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Minimal mitral regurgitation. Mitral regurgitation (mitral valve insufficiency). Diagnosis of mitral insufficiency

– valvular heart disease, characterized by incomplete closure or prolapse of the leaflets of the left atrioventricular valve during systole, which is accompanied by reverse pathological blood flow from the left ventricle to the left atrium. Mitral insufficiency leads to shortness of breath, fatigue, palpitations, cough, hemoptysis, swelling in the legs, and ascites. The diagnostic algorithm for detecting mitral insufficiency involves comparing data from auscultation, ECG, PCG, radiography, echocardiography, cardiac catheterization, and ventriculography. For mitral regurgitation, drug therapy and cardiac surgery (mitral valve replacement or plastic surgery) are performed.

General information

Mitral valve insufficiency is a congenital or acquired heart defect caused by damage to the valve leaflets, subvalvular structures, chords, or overstretching of the valve ring, leading to mitral regurgitation. Isolated mitral regurgitation is rarely diagnosed in cardiology, but in the structure of combined and concomitant heart defects it occurs in half of the cases.

In most cases, acquired mitral regurgitation is combined with mitral stenosis (combined mitral heart disease) and aortic defects. Isolated congenital mitral regurgitation accounts for 0.6% of all congenital heart defects; in complex defects it is usually combined with ASD, VSD, patent ductus arteriosus, coarctation of the aorta. In 5-6% of healthy individuals, echocardiography reveals some degree of mitral regurgitation.

Causes

Acute mitral regurgitation can develop due to ruptures of the papillary muscles, chordae tendineae, rupture of the mitral valve leaflets during acute myocardial infarction, blunt cardiac trauma, and infective endocarditis. Rupture of the papillary muscles due to myocardial infarction is accompanied by death in 80–90% of cases.

The development of chronic mitral regurgitation can be caused by damage to the valve due to systemic diseases: rheumatism, scleroderma, systemic lupus erythematosus, eosinophilic Loeffler's endocarditis. Rheumatic heart disease accounts for about 14% of all cases of isolated mitral regurgitation.

Ischemic dysfunction of the mitral complex is observed in 10% of patients with post-infarction cardiosclerosis. Mitral regurgitation can result from mitral valve prolapse, tear, shortening or lengthening of the chordae tendineae and papillary muscles. In some cases, mitral regurgitation is a consequence of systemic connective tissue defects in Marfan and Ehlers-Danlos syndromes.

Relative mitral regurgitation develops in the absence of damage to the valve apparatus during dilatation of the left ventricular cavity and expansion of the fibrous ring. Such changes occur in dilated cardiomyopathy, progressive arterial hypertension and coronary artery disease, myocarditis, and aortic heart defects. More rare causes of mitral regurgitation include leaflet calcification, hypertrophic cardiomyopathy, etc.

Congenital mitral insufficiency occurs with fenestration, splitting of the mitral leaflets, parachute deformation of the valve.

Classification

According to the course, mitral insufficiency is acute and chronic; by etiology - ischemic and non-ischemic. There is also a distinction between organic and functional (relative) mitral insufficiency. Organic failure develops when there is a structural change in the mitral valve itself or the tendon threads that hold it. Functional mitral regurgitation is usually a consequence of expansion (mitralization) of the left ventricular cavity due to hemodynamic overload caused by myocardial diseases.

Taking into account the severity of regurgitation, 4 degrees of mitral regurgitation are distinguished: with minor mitral regurgitation, moderate, severe and severe mitral regurgitation.

The clinical course of mitral regurgitation is divided into 3 stages:

I (compensated stage)- minor mitral valve insufficiency; Mitral regurgitation accounts for 20-25% of systolic blood volume. Mitral insufficiency is compensated by hyperfunction of the left heart.

II (subcompensated stage)- mitral regurgitation accounts for 25-50% of systolic blood volume. Blood stasis in the lungs and a slow increase in biventricular overload develop.

III (decompensated stage)- pronounced mitral valve insufficiency. The return of blood to the left atrium during systole is 50-90% of the systolic volume. Total heart failure develops.

Features of hemodynamics in mitral insufficiency

Due to incomplete closure of the mitral valve leaflets during systole, a regurgitant wave occurs from the left ventricle to the left atrium. If the reverse blood flow is insignificant, mitral insufficiency is compensated by increased heart function with the development of adaptive dilatation and hyperfunction of the left ventricle and left atrium of the isotonic type. This mechanism can restrain the increase in pressure in the pulmonary circulation for quite a long time.

Compensated hemodynamics in mitral regurgitation is expressed by an adequate increase in stroke and minute volumes, a decrease in end-systolic volume and the absence of pulmonary hypertension.

In severe forms of mitral regurgitation, the volume of regurgitation prevails over the stroke volume, and cardiac output is sharply reduced. The right ventricle, experiencing increased load, quickly hypertrophies and dilates, resulting in severe right ventricular failure.

In acute mitral regurgitation, adequate compensatory dilation of the left heart does not have time to develop. In this case, a rapid and significant increase in pressure in the pulmonary circulation is often accompanied by fatal pulmonary edema.

Symptoms of mitral regurgitation

During the compensation period, which can last several years, mitral regurgitation may be asymptomatic. In the subcompensation stage, subjective symptoms appear, expressed by shortness of breath, fatigue, tachycardia, anginal pain, cough, hemoptysis. With increasing venous stagnation in the pulmonary circulation, attacks of nocturnal cardiac asthma may occur.

The development of right ventricular failure is accompanied by the appearance of acrocyanosis, peripheral edema, liver enlargement, swelling of the neck veins, and ascites. When the recurrent laryngeal nerve is compressed by the dilated left atrium or pulmonary trunk, hoarseness or aphonia occurs (Ortner's syndrome). In the decompensation stage, more than half of patients with mitral insufficiency have atrial fibrillation.

Diagnostics

The main diagnostic data indicating mitral regurgitation are obtained during a thorough physical examination, confirmed by electrocardiography, phonocardiography, chest radiography and fluoroscopy, echocardiography and Doppler study of the heart.

Due to hypertrophy and dilatation of the left ventricle in patients with mitral insufficiency, a cardiac hump develops, an intensified diffuse apical impulse appears in the V-VI intercostal space from the midclavicular line, and pulsation in the epigastrium. Percussion determines the expansion of the boundaries of cardiac dullness to the left, up and to the right (with total heart failure). Auscultatory signs of mitral insufficiency are weakening, sometimes complete absence of the first sound at the apex, systolic murmur over the apex of the heart, accent and splitting of the second sound over the pulmonary artery, etc.

The information value of a phonocardiogram lies in the ability to characterize the systolic murmur in detail. ECG changes in mitral regurgitation indicate hypertrophy of the left atrium and ventricle, and in pulmonary hypertension - right ventricular hypertrophy. X-rays show an increase in the left contours of the heart, as a result of which the shadow of the heart acquires a triangular shape, congestive roots of the lungs.

Echocardiography allows you to determine the etiology of mitral regurgitation, assess its severity, and the presence of complications. Using Doppler echocardiography, regurgitation through the mitral orifice is detected, its intensity and magnitude are determined, which together makes it possible to judge the degree of mitral regurgitation. In the presence of atrial fibrillation, transesophageal echocardiography is used to identify blood clots in the left atrium. To assess the severity of mitral regurgitation, probing of the cardiac cavities and left ventriculography are used.

Treatment of mitral regurgitation

In case of acute mitral regurgitation, the administration of diuretics and peripheral vasodilators is required. To stabilize hemodynamics, intra-aortic balloon counterpulsation can be performed. No special treatment is required for mild asymptomatic chronic mitral regurgitation. In the subcompensated stage, ACE inhibitors, beta-blockers, vasodilators, cardiac glycosides, and diuretics are prescribed. With the development of atrial fibrillation, indirect anticoagulants are used.

In case of mitral regurgitation of moderate and severe severity, as well as the presence of complaints, cardiac surgery is indicated. The absence of calcification of the leaflets and the preserved mobility of the valve apparatus makes it possible to resort to valve-sparing interventions - mitral valve repair, annuloplasty, shortening of the chordae, etc. Despite the low risk of developing infective endocarditis and thrombosis, valve-sparing operations are often accompanied by relapse of mitral regurgitation, which limits their implementation to a fairly narrow range range of indications (mitral valve prolapse, ruptures of valve structures, relative valve insufficiency, dilatation of the valve ring, planned pregnancy).

In the presence of valve calcification and severe thickening of the chordae, mitral valve replacement with a biological or mechanical prosthesis is indicated. Specific postoperative complications in these cases may include thromboembolism, atrioventricular block, secondary infective endocarditis of prostheses, and degenerative changes in bioprostheses.

