Acute mitral insufficiency. Detachment of the chord of the mitral valve treatment

The patient called the SMP (ECG was not taken). The condition is regarded as an attack of bronchial asthma. After the intervention, the patient's condition improved. The patient went to work the next day. He did not seek medical help. But since that time, he began to notice shortness of breath with moderate physical exertion (ascent to the 3rd floor). Three months later, during the next medical examination, atrial fibrillation was recorded on the ECG. At the outpatient stage, echocardiography was performed: there is a rounded formation, with clear contours, 2*2 cm in size, based on the anterior leaflet of the mitral valve (myxoma?)

The ambulance crew took the patient to the hospital for examination and selection of therapy.

It is also known from the anamnesis that for 25 years he has been working as a “tunnel driller”. Work is associated with everyday heavy physical labor (weight lifting).

Objective examination data: general condition of the patient of moderate severity. Consciousness is clear. Integuments of normal coloring, normal humidity. There are no edemas of the lower extremities. Lymph nodes are not enlarged. Breathing on auscultation is hard, no wheezing. NPV 16 per min. The area of the heart is not changed. The apex beat is not defined. On auscultation, the heart sounds are muffled, arrhythmic. A systolic murmur is heard at the apex. BP 140/90 mm Hg HR=PS 72 beats/min.

ECG: atrial fibrillation. Heart rate 100 per minute. No acute focal changes.

Echocardiography: aortic root - 3.2 cm; aortic valve: leaflets are not calcified, opening - 2.0 cm. LA diameter - 6.0 cm, volume ml. IVS - 1.3 cm, GL - 1.3 cm, CDR - 5.7 cm, CSR - 3.8 cm, LVMI 182.5 g / m2, IOT - 0.46, EDV - 130 ml, CSD - 55 ml, VW - 58%. Violations of local contractility were not identified. AP 22 cm2, RV PSAX 3.4 cm, RV basal diameter 3.7 cm, free wall thickness 0.4 cm, TAPSE 2.4 cm IVC 1.8 cm, inspiratory collapse< 50%.

The study was conducted against the background of atrial fibrillation. SDLA - 45 mm Hg.

In the cavity of the LA in systole, a part of the chord of the anterior leaflet of the mitral valve is visualized.

Conclusion: Concentric hypertrophy of the left ventricle. Dilatation of both atria. Detachment of the chord of the anterior leaflet of the mitral valve with the formation of severe insufficiency. Insufficiency of TC of a small degree. Signs of pulmonary hypertension.

Mitral valve prolapse

Mitral valve prolapse (MVP) is a clinical pathology in which one or two leaflets of this anatomical formation prolapse, that is, bend into the cavity of the left atrium during systole (heart contraction), which should not normally occur.

Diagnosis of MVP became possible due to the use of ultrasound techniques. Mitral leaflet prolapse is probably the most common pathology in this area and occurs in more than six percent of the population. In children, the anomaly is detected much more often than in adults, and in girls it is found about four times more often. In adolescence, the ratio of girls to boys is 3:1, and for women and men 2:1. In the elderly, the difference in the frequency of occurrence of MVP in both sexes is leveled. This disease also occurs during pregnancy.

Anatomy

The heart can be imagined as a kind of pump that makes blood circulate through the vessels of the whole body. Such movement of fluid becomes possible by maintaining the proper level of pressure in the cavity of the heart and the work of the muscular apparatus of the organ. The human heart consists of four cavities called chambers (two ventricles and two atria). The chambers are separated from each other by special "doors", or valves, each of which consists of two or three shutters. Thanks to this anatomical structure of the main motor of the human body, each cell of the human body is supplied with oxygen and nutrients.

There are four valves in the heart:

Mitral. It separates the cavity of the left atrium and ventricle and consists of two valves - anterior and posterior. Anterior leaflet prolapse is much more common than the posterior leaflet. Special threads, called chords, are attached to each of the valves. They provide valve contact with muscle fibers, which are called papillary or papillary muscles. For the full-fledged work of this anatomical formation, joint coordinated work of all components is necessary. During cardiac contraction - systole - the cavity of the muscular cardiac ventricle decreases, and accordingly the pressure in it increases. At the same time, the papillary muscles are included in the work, which close the exit of blood back to the left atrium, from where it poured out from the pulmonary circulation, enriched with oxygen, and, accordingly, the blood enters the aorta and further, through the arterial vessels, is delivered to all organs and tissues.
Tricuspid (tricuspid) valve. It consists of three wings. Located between the right atrium and ventricle.
aortic valve. As described above, it is located between the left ventricle and the aorta and does not allow blood to return to the left ventricle. During systole, it opens, releasing arterial blood into the aorta under high pressure, and during diastole, it closes, which prevents back flow of blood to the heart.
Pulmonary valve. It lies between the right ventricle and the pulmonary artery. Similar to the aortic valve, it prevents blood from returning to the heart (right ventricle) during diastole.

