  • severe fatigue;
  • swelling of the legs and ankles;
  • pain and shortness of breath when walking and lifting heavy objects;
  • dizziness accompanied by fainting.

If such symptoms occur, you should immediately seek advice from a qualified specialist. He will help you understand why the heart valves are not working and develop the required course of treatment. Initially, patients are prescribed conservative methods treatment. They are aimed at removing pain, adjusting heart rhythm and preventing possible complications. Similar methods are prescribed after operations of the cardiovascular system; they help prevent relapses.

To determine more effective method Treatment by a doctor must take into account the severity of the disease, the patient’s age and all individual contraindications. Patients are prescribed medications that will increase the intensity of the heart muscle, and its functionality should improve. In the case when medicinal methods Treatments do not help, then surgery is prescribed.

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Surgical methods of treatment

Heart valve diseases are physical illnesses, therefore for full recovery heart failure, surgical intervention may be prescribed. Most often, during such operations, damaged valves are replaced.

Before the operation it is prescribed diagnostic examination patients, which will help identify damaged valves and identify the severity of the disease. In addition, during such examinations, doctors should obtain information about the structure of the heart and underlying diseases of the body.

To increase the effectiveness of surgical intervention, a similar procedure is combined with simultaneous bypass surgery, with the treatment of an aortic aneurysm or with atrial fibrillation.

Currently, there are two main types of surgery for the treatment of the cardiovascular system. The first type is gentle. It involves the restoration of damaged valves. The second type of operation is more complex: during it, a complete replacement is performed damaged organ.

If cardiologists prescribe surgical restoration, then in this case the use of individual parts is not provided. It lends itself best to such restoration. Sometimes reconstructive operations help improve the functioning of the tricuspid and aortic systems.

During reconstructive surgery, the degree of possible infection of the body is reduced, since there will be no rejection of foreign materials. In addition, patients will not need to take anticoagulants, which help thin the blood, for the rest of their lives.

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Valve replacement surgery

Complete replacement of heart valves is prescribed in cases where the restoration procedure is impossible. Most often, a complete replacement is performed when the aortic valves malfunction.

During this type of surgery, the damaged organ is completely replaced. During this process, the flap is changed, which is sewn to the original ring. For this purpose, biocompatible materials are used with body tissues to prevent their rejection.

After a complete replacement of the internal valves, all patients are prescribed mandatory pills that can thin the blood. Some of these medications include Coumadin, Marevan, or Warfarin. They will help significantly reduce the formation of large blood clots and delay their clotting. This quality will help prevent strokes or heart attacks. In addition, all patients after surgery must undergo blood tests, which will help track and evaluate the performance of the heart and the effectiveness of the medications taken.

Cardiac organ prostheses can have different structures: biological and mechanical.

Biological ones are made from bioprosthetic tissue based on internal organs cows or pigs. Less commonly, human donor material can be used. To facilitate their installation, several artificial components are used that will help to properly place and attach the implanted organ.

Biological prostheses work for quite a long time without causing failures. heart rate. The duration of their work can reach 15-20 years, while patients do not need to take anticoagulants daily.

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