Prognosis and prevention

Progression of regurgitation with mitral regurgitation is observed in 5–10% of patients. The five-year survival rate is 80%, the ten-year survival rate is 60%. The ischemic nature of mitral regurgitation quickly leads to severe circulatory impairment and worsens prognosis and survival. Postoperative relapses of mitral insufficiency are possible.

Mild to moderate mitral regurgitation is not a contraindication to pregnancy and childbirth. With a high degree of deficiency, additional examination with a comprehensive risk assessment is necessary. Patients with mitral regurgitation should be observed by a cardiac surgeon, cardiologist and rheumatologist. Prevention of acquired mitral valve insufficiency involves preventing diseases leading to the development of the defect, mainly rheumatism.

From this article you will learn: what mitral valve insufficiency is, why it develops, and how it manifests itself. Degrees of the disease and their characteristics. How to get rid of mitral valve insufficiency.

Article publication date: 05/22/2017

Article updated date: 05/29/2019

Mitral valve insufficiency is a defect in which its leaflets are unable to close completely. Because of this, regurgitation (backflow of blood) from the left ventricle into the left atrium occurs.

The disease is dangerous because it leads to impaired circulation and related disorders of internal organs.

Valve disease can be completely cured with surgery. Conservative treatment is more symptomatic.

Treatment is provided by a cardiologist, cardiac surgeon, and rheumatologist.

Causes

This is an acquired defect, not congenital. Its causes can be diseases that damage the connective tissues of the body (since valves are made of connective tissue), and abnormalities of the valve itself.

Possible causes of mitral valve disease:

Systemic diseases Heart diseases Valve abnormalities
Rheumatism is a disease in which lymphocytes (immune cells) attack the connective tissue cells of their own body. Myocardial infarction – retraction of one or both of its leaflets into the cavity of the left atrium
Lupus erythematosus is a disease in which antibodies produced by the immune system damage the DNA of connective tissue cells. Endocarditis (inflammation of the inner lining of the heart) Age-related degenerative changes in the mitral valve
Marfan syndrome is a genetic disease in which the production of fibrillin 1, a structural component of connective tissue that gives it strength and elasticity, is impaired. Cardiac ischemia
Heart injuries

Symptoms, degrees and stages

The disease can occur in acute and chronic forms.

Acute mitral regurgitation occurs when the chordae tendineae or papillary muscles rupture during a heart attack or during infective endocarditis, as well as during cardiac injury.

Chronic develops gradually (in 5 stages) due to chronic diseases such as rheumatism, systemic lupus erythematosus, coronary heart disease, as well as due to pathologies of the mitral valve itself (its prolapse, degeneration).

Symptoms of acute bicuspid valve insufficiency:

  • A sharp drop in blood pressure leading to cardiogenic shock.
  • Left ventricular failure.
  • Pulmonary edema (manifested by suffocation, coughing, wheezing, sputum production).
  • Atrial extrasystoles.
  • Atrial fibrillation.

Degrees of mitral regurgitation

The severity of the defect can be determined by echocardiography (ultrasound of the heart). It depends on the volume of blood that flows back into the left atrium and the size of the hole that remains when the valve leaflets close.

Characteristics of degrees of severity:

Stages of the disease: characteristics and symptoms

Depending on the severity of the defect, the severity of circulatory disorders and the symptoms that bother the patient, 5 stages are distinguished:

  1. Compensation stage. It is characterized by grade 1 mitral valve insufficiency (regurgitation volume less than 30 ml). There are no circulatory disorders in the small and large circles. The patient is not bothered by any symptoms. The disease can be detected by chance during a routine medical examination.
  2. Subcompensation stage. The severity according to echocardiography is moderate. The reverse flow of blood into the left atrium leads to its expansion (dilatation). To compensate for circulatory disorders, the left ventricle is forced to contract more intensely, which leads to its increase - hypertrophy. With intense physical activity, shortness of breath and increased heart rate appear, which indicates that there is still a slight disturbance of blood circulation in the pulmonary (small) circle. Slight swelling of the legs (feet and legs) is possible.
  3. Stage of decompensation. The severity of regurgitation is 2–3. At this stage, blood circulation is disrupted in both the small and large circles. This is expressed by shortness of breath during any physical exertion, significant enlargement of the left ventricle, pressing, aching or stabbing pain in the left half of the chest (usually after physical activity), and periodic disturbances in heart rhythm.
  4. Dystrophic stage. Degree of severity – third (regurgitation more than 60 ml or 50%). The functioning of not only the left, but also the right ventricle is impaired. Echocardiography or chest x-ray may reveal hypertrophy of both ventricles. Blood circulation in both circles is significantly worsened. Because of this, severe swelling appears in the legs, pain both on the left and in the right hypochondrium (can also occur at rest), shortness of breath after minor physical activity or at rest, attacks of cardiac asthma (choking, coughing). Kidney and liver disorders appear. At this stage, tricuspid valve insufficiency may also be added to mitral valve insufficiency.
  5. Terminal stage. Corresponds to stage 3 of chronic heart failure. The functioning of all parts of the heart is impaired. The heart is no longer able to properly supply blood to all organs. The patient is concerned about shortness of breath at rest, frequent attacks of cardiac asthma, intolerance to any physical activity, swelling of the limbs and abdomen, pain in the heart, arrhythmias (atrial fibrillation,). Irreversible dystrophic changes develop in the internal organs (primarily the kidneys and liver). The prognosis is extremely unfavorable. Treatment is no longer effective.

Diagnostics

To identify the disease, one or more procedures are used:

  • conventional echocardiography;
  • transesophageal echocardiography;
  • X-ray of the chest organs;

Treatment

It can be surgical or medical. However, drug treatment cannot completely eliminate the pathology. Mitral regurgitation can only be completely cured through surgery.

Treatment tactics

In the acute form of mitral regurgitation, medications are urgently administered to relieve symptoms, and then surgery is performed.

In the chronic form, treatment tactics depend on the stage.

Stage Method of treatment
First stage (compensation stage) Surgical treatment is not indicated in most cases. It is possible to prescribe medications.
Second stage (subcompensation stage) Both drug treatment and surgical treatment are possible (the larger the volume of regurgitation, the more surgical intervention is needed).
Third stage (decompensation stage) An operation is required.
Fourth stage (dystrophic) Surgery is prescribed.
Fifth stage (terminal) It is incurable, as it leads to irreversible changes in the internal organs. It is possible to prescribe medications to relieve symptoms, but this does not affect the further prognosis and life expectancy.

Drug treatment

In the acute form of the disease, nitrates (Nitroglycerin) and non-glycoside inotropic drugs (for example, Dobutamine) are administered to the patient as first aid. After this, emergency surgery is performed.

In the chronic form, treatment should be aimed both at improving the functioning of the heart and blood circulation, and at getting rid of the underlying disease.

To correct circulatory disorders, diuretics, beta-blockers, aldosterone antagonists, nitrates, antiarrhythmic drugs, and ACE inhibitors are used. If the risk of thrombosis is increased, antiplatelet agents are used.

Treatment of the underlying disease that caused the mitral valve pathology:

Disease Drugs
Rheumatism Corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), antibacterial agents.
lupus erythematosus Corticosteroids, NSAIDs, immunosuppressants, TNF inhibitors.
Marfan syndrome Symptomatic for the prevention of cardiovascular complications: beta-blockers.
Endocarditis Antibiotics – as the main treatment; and thrombolytics - to prevent the progression of cardiovascular complications.
Cardiac ischemia Statins, fibrates, natural lipid-lowering agents - to influence the pathological process; nitrates, ACE inhibitors, antiarrhythmics, beta-blockers, antiplatelet agents - against cardiovascular complications.

Captopril is a representative of the class of ACE inhibitors

Surgery

It is prescribed for the acute form of the disease, as well as for the second and higher stages of the chronic form.

In modern surgical practice, two types of operations are used:

  1. Valve plastic surgery. This is the reconstruction of your own valve (suturing its valves and chordae tendineae).
  2. Valve replacement. This is its replacement with a prosthesis of artificial or biological origin.

By performing the operation on time, you can prevent further progression of the defect and associated heart failure.

Prevention

Preventive measures consist of treating the underlying disease even before the onset of mitral regurgitation (timely treatment of endocarditis with antibiotics, correct use of medications prescribed by a doctor for rheumatism, etc.).

Eliminate factors that increase the risk of heart disease: smoking, alcoholism, frequent consumption of fatty, salty and spicy foods, improper drinking regimen, lack of sleep, low mobility, obesity, stress, poor distribution of work and rest time.

Living with mitral regurgitation

If the defect is of the first degree of severity and is in the stage of compensation, you can only get by with observation from a doctor and taking a minimum amount of medication. Visit a cardiologist and do an echocardiogram every six months.

Physical activity within reasonable limits is not contraindicated, however, competitive sports activities are excluded at any stage of the disease.

As for pregnancy, at an early stage of the defect without significant circulatory disorders, it is possible, but childbirth will take place via cesarean section. For stage 2 or higher disease, successful pregnancy is possible only after the defect is eliminated.

After valve replacement, follow a healthy lifestyle to prevent cardiovascular disease. If you need any operations (including dental) or invasive diagnostic procedures in the future, notify your doctor in advance about the presence of a prosthetic valve, as you will be prescribed special medications to prevent inflammation and blood clots in the heart.

Forecast

The prognosis depends on the cause of the defect.

  • In most cases, it is unfavorable, since the underlying diseases (rheumatism, lupus, Marfan syndrome, coronary heart disease) are difficult to treat and cannot be completely stopped. Thus, the disease can lead to other damage to the heart, blood vessels and internal organs.
  • If the defect was caused by endocarditis or degenerative changes in the valve itself, the prognosis is more comforting. Cure is possible if timely surgery for plastic surgery or valve replacement is performed. The installed prosthesis will last from 8 to 20 years or more, depending on the type.
  • The prognosis for a defect of 1st degree of severity, which is not accompanied by circulatory disorders, can be favorable. With proper monitoring tactics, as well as treatment of the underlying disease, mitral regurgitation may not progress for many years.

Mitral insufficiency is a type of valvular heart disease. Pathogenesis is caused by incomplete closure of the mitral orifice, which is preceded by disturbances in the structure of the leaflets and tissues located under the valves.

The pathology is characterized by regurgitation of blood into the left atrium from the left ventricle. Let us consider in detail what it is, the nature of development and the clinical picture of the course of mitral valve insufficiency in degrees 1, 2 and 3 of the disease, methods of its treatment and the prognosis for returning to normal life.

MVR (mitral valve insufficiency) is the most common cardiac anomaly. Of all the sick 70% suffer from an isolated form of cerebrovascular accident. Typically, rheumatic endocarditis is the main underlying cause of the disease. Often a year after the first attack there is a heart condition, which is quite difficult to cure.

The highest risk group includes people with valvulitis.. This disease damages the valve leaflets, as a result of which they undergo processes of wrinkling, destruction, and gradually become shorter than their original length. If valvulitis is at an advanced stage, calcification develops.

Additionally, as a result of these diseases, the length of the chords is reduced, and dystrophic and sclerotic processes occur in the papillary muscles.

Septic endocarditis leads to the destruction of many cardiac structures, so NMC has the most severe manifestations. The valve flaps do not fit together tightly enough. When they are not completely closed through the valve, too much blood coming out, which provokes its reboot and the formation of stagnant processes, an increase in pressure. All signs lead to increasing insufficiency of uric acid.

Causes and risk factors

NMC affects people with one or more of the following pathologies:

  1. Congenital predisposition.
  2. Connective tissue dysplasia syndrome.
  3. Mitral valve prolapse, characterized by regurgitation of 2 and 3 degrees.
  4. Destruction and breakage of the chords, rupture of the valves of the mitral valve due to injuries in the chest area.
  5. Rupture of valves and chords during development.
  6. Destruction of the apparatus connecting the valves in endocarditis resulting from connective tissue diseases.
  7. Infarction of part of the mitral valve with subsequent scar formation in the subvalvular region.
  8. Changes in the shape of the valves and tissues located under the valves when rheumatism.
  9. Enlargement of the mitral annulus during dilatation cardiomyopathy.
  10. Insufficiency of valve function in the development of hypertrophic cardiomyopathy.
  11. MK insufficiency due to surgery.

Types, forms, stages

With NMC the total stroke volume of the left ventricle is estimated. Depending on its quantity, the disease is divided into 4 degrees of severity (the percentage indicates the part of the blood that is redistributed incorrectly):

  • I (the softest) - up to 20%.
  • II (moderate) - 20-40%.
  • III (medium form) - 40-60%.
  • IV (heaviest) - over 60%.

According to the forms of its course, the disease can be divided into acute and chronic:

When determining the features of movement of the mitral valves, there are 3 types of pathology classification:

  • 1 - standard level of mobility of the leaflets (in this case, painful manifestations consist of dilatation of the fibrous ring, perforation of the leaflets).
  • 2 - destruction of the valves (the chords take the greatest damage, as they are stretched or ruptured, and a violation of the integrity of the papillary muscles also occurs.
  • 3 - decreased mobility of the valves (forced connection of commissures, reduction in the length of the chords, as well as their fusion).

Danger and complications

With the gradual progression of NMC, the following disorders appear:

  1. thromboembolism due to constant stagnation of a large part of the blood.
  2. Valve thrombosis.
  3. Stroke. Previously occurring valve thrombosis is of great importance in the risk factors for stroke.
  4. Atrial fibrillation.
  5. Symptoms of chronic heart failure.
  6. Mitral regurgitation (partial failure of the mitral valve to perform functions).

Mitral valve insufficiency is a type of valvular heart disease. Pathogenesis is caused by incomplete closure of the mitral orifice, which is preceded by disturbances in the structure of the leaflets and tissues located under the valves. The pathology is characterized by regurgitation of blood into the left atrium from the left ventricle.

Symptoms and signs

The severity and severity of MCT depends on the degree of its development in the body:

  • Stage 1 the disease has no specific symptoms.
  • Stage 2 does not allow patients to carry out physical activity in an accelerated mode, since shortness of breath, tachycardia, pain in the chest, loss of heart rhythm, and discomfort immediately appear. Auscultation with mitral insufficiency determines increased tone intensity and the presence of background noise.
  • Stage 3 characterized by left ventricular failure and hemodynamic pathologies. Patients suffer from constant shortness of breath, orthopnea, increased heart rate, chest discomfort, and their skin is paler than in a healthy state.

Find out more about mitral regurgitation and hemodynamics with it from the video:

When to see a doctor and which one

When identifying symptoms characteristic of MCT, it is necessary contact a cardiologist immediately, to stop the disease in its early stages. In this case, you can avoid the need to consult with other doctors.

Sometimes there is suspicion of a rheumatoid etiology of the disease. Then you should visit a rheumatologist for diagnosis and proper treatment. If there is a need for surgical intervention, treatment and subsequent the problem is resolved by a cardiac surgeon.

Symptoms of mitral regurgitation may be similar to those of other acquired heart defects. We wrote more about how they manifest themselves.

Diagnostics

Common methods for detecting NMC:


Learn more about symptoms and diagnosis from the video:

It is necessary to distinguish NMC from other heart pathologies:

  1. Myocarditis in severe form.
  2. Congenital and acquired heart defects of related etiology.
  3. Cardiomyopathies.
  4. MK prolapse.

and how to cure this problem? You will find all the details in the available review.

About the symptoms of aortic valve insufficiency and the differences between this heart defect and the one described in this article in another material.

Also read the information about how Behçet's disease appears and how dangerous it is, and the methods of treating this disease.

Therapy methods

If symptoms of cervical urinary tract are severe, surgical intervention is indicated for the patient. The operation is performed urgently for the following reasons:

  1. In the second and later stages, despite the fact that the volume of blood ejected is 40% of its total amount.
  2. In the absence of effect from antibacterial therapy and worsening of infectious endocarditis.
  3. Increased deformation, sclerosis of the valves and tissues located in the subvalvular space.
  4. In the presence of signs of progressive left ventricular dysfunction together with general heart failure occurring at 3-4 degrees.
  5. Heart failure in the early stages can also be a reason for surgery, however, to form an indication, thromboembolism of large vessels located in the systemic circulation must be detected.

The following operations are practiced:

  • Valve-sparing reconstructive surgeries are necessary to correct cerebrovascular accidents in childhood.
  • Commissuroplasty and decalcification of the leaflets are indicated for severe MV insufficiency.
  • Chordoplasty is intended to normalize the mobility of the valves.
  • Translocation of cords is indicated when they fall off.
  • Fixation of parts of the papillary muscle is carried out using Teflon gaskets. This is necessary when separating the head of the muscle from the remaining components.
  • Prosthetics of the chords is necessary when they are completely destroyed.
  • Valvuloplasty avoids leaflet rigidity.
  • Anuloplasty is intended to relieve the patient of regurgitation.
  • Valve replacement is carried out when it is severely deformed or when fibrosclerosis develops irreparably and interferes with normal functioning. Mechanical and biological prostheses are used.

Learn about minimally invasive operations for this disease from the video:

What to expect and preventive measures

With the development of cerebrovascular accident, the prognosis determines the severity of the disease, that is, the level of regurgitation, the occurrence of complications and irreversible changes in cardiac structures. Survival rate 10 years after diagnosis is higher than for similar severe pathologies.

If valve insufficiency is mild or moderate, women have the ability to bear and give birth to children. When the disease becomes chronic, all patients should undergo an annual ultrasound and visit a cardiologist. If worsening occurs, you should visit the hospital more often.

If the condition worsens, surgical intervention is undertaken, so patients should always be prepared for this measure of cure for the disease.

Prevention of NMC consists in preventing or promptly treating diseases that cause this pathology. All diseases or manifestations of mitral valve insufficiency due to an abnormal or reduced valve must be quickly diagnosed and promptly treated.

NMC is a dangerous pathology that leads to severe destructive processes in the heart tissue, and therefore requires proper treatment. Patients, if they follow the doctor’s recommendations, may, some time after starting treatment,

How to get rid of mitral valve insufficiency.

Mitral valve insufficiency is a defect in which its leaflets are unable to close completely. Because of this, regurgitation (backflow of blood) from the left ventricle into the left atrium occurs.

The disease is dangerous because it leads to heart failure, circulatory disorders and related disorders of internal organs.

Valve disease can be completely cured with surgery. Conservative treatment is more symptomatic.

Treatment is provided by a cardiologist, cardiac surgeon, and rheumatologist.

Causes

This is an acquired defect, not congenital. Its causes can be diseases that damage the connective tissues of the body (since valves are made of connective tissue), heart disease and abnormalities of the valve itself.

Possible causes of mitral valve disease:

Symptoms, degrees and stages

The disease can occur in acute and chronic forms.

Acute mitral regurgitation occurs when the chordae tendineae or papillary muscles rupture during a heart attack or during infective endocarditis, as well as during cardiac injury.

Chronic develops gradually (in 5 stages) due to chronic diseases such as rheumatism, systemic lupus erythematosus, coronary heart disease, as well as due to pathologies of the mitral valve itself (its prolapse, degeneration).

Symptoms of acute bicuspid valve insufficiency:

  • A sharp drop in blood pressure leading to cardiogenic shock.
  • Left ventricular failure.
  • Pulmonary edema (manifested by suffocation, coughing, wheezing, sputum production).
  • Atrial extrasystoles.
  • Atrial fibrillation.

Degrees of mitral regurgitation

The severity of the defect can be determined by echocardiography (ultrasound of the heart). It depends on the volume of blood that flows back into the left atrium and the size of the hole that remains when the valve leaflets close.

Characteristics of degrees of severity:

Stages of the disease: characteristics and symptoms

Depending on the severity of the defect, the severity of circulatory disorders and the symptoms that bother the patient, 5 stages are distinguished:

  1. Compensation stage. It is characterized by grade 1 mitral valve insufficiency (regurgitation volume less than 30 ml). There are no circulatory disorders in the small and large circles. The patient is not bothered by any symptoms. The disease can be detected by chance during a routine medical examination.
  2. Subcompensation stage. The severity according to echocardiography is moderate. The reverse flow of blood into the left atrium leads to its expansion (dilatation). To compensate for circulatory disorders, the left ventricle is forced to contract more intensely, which leads to its increase - hypertrophy. With intense physical activity, shortness of breath and increased heart rate appear, which indicates that there is still a slight disturbance of blood circulation in the pulmonary (small) circle. Slight swelling of the legs (feet and legs) is possible.
  3. Stage of decompensation. The severity of regurgitation is 2–3. At this stage, blood circulation is disrupted in both the small and large circles. This is expressed by shortness of breath during any physical exertion, significant enlargement of the left ventricle, pressing, aching or stabbing pain in the left half of the chest (usually after physical activity), and periodic disturbances in heart rhythm.
  4. Dystrophic stage. Degree of severity – third (regurgitation more than 60 ml or 50%). The functioning of not only the left, but also the right ventricle is impaired. Echocardiography or chest x-ray may reveal hypertrophy of both ventricles. Blood circulation in both circles is significantly worsened. Because of this, severe swelling appears in the legs, pain both on the left and in the right hypochondrium (can also occur at rest), shortness of breath after minor physical activity or at rest, attacks of cardiac asthma (choking, coughing). Kidney and liver disorders appear. At this stage, tricuspid valve insufficiency may also be added to mitral valve insufficiency.
  5. Terminal stage. Corresponds to stage 3 of chronic heart failure. The functioning of all parts of the heart is impaired. The heart is no longer able to properly supply blood to all organs. The patient is concerned about shortness of breath at rest, frequent attacks of cardiac asthma, interruptions in heart function, intolerance to any physical activity, swelling of the limbs and abdomen, pain in the heart, arrhythmias (atrial fibrillation, atrial extrasystoles). Irreversible dystrophic changes develop in the internal organs (primarily the kidneys and liver). The prognosis is extremely unfavorable. Treatment is no longer effective.

Diagnostics

To identify the disease, one or more procedures are used:

  • conventional echocardiography;
  • transesophageal echocardiography;
  • X-ray of the chest organs;

Treatment

It can be surgical or medical. However, drug treatment cannot completely eliminate the pathology. Mitral regurgitation can only be completely cured through surgery.

Treatment tactics

In the acute form of mitral regurgitation, medications are urgently administered to relieve symptoms, and then surgery is performed.

In the chronic form, treatment tactics depend on the stage.

Drug treatment

In the acute form of the disease, nitrates (Nitroglycerin) and non-glycoside inotropic drugs (for example, Dobutamine) are administered to the patient as first aid. After this, emergency surgery is performed.

In the chronic form, treatment should be aimed both at improving the functioning of the heart and blood circulation, and at getting rid of the underlying disease.

To correct circulatory disorders, diuretics, beta-blockers, aldosterone antagonists, nitrates, antiarrhythmic drugs, and ACE inhibitors are used. If the risk of thrombosis is increased, antiplatelet agents are used.

Treatment of the underlying disease that caused the mitral valve pathology:

Surgery

It is prescribed for the acute form of the disease, as well as for the second and higher stages of the chronic form.

In modern surgical practice, two types of operations are used:

  1. Valve plastic surgery. This is the reconstruction of your own valve (suturing its valves and chordae tendineae).
  2. Valve replacement. This is its replacement with a prosthesis of artificial or biological origin.

By performing the operation on time, you can prevent further progression of the defect and associated heart failure.

Prevention

Preventive measures consist of treating the underlying disease even before the onset of mitral regurgitation (timely treatment of endocarditis with antibiotics, correct use of medications prescribed by a doctor for rheumatism, etc.).

Eliminate factors that increase the risk of heart disease: smoking, alcoholism, frequent consumption of fatty, salty and spicy foods, improper drinking regimen, lack of sleep, low mobility, obesity, stress, poor distribution of work and rest time.

Living with mitral regurgitation

If the defect is of the first degree of severity and is in the stage of compensation, you can only get by with observation from a doctor and taking a minimum amount of medication. Visit a cardiologist and do an echocardiogram every six months.

Physical activity within reasonable limits is not contraindicated, however, competitive sports activities are excluded at any stage of the disease.

As for pregnancy, at an early stage of the defect without significant circulatory disorders, it is possible, but childbirth will take place via cesarean section. For stage 2 or higher disease, successful pregnancy is possible only after the defect is eliminated.

After valve replacement, follow a healthy lifestyle to prevent cardiovascular disease. If you need any operations (including dental) or invasive diagnostic procedures in the future, notify your doctor in advance about the presence of a prosthetic valve, as you will be prescribed special medications to prevent inflammation and blood clots in the heart.

Forecast

The prognosis depends on the cause of the defect.

  • In most cases, it is unfavorable, since the underlying diseases (rheumatism, lupus, Marfan syndrome, coronary heart disease) are difficult to treat and cannot be completely stopped. Thus, the disease can lead to other damage to the heart, blood vessels and internal organs.
  • If the defect was caused by endocarditis or degenerative changes in the valve itself, the prognosis is more comforting. Cure is possible if timely surgery for plastic surgery or valve replacement is performed. The installed prosthesis will last from 8 to 20 years or more, depending on the type.
  • The prognosis for a defect of 1st degree of severity, which is not accompanied by circulatory disorders, can be favorable. With proper monitoring tactics, as well as treatment of the underlying disease, mitral regurgitation may not progress for many years.

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Mitral valve insufficiency

The mitral valve is a valve located between the left atrium and the left ventricle of the heart that prevents regurgitation of blood into the left atrium during systole.

Mitral valve insufficiency or mitral regurgitation is the inability of the valve to prevent regurgitation of blood from the left ventricle into the left atrium.

Regurgitation is the rapid flow of blood in the direction opposite to normal movement, occurring during systole.

Mitral regurgitation rarely occurs in isolation (about 2% of the total number of heart diseases). It is accompanied by aortic valve defects and mitral stenosis.

There are functional (relative) and organic mitral insufficiency.

Functional mitral regurgitation is caused by acceleration of blood flow during dystonia, changes in the tone of papillary muscle fibers, dilatation (expansion) of the left ventricle, which provides hemodynamic overload of the heart.

Organic mitral regurgitation develops as a result of anatomical damage to the connective tissue plates of the valve itself, as well as the tendon strands that fix the valve.

Hemodynamic disorders of these types of mitral insufficiency are of the same nature.

Hemodynamic disturbances in various forms of mitral insufficiency

Systole is a series of successive contractions of the ventricular and atrium myocardium of a certain phase of the cardiac cycle.

Aortic pressure significantly exceeds left atrial pressure, which promotes regurgitation. During systole, reverse blood flow occurs in the left atrium, caused by incomplete covering of the atrioventricular orifice by the valve leaflets. As a result, an additional portion of blood enters diastole. During ventricular diastole, a significant volume of blood flows from the atrium into the left ventricle. As a result of this disorder, overload occurs on the left side of the heart, which increases the force of contraction of the heart muscle. Myocardial hyperfunction is observed. At the initial stages of development of mitral insufficiency, good compensation occurs.

Mitral regurgitation leads to hypertrophy of the left ventricle and left atrium, resulting in increased pressure in the pulmonary vessels. Spasm of the pulmonary arterioles causes pulmonary hypertension, resulting in the development of right ventricular hypertrophy and tricuspid valve insufficiency.

Mitral valve insufficiency: symptoms, diagnosis

With good compensation of mitral valve insufficiency, symptoms do not appear. Severe mitral regurgitation is characterized by the following symptoms:

  • Shortness of breath and irregular heart rhythms during physical activity (then at rest);
  • Cardialgia;
  • Increased fatigue;
  • Cardiac asthma (attacks of severe shortness of breath);
  • Pain, swelling in the right hypochondrium, caused by an enlarged liver;
  • Edema of the lower extremities;
  • Dry cough with a small amount of sputum, in rare cases with blood;
  • Pain in the heart area of ​​a stabbing, pressing, aching nature, not associated with physical activity.

With compensated mitral valve insufficiency, symptoms may not appear for several years. The severity of symptoms is determined by the strength of regurgitation.

To diagnose mitral insufficiency, the following methods are used:

  • An ECG can reveal signs of overload and hypertrophy of the left ventricle and atrium, and in the third stage - of the right heart;
  • EchoCG - determination of hypertrophy and dilatation of the left heart;
  • X-ray examination of the chest organs - determining the degree of pulmonary venous hypertension, the degree of protrusion of the atrial arches;
  • Ventriculography – determining the presence and degree of regurgitation;
  • Ventricular catheterization – determination of pressure dynamics in the ventricles of the heart.

Currently, there is an overdiagnosis of mitral insufficiency. Modern research methods have shown that a minimal degree of regurgitation can be present in a healthy body.

Mitral valve insufficiency 1st degree: clinical picture

Mitral valve insufficiency of the 1st degree is characterized by compensation of hemodynamics and the inability of the valve to prevent the reverse flow of blood, which is achieved by hyperfunction of the left ventricle and atrium. This stage of the disease is characterized by the absence of symptoms of circulatory failure and the patient’s well-being during physical activity. When diagnosing mitral valve insufficiency of the 1st degree, a slight expansion of the borders of the heart to the left and the presence of systolic murmurs are detected. There are no signs of valve dysfunction on the electrocardiogram.

Mitral valve insufficiency 2nd degree: clinical picture

Mitral valve insufficiency of the 2nd degree is characterized by the development of a passive form of venous pulmonary hypertension. This stage is characterized by a number of symptoms of circulatory disorders: shortness of breath and rapid heartbeat during physical activity and at rest, cough, attacks of cardiac asthma, hemoptysis. When diagnosing mitral valve insufficiency of the 2nd degree, expansion of the borders of the heart to the left (1 - 2 cm), to the right (up to 0.5 cm) and upward, and systolic murmurs are detected. The electrocardiogram shows changes in the atrial component.

Mitral valve insufficiency 3rd degree: clinical picture

With mitral valve insufficiency of the 3rd degree, right ventricular hypertrophy develops, which is accompanied by characteristic symptoms: liver enlargement, development of edema, increased venous pressure.

Diagnosis of mitral valve insufficiency of the 3rd degree reveals a significant expansion of the boundaries of the heart muscle and intense systolic murmurs. An electrocardiogram shows the presence of a mitral wave and signs of left ventricular hypertrophy.

Treatment of mitral valve insufficiency, prognosis

Treatment of mitral valve regurgitation is governed by a single rule: a patient diagnosed with mitral regurgitation is a surgical patient. This pathology is not subject to drug correction. The task of the cardiologist is to properly prepare the patient for surgery.

Conservative treatment of mitral valve insufficiency is aimed at controlling the heart rate, as well as preventing thromboembolic complications and reducing the degree of regurgitation. Symptomatic treatment is also used.

During surgery, the mitral valve is implanted.

Prognosis for mitral regurgitation depends entirely on the degree of regurgitation, the severity of the valve defect and the dynamics of the disease.

Video from YouTube on the topic of the article:

The information is generalized and is provided for informational purposes. At the first signs of illness, consult a doctor. Self-medication is dangerous to health!

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Mitral valve insufficiency: causes, diagnosis and treatment of valve defect

Return blood flow in the left chambers of the heart disrupts normal pumping function. Mitral valve insufficiency of the 1st degree is manifested by minimal symptoms that do not create difficulties for everyday life. As valvular insufficiency worsens, clinical manifestations increase, which requires a full range of therapeutic and diagnostic procedures. Treatment tactics and prognosis for life depend on the stage of the disease and the presence of cardiac complications.

Causes of valve pathology

Regurgitation is a condition of blood circulation when, against the background of a malfunction of the valve apparatus, the possibility of non-physiological reflux of blood back into the atrium arises. The main reasons for the malfunction of the mitral valve are the following factors:

  • rheumatic disease;
  • cardiac defects of congenital origin;
  • atherosclerosis;
  • infectious-septic endocarditis;
  • ischemia of the heart muscle (CHD);
  • systemic types of pathology (scleroderma, arthritis, lupus);
  • traumatic damage to smooth muscle tissue or chordae tendineae;
  • cardiovascular diseases contributing to left ventricular dilatation.

The most common cause of pathology is infection. Cicatricial post-inflammatory changes in the valve between the atrium and the ventricle form regurgitant blood flow and the main manifestations of the disease.

Types of disease

Depending on the causative factors, there are 2 groups of mitral valve pathology:

  • rheumatic origin (direct damaging effect on the valve);
  • non-rheumatic pathology (pathological changes in the perivalvular structures - tendon cords, muscle tissue or valve ring).

It is important to distinguish the anatomical and functional type of cardiac pathology. In the first case, regurgitation occurs against the background of organic changes in the valve. The second option is relative insufficiency caused by overstretching (dilatation) of the valve ring due to myocarditis, cardiomyopathy or coronary artery disease.

Depending on the severity of symptoms, there are 3 successive stages of the disease:

  1. Compensatory (1st degree) – minimal manifestations of the disease;
  2. Mitral valve insufficiency of the 2nd degree (subcompensation) - problems arise during physical activity;
  3. Decompensation (grade 3) – symptoms appear at rest.

Hemodynamic changes caused by the anatomical defect of the valve are of great importance for clinical manifestations. At the initial stage of the disease, when an increased amount of blood enters the left atrium (inflow from the veins and regurgitation), compensatory hypertrophy occurs, ensuring the absence of pronounced symptoms. Then the cardiac muscle of the left ventricle hypertrophies, which has to work hard to ensure adequate blood flow to the aorta.

Stage 3 decompensation or mitral valve insufficiency occurs when the heart is unable to provide systemic blood flow.

Symptoms of valve insufficiency

The long-term absence of manifestations of the disease is due to slow organic changes and compensatory capabilities of the heart muscle. Primary signs of mitral valve insufficiency occur against the background of a serious unexpected load and are manifested by the following complaints:

  • severe lack of air (shortness of breath);
  • severe weakness with rapid fatigue;
  • tachycardia (increased heart rate);
  • cardiac arrhythmia.

As the insufficiency of the mitral valve function increases, the symptoms intensify: swelling of the legs occurs, suffocation, coughing and shortness of breath in the absence of movement can be bothersome.

The prognosis for recovery depends on the timeliness of visiting a doctor - it is optimal to start therapy at the stage of a compensated type of pathology.

Diagnostic principles

Listening to heart sounds (auscultation) during the initial examination will allow the doctor to suggest the presence of pathology. Typical auscultatory signs include:

  • pansystolic murmur;
  • weakening or absence of the first tone;
  • third tone, the presence of which indicates severe regurgitation;
  • accent of the second tone over the pulmonary artery.

An experienced specialist, having assessed auscultatory signs, will make a preliminary diagnosis and refer for additional examination:

  1. Electrocardiography, which can reveal signs of hypertrophy of the atrium and ventricle on the left;
  2. X-ray of the chest area (detecting an enlarged heart, identifying signs of pulmonary hypertension and valve calcification);
  3. Echocardiography with Doppler (assessment of anatomical changes, detection of regurgitant blood flow);
  4. Contrast angiocardiography (the optimal and most reliable method for diagnosing pathology).

Cardiac ultrasound can assess the severity of mitral regurgitation.

  • reverse cast no more than 30%;
  • the area of ​​the valve defect is no more than 0.2 cm2;
  • regurgitant blood does not reach the middle of the atrium.

Against the background of subcompensation:

  • return blood flow reaches the middle of the atrium and is up to 50%;
  • the area of ​​the unclosed hole is 0.2-0.4 cm2.

With decompensation, regurgitant reflux exceeds 50%, blood fills the entire atrium, and the valve defect is more than 0.4 cm 2.

An important factor for choosing treatment tactics is to identify the cause of valvular pathology: therapy for rheumatic lesions differs from functional disorders associated with myocarditis or the consequences of coronary artery disease.

Treatment tactics

The choice of therapy method is determined by the following criteria:

  • causative factor of valve pathology;
  • stage of the disease;
  • the presence of concomitant diseases (hypertension, ischemic heart disease, endocrine pathology, atherosclerosis).

In case of insufficiency of mitral valve function, treatment can be medicinal and surgical.

Conservative methods

The main goals of therapy are to reduce the load on the left chambers of the heart and prevent complications. The following methods are used for this:

  • antibiotic therapy;
  • antimicrobial prevention of endocarditis and relapses of rheumatism;
  • limiting physical activity;
  • diet therapy with salt restriction;
  • anticoagulants;
  • symptomatic drugs (hypotensive, diuretic, antiarrhythmic drugs and cardiac glycosides).

It is necessary to regularly see a doctor even if there are no symptoms during the initial stage of mitral regurgitation.

Surgery

Against the background of decompensation with a pronounced degree of regurgitation, when drug therapy is ineffective, 2 surgical treatment options are used:

  • reconstructive valve surgery;
  • valve replacement.

The choice of method is individual - for each specific patient, a different version of the operation is selected. The prognosis largely depends on the timeliness of the surgical intervention performed. Possible postoperative complications include septic endocarditis, thromboembolism, and prosthetic malfunction.

Risk of dangerous complications

Against the background of effective therapy and in the long-term postoperative period, unpleasant consequences and illnesses are possible. Dangerous complications of the rheumatic variant of valvular insufficiency are the following pathologies:

  • left ventricular congestive heart failure;
  • septic endocarditis;
  • atrial fibrillation;
  • cor pulmonale with typical symptoms of pulmonary hypertension;
  • vascular thromboembolism with a high risk of sudden death.

After valve surgery, the prognosis is better and the risk of complications is lower than when using an artificial valve prosthesis.

The main factor in the occurrence of regurgitant blood flow in the left chambers of the heart is rheumatic damage to the valve apparatus.

At the beginning of the disease there are no symptoms, but as the disease progresses and the backflow of blood into the left atrium increases, the manifestations of cardiac pathology increase.

The basis of primary diagnosis is ECG and echocardiography. In difficult cases, the doctor will refer you for a contrast study (angiocardiography). Drug treatment will be effective if the disease is detected early. Against the background of decompensation, surgery will be required to restore the functions of the valve apparatus.

Mitral valve insufficiency in children and adults is a common defect

The health of the heart depends on whether there are congenital abnormal changes in its structure. However, not everyone knows that smoldering foci of infection can also provoke heart disease. There are other diseases that can initiate this.

Knowing what affects the activity of the heart, what signs of the onset of a pathological process will help you seek help from a doctor in time and avoid worsening the situation.

Features of the disease

Nature has established that the flow of blood from the left atrium through the valve into the corresponding ventricle has no return. Disturbances of various kinds make it possible, during a push of blood (systole), to send some part of its volume back into the atrium. An anomaly of this kind can be detected at any age. For all age categories, pathology has the same causes and manifestations. The disorder refers to heart defects that are very common.

Mitral regurgitation is, in other words, a valve that is designed to allow blood from the left atrium to enter the corresponding ventricle and prevent its backflow, does not fully cope with the task. The reasons why this happens are varied.

The defect can be congenital or appear as a result of negative changes. Then it is classified as an acquired defect.

More often, a concomitant problem is aortic heart defects and narrowing of the mitral valve. The patient may have these complementary disorders all at once or one of several variants.

Pathology can develop at different speeds.

Mitral insufficiency (scheme)

Forms

The chronic form is detected over a period of time as a result of:

  • changes in the tissues of heart structures as a consequence of diseases,
  • development of pathology due to abnormal congenital features,
  • if the valve was replaced, there is a possible violation of the implant structure.

The acute form of the pathology manifests itself in a short period of time. Crisis situations lead to such cases:

  • myocardial infarction,
  • rupture of the leaflets due to infective endocarditis,
  • other acute conditions.

The following video contains detailed information about mitral regurgitation, presented in an accessible form:

Degrees

The disorder is classified according to the level of blood volume return. Degrees:

  • 1st. The problem is minor. The volume of blood in its reverse stroke during the ventricular impulse (systole) reaches the surface of the valve. The situation does not cause disruptions in the functioning of the heart and is normal.
  • 2nd. The movement of blood into the atrium relative to the mitral valve is approximately one and a half centimeters. The violation is considered a moderate deviation from the norm.
  • 3rd. The return of blood reaches the midline of the atrium. This abnormal blood movement is considered a severe disorder.
  • 4th. When the blood in its reverse movement reaches the upper part of the atrium. The situation is classified as severe heart damage.

Causes of mitral valve insufficiency

Regurgitation (return of blood) is caused by reasons inside the body:

  1. The problem may be associated with the following functional disorders:
    • The tendon threads that serve as the connecting link between the heart muscle and the papillary muscles are torn or stretched.
    • The muscles that are responsible for the movement of the valve leaflets (papillary) have changed their tone, and now it does not correspond to the norm.
    • The ring to which the valve flaps are attached has stretched.
    • The ventricle of the left half increased in volume.
  2. The return of blood may be due to the functional inferiority of the valve itself. The double-leaf design does not ensure tight closure of the doors when closing.

Congenital disease

In the case of mitral regurgitation from birth, the causes may be factors that influenced the development of the fetus during pregnancy:

    • stressful situations,
    • unfavorable environmental conditions,
    • contact with substances whose effects are harmful to the body;
    • influence of ionizing radiation,
    • taking pills without consulting a specialist.

Consequences of past illnesses

Mitral insufficiency occurs as a consequence of previous diseases:

  • A tumor process that interferes with the release of the ventricle.
  • Damage or pathological change in elements in the structure of the heart as a result of:
    • myocardial infarction,
    • myocarditis,
    • dilated cardiomyopathy,
    • rheumatism,
    • infective endocarditis,
    • lupus erythematosus.

Symptoms

  • The correct distribution of blood in the body is disrupted, so the patient feels weak performance and loss of strength.
  • Congestion in the blood supply to the lungs is manifested by shortness of breath.
  • The process that contributed to the valve damage can compromise the health of the heart muscle. As a result, arrhythmia occurs.
  • Stagnation of blood in the lungs initiates a cough. At the beginning of the disease it has a dry character. Subsequently, sputum appears with blood streaks.

Diagnostics

The doctor analyzes the patient’s symptoms, asks about the history of the disease and whether relatives have such problems. After this, he selects methods for examining the patient.

  • Echocardiography is a method that will determine the possibility of returning blood volume to the atrium based on the state of functional structures. When performing Doppler echocardiography, you can see if there is regurgitation during systole.
  • Magnetic resonance imaging allows you to see an image of the heart in all its structural details.
  • Catheterization – the pressure in individual chambers of the heart can be measured. These indicators make it possible to establish mitral insufficiency.
  • A phonocardiogram complements and clarifies the examination of the patient by listening with a stethoscope. Allows you to determine the noise in the area of ​​the mitral valve when the ventricle sends blood into the aorta (systole).
  • Electrocardiogram – makes it possible to study irregular heart rhythms.
  • A blood test shows whether there is an inflammatory process in the body.
  • Coronarocardiography is a method of monitoring the condition of blood vessels using a dye. It shows the movement of blood in the heart and blood vessels in the image.
  • X-ray is a picture of the chest area. Changes in the size and shape of the heart are determined.

Treatment

If mitral insufficiency is up to the second degree, then often this situation does not require help. It is important to cure the disease that initiated the disorders that led to mitral regurgitation.

Therapeutic

  • Treatment courses are prescribed to prevent the development of infectious processes.
  • Hardening procedures are recommended.
  • Physiotherapeutic treatment.
  • The direction of assistance is chosen to suppress the pathology that caused negative changes in the heart.
  • The doctor refers you to a sanatorium-resort treatment, where there is the necessary specialization.

Medication

If there are complications associated with the return of blood to the atrium, then medications are used to maintain the patient’s condition.

  • Potassium supplements – support the condition of the myocardium,
  • diuretics - to avoid swelling,
  • nitrates – to improve blood circulation,
  • cardiac glycosides - alleviate the condition in case of heart failure.

Operation

In case of pathology development to the third and fourth degrees, surgical intervention is recommended. With the help of radical surgery, according to indications in a particular case, the following is performed:

  • correction of structural defects through plastic surgery,
  • valve replacement.

If the pathology is severe and surgical intervention is not possible due to the patient’s condition, his health is maintained with the help of medications and therapeutic procedures.

The video below explains in more detail how the operation for mitral heart failure occurs:

Disease prevention

If we talk about preventing congenital mitral valve insufficiency, then during pregnancy it is necessary to exclude any harmful influence on it:

  • do not be in an area where there may be ionizing radiation;
  • do not come into contact with harmful chemicals,
  • stay in an area with good environmental conditions.

To prevent the occurrence of an acquired disease, observe:

  • treat infectious diseases in a timely manner; prevent smoldering foci of infection;
  • prevent the occurrence of other pathologies that can cause mitral regurgitation;
  • lead a healthy lifestyle,
  • eliminate acute stressful situations,
  • give the body a feasible systematic load, for example: walking, swimming.

Complications

  • pulmonary hypertension,
  • the electrical impulse between the parts of the heart may be disrupted,
  • atrial fibrillation, and there may also be other rhythm disturbances;
  • inflammatory processes in the inner membranes of the heart muscles,
  • heart failure.

We will tell you about the prognosis for proper treatment of mitral valve insufficiency of degrees 1, 2, 3 at the end of the article.

Forecast

The prospect depends on several components:

  • condition of the heart muscles,
  • how realistic is it to cure the disease that caused the pathology; its heaviness;
  • the degree of abnormal valve function.

With mitral regurgitation of the third degree, heart failure may develop. From the moment of diagnosis, almost all patients live more than five years. More than 4/5 of the total number of patients with this problem live ten years or more.

With the second degree of development of the pathology, patients may not experience any health problems for several years.

The following video presents a consultation with a renowned physician regarding mitral regurgitation.

Ischemic mitral regurgitation is a serious disease with a poor prognosis. The progressive and often insidious course caused by coronary pathology significantly distinguishes ischemic mitral regurgitation from mitral regurgitation associated with other causes.

Ischemic mitral regurgitation is a consequence of myocardial infarction, which always precedes the appearance of mitral regurgitation. In this case, the state of the valves and subvalvular structures does not change. Thus, the term ischemic mitral regurgitation excludes other etiological causes of mitral regurgitation - infectious, degenerative connective tissue diseases, rupture of chordae, congenital cusp prolapse, etc. Mitral regurgitation associated with ischemic cardiomyopathy and left ventricular dysfunction is a similar phenomenon, but still etiologically different from true ischemic mitral insufficiency. Intermittent mitral regurgitation caused by transient ischemia, as a rule, occurs infrequently and manifests in parallel with angina pectoris.

Ischemic mitral regurgitation can develop acutely due to rupture of the papillary muscle or gradually, due to post-infarction remodeling of the left ventricular cavity. Thus, ischemic mitral regurgitation is not a disease of the valve, but of the myocardium. However, mitral regurgitation associated with other causes also has secondary effects on the myocardium.

In 17-55% of patients after acute myocardial infarction, a systolic murmur of mitral regurgitation or echocardiographic confirmation of mitral regurgitation appears. Among patients who underwent cardiac catheterization within 6 hours after myocardial infarction, 18% were diagnosed with mitral regurgitation. In 3.4% of these patients, stage III mitral regurgitation was observed, in 7.2% - stage II, however, in many patients these phenomena disappear over time. The most typical occurrence of mitral regurgitation is after transmural posterior myocardial infarction.

Rupture of the papillary muscle is the most dangerous prognostic sign. The posterior papillary muscle is involved in myocardial infarction 3-6 times more often than the anterior one. In most cases, a partial rupture is characteristic. Complete rupture usually occurs within the first week after acute myocardial infarction, while partial rupture may be delayed for up to 3 months.

Acute myocardial infarction can also lead to the development of severe mitral regurgitation without rupture of the papillary muscle. This is due to dysfunction of the latter when it is involved in the area of ​​infarction, often hemorrhagic.

Chronic mitral regurgitation is associated with distortion of the posterior papillary muscle due to dilatation of the left ventricular cavity, which takes on the shape of a ball. In parallel with this, there is an expansion (> 3 cm in diameter) of the left atrioventricular opening. The mitral valve annulus tends to expand in proportion to the volume of the left ventricular cavity.

The mitral valve consists of six anatomical components: leaflets, chords, annulus, papillary muscles, left ventricular wall and left atrium. The mitral annulus has a saddle shape (a hyperbolic paraboloid with bidirectional curvature). In the area of ​​the geometric center, the fibrous ring of the mitral valve has a bend in the cephalic direction, and in the area of ​​the commissures - in the caudal direction.

During isovolumic contraction of the left ventricle and closure of the mitral valve, the left atrium is filled until the aortic valve opens. At this time, the flow through the mitral valve rapidly decreases, the leaflets close and bend towards the atrium. During systole, the left atrium quickly fills, the valve ring moves slightly towards the atrium and then gradually descends 1-1.5 cm towards the apex during ventricular systole. In addition, the ring contracts asymmetrically, reducing valve area by an average of 27%. Immediately after the end of atrial systole, when the pressure in the left ventricle exceeds the pressure in the atrium, the leaflets move closer to each other within 20-60 milliseconds. Considering that the area of ​​the mitral valve leaflets is twice the area of ​​the left atrioventricular orifice, the line of their closure is in the plane of the mitral valve annulus. When the valve closes, 30% of the anterior and 50% of the posterior leaf are in close contact with each other. Chordal tension limits the upward movement of the leaflets; the tension peaks in early systole, decreases slowly in late systole, and falls rapidly in early diastole. The papillary muscles begin to shorten (2-4 mm) during late diastole, synchronously with the myocardium of the left ventricular wall. During systole, the ventricle twists counterclockwise.

The area of ​​the mitral valve reaches its maximum during diastole (up to 3.9±0.7 cm 2 /m 2), while its shape changes asymmetrically: the maximum lengthening of the perimeter of the mitral ring occurs due to an increase in the posterior semicircle. Although peak flow through the valve occurs in diastole, the leaflets reach their maximum open position before peak flow is reached and begin to close while flow is still accelerating.

The left ventricle, during early diastole and the period of rapid filling, expands primarily along the transverse axis and much less along the longitudinal axis. During early diastole, the wall thickness of the left ventricle decreases and the ventricle rapidly unwinds, rotating clockwise, slowing to a speed in mid-diastole and late diastole.

Mechanism of ischemic mitral regurgitation

Acute ischemic mitral regurgitation

Numerous studies have shown that the loss of papillary muscle contraction alone as a result of acute ischemia does not lead to mitral regurgitation. The resulting changes in the dynamics of contraction of the papillary muscle not only cause leaflet prolapse due to the effect of decreasing tension, but also affect the cooptation of the leaflets. Thus, ischemic mitral regurgitation is the result of a violation of the complex geometric and temporal parameters of the mitral apparatus, which cannot be proven by standard diagnostic methods and cannot be noticeable in a stopped heart during surgery.

Chronic ischemic mitral regurgitation

Chronic ischemic mitral regurgitation in most patients develops due to limited mobility of the leaflets due to fibrosis and atrophy of the papillary muscles, while lengthening of the chordae and papillary muscles is not observed. In patients with pre-existing mitral valve prolapse, myocardial infarction may cause the previously competent valve to become regurgitated. In this case, the area of ​​the mitral annulus expands by 60% during the entire period of systolic ejection due to the fact that the more mobile part of the base of the posterior leaflet is stretched simultaneously with the distortion of the posterior papillary muscle.

Thus, geometric changes in the mitral apparatus that lead to its acute insufficiency are often repeated, but extremely subtle (< 5 мм) и недоступны клиническим методам исследования. Хроническая митральная недостаточность приводит к большим изменениям (1-2 см), которые вызывают умеренное расширение кольца и комплексное натяжение створок, нарушающее их кооптацию.

Pathophysiology

Acute mitral regurgitation immediately leads to left ventricular volume overload, increasing left ventricular preload and reducing systolic output. The amount of regurgitation depends on the degree of valve incompetence. Mitral regurgitation increases early diastolic filling of the ventricle and reduces systolic tension and elasticity of the ventricular wall. Myocardial oxygen consumption does not change due to decreased wall tension in late systole. An increase in minute volume of blood circulation is achieved by increasing stroke volume. However, if mitral regurgitation is large enough, flow through the aortic valve, i.e. cardiac output, is reduced. Left atrial pressure and pulmonary artery wedge pressure increase, the latter leading to right ventricular failure.

Natural course

Mitral regurgitation after acute myocardial infarction disappears during the hospital period in 15% of patients; in another 15% of patients, the symptoms of mitral regurgitation are eliminated within several months. At the same time, among patients with the absence of mitral regurgitation, in 12% it appears in the late period after myocardial infarction.

Even mild mitral regurgitation doubles in-hospital and 3-year mortality compared with patients without mitral regurgitation. Without surgical intervention, the average survival rate after rupture of the papillary muscles does not exceed 3-4 days. Some patients with a partial tear or tear of one head of the papillary muscle survive several weeks or months after a myocardial infarction. With severe (III or IV) degree of mitral regurgitation, hospital mortality is 24%, and one-year mortality is 52%.

Chronic mitral insufficiency stage I. in patients with symptoms of coronary insufficiency increases 1-year mortality to 10%, stage II. - up to 17%, III degree. - up to 40%, compared with 6% mortality in patients without mitral regurgitation.

Clinic, diagnosis and treatment of acute ischemic mitral regurgitation

Acute severe ischemic mitral regurgitation complicates the course of the disease in 0.4-0.9% of all patients with myocardial infarction. In 23 patients it was associated with rupture of the posterior papillary muscle, despite the fact that anterior myocardial infarction occurs more frequently. The average age of patients is 60 years. Mitral regurgitation is more common in men than in women. Rupture of the papillary muscle can occur as early as the first day after a heart attack, and almost always within 7 days (on average 4 days).

Acute ischemic mitral regurgitation usually presents with chest pain and/or shortness of breath. Most patients develop a blowing holosystolic murmur with emphasis at the apex. Rupture of the papillary muscle often manifests clinically as pulmonary edema or cardiogenic shock, systemic hypotension, oliguria, and acidosis, and requires prompt intervention to save life.

Most patients remain in sinus rhythm. In 50% of patients, changes characteristic of acute myocardial infarction are present - ST segment elevation in the anteroseptal, lateral or, more often, posterior wall of the left ventricle. Blockade of the right or left bundle branch is typical for patients with post-infarction VSD.

A chest x-ray shows signs of venous stagnation. The heart shadow, as a rule, is not enlarged.

Transthoracic and transesophageal echocardiography allow one to assess the degree of mitral regurgitation and confirm the absence of pathology on the part of the mitral valve leaflets and impaired contractility of the left ventricular wall, as well as pathology on the part of the papillary muscles. The left atrium is usually not enlarged. The ejection fraction decreases, but does not reflect the degree of left ventricular damage.

Despite hemodynamic instability, most patients require diagnostic cardiac catheterization, primarily to determine coronary pathology. Approximately half of the patients have a single-vessel lesion, most often the right coronary artery, while the other half have a three-vessel lesion. Left ventriculography shows an increase in the volume of the left ventricle, severe mitral valve insufficiency, and an increase in left ventricular pressure. The ejection fraction generally does not decrease below 40%. Probing of the right heart usually reveals increased pulmonary artery pressure and “v” waves reaching 40 mm Hg or higher. Mixed venous blood oxygen saturation is often significantly below 50%, which reflects a decrease in cardiac output with a decrease in the index to 1.0-2.9 l.min/m 2.

The urgency and aggressiveness of surgical treatment depends on the presence or absence of cardiogenic shock and/or heart failure. In the intensive care unit, continuous monitoring of ECG, central hemodynamics (including pulmonary artery wedge pressure and cardiac output), peripheral oxygen saturation, blood gases (both arterial and venous), oxygen saturation and pH should be established.

The adequacy of hemodynamics must be assessed before fatal consequences develop. The criteria for cardiogenic shock are: systemic hypotension (systolic blood pressure< 80 мм рт.ст., среднее давление < 55 мм рт. ст.), насыщение смешанной венозной крови кислородом < 50%, сердечный индекс < 2,0 л.мин/м2, метаболический ацидоз, олигурия и снижение периферической микроциркуляции (бледность кожных покровов, холодные конечности, слабый периферический пульс). В этой связи, все необходимые диагностические исследования должны быть выполнены настолько быстро насколько возможно.

In patients with no critical changes in hemodynamics, additional infusion of crystalloid or colloid solutions that can increase cardiac output and restore diuresis is possible. Narcotic analgesics are used that are less likely to damage myocardial function or cause hypotension. Inotropes, as well as peripheral vasodilators, are used to maintain cardiac output. In the most critical patients, failure to respond to drug therapy warrants the use of intra-aortic counterpulsation.

For patients with acute myocardial infarction and stage I or II mitral insufficiency. Urgent myocardial revascularization can prevent the progression of mitral regurgitation, the development of cardiogenic shock and heart failure. This can be achieved by thrombolysis, PTCA, or stenting. Immediate surgery is the treatment of choice for most patients, but in patients without papillary muscle rupture, PTCA or thrombolytic therapy may be used in the hope of reducing the size of the myocardial infarction and thus mitral regurgitation. Theoretically, PTCA or thrombolysis performed within 4 hours of the onset of acute myocardial infarction can reduce both the size and severity of mitral regurgitation. However, in many patients they are not able to provide a favorable outcome.

Surgery for acute ischemic mitral regurgitation is often emergency. In some cases, in critically ill patients, in order to reduce the time of connecting artificial blood circulation, the internal mammary artery is not taken. Extracorporeal circulation is carried out in normothermia mode, myocardial protection is hypothermic blood ante- and retrograde cardioplegia. Before manipulation of the mitral valve, distal anastomoses are performed on the posterior and lateral surfaces of the heart, since performing this procedure after valve replacement can lead to rupture of the posterior wall of the left ventricle.

Most patients with acute ischemic mitral regurgitation have a small left atrium, which makes valve manipulation difficult, so for better exposure, an approach through the right atrium with incision of the interatrial septum and the roof of the left atrium can be used.

Mitral valve replacement is the operation of choice, especially for patients in critical condition, since plastic procedures on the valve, if unsuccessful, will require repeated cardiac arrest. The choice of prosthesis (mechanical or biological) depends on the patient’s age, life expectancy, and possible problems with constant anticoagulant therapy. During prosthetics, it is necessary to preserve the subvalvular structures to prevent damage to the fibrous framework of the left ventricle and reduce the ejection fraction.

In the intra- and early postoperative period, inotropic drugs and peripheral vasodilators are initially used, but if adequate cardiac output cannot be maintained with these drugs, counterpulsation or one of the left ventricular bypass options must be used immediately. If acute heart failure and the use of mechanical circulatory support are predicted at the preoperative stage, then in such a situation it is better to use a bioprosthesis, since it is not susceptible to thrombosis during operation of the circulatory support device.

results

The immediate results of emergency mitral valve replacement for ischemic mitral regurgitation to date leave much to be desired. In-hospital mortality ranges from 31% to 69%. Most surgeons do not recommend plastic surgery in emergencies for the reasons outlined above. Preservation of the notochordal apparatus, which improves left ventricular function, can reduce mortality to 22%. However, with drug treatment the mortality rate approaches 100%. Factors influencing mortality include advanced age, cardiogenic shock, comorbidities, number of myocardial infarctions, and delay in surgery. The 5-year survival rate among patients who survived the postoperative period is 50%.

Clinic, diagnosis and treatment of chronic ischemic mitral regurgitation

In 10.9-19.0% of patients with symptoms of coronary pathology and in 3.5-7.0% of patients, concomitant mitral regurgitation is detected during myocardial revascularization. Most of them have I or II degrees. mitral insufficiency.

In patients with chronic ischemic mitral regurgitation, the spectrum of clinical manifestations is determined by three factors:

1) the presence and severity of ischemia,

2) degree of mitral regurgitation and

3) severity of left ventricular dysfunction.