Normally, the work of the heart can be represented as follows. In the lungs, the blood is enriched with oxygen and enters the heart, or rather, its left atrium (it has thin muscle walls, and is only a “reservoir”). From the left atrium, it pours into the left ventricle (represented by a “powerful muscle” capable of pushing out the entire incoming volume of blood), from where it spreads through the aorta to all organs of the systemic circulation (liver, brain, limbs and others) during the systole period. Having transferred oxygen to the cells, the blood takes carbon dioxide and returns to the heart, this time to the right atrium. From its cavity, the fluid enters the right ventricle and during systole is expelled into the pulmonary artery, and then into the lungs (pulmonary circulation). The cycle is repeated.

What is prolapse and why is it dangerous? This is a condition of defective operation of the valvular apparatus, in which during muscle contraction, the blood outflow tracts are not completely closed, and, therefore, part of the blood during the systole period returns back to the heart. So with mitral valve prolapse, fluid during systole partially enters the aorta, and partially from the ventricle is pushed back into the atrium. This return of blood is called regurgitation. Usually, with the pathology of the mitral valve, the changes are insignificant, so this condition is often considered as a variant of the norm.

Causes of mitral valve prolapse

There are two main causes of this pathology. One of them is a congenital disorder in the structure of the connective tissue of the heart valves, and the second is a consequence of previous diseases or injuries.

Congenital mitral valve prolapse is quite common and is associated with a hereditary defect in the structure of the connective tissue fibers that serve as the basis of the valves. With this pathology, the threads (chords) connecting the valve with the muscle are lengthened, and the valves themselves become softer, more pliable and more easily stretched, which explains their loose closure at the time of the heart systole. In most cases, congenital MVP proceeds favorably, without causing complications and heart failure, therefore, it is most often considered a feature of the body, and not a disease.
Heart diseases that can cause changes in the normal anatomy of the valves:
- Rheumatism (rheumatic heart disease). As a rule, a heart attack is preceded by a sore throat, a couple of weeks after which an attack of rheumatism (joint damage) occurs. However, in addition to the visible inflammation of the elements of the musculoskeletal system, heart valves are involved in the process, which are subjected to a much greater destructive effect of streptococcus.
- Ischemic heart disease, myocardial infarction (heart muscle). With these diseases, there is a deterioration in blood supply or its complete cessation (in the case of myocardial infarction), including the papillary muscles. Chord breaks may occur.
- Chest injury. Strong blows in the chest area can provoke a sharp separation of the valvular chords, which leads to serious complications if assistance is not provided in a timely manner.

Mitral valve prolapse classification

There is a classification of mitral valve prolapse depending on the severity of regurgitation.

I degree is characterized by a deflection of the sash from three to six millimeters;
II degree is characterized by an increase in the amplitude of the deflection up to nine millimeters;
III degree is characterized by the severity of the deflection of more than nine millimeters.

Mitral valve prolapse symptoms

As mentioned above, mitral valve prolapse in the vast majority of cases is almost asymptomatic and is diagnosed by chance during a preventive medical examination.

The most common symptoms of mitral valve prolapse include:

Cardialgia (pain in the region of the heart). This symptom occurs in about 50% of cases of MVP. Pain is usually localized in the region of the left half of the chest. They can be both short-term in nature and stretch for several hours. Pain can also occur at rest or with severe emotional stress. However, it is often not possible to associate the occurrence of a cardialgic symptom with any provoking factor. It is important to note that the pain is not stopped by taking nitroglycerin, which happens with coronary heart disease;
Feeling short of breath. Patients have an irresistible desire to take a deep breath "full chest";
Feeling of interruptions in the work of the heart (either a very rare heartbeat, or, on the contrary, rapid (tachycardia);
Dizziness and fainting. They are caused by heart rhythm disturbances (with a short-term decrease in blood flow to the brain);
Headaches in the morning and at night;
An increase in temperature, without any reason.

Diagnosis of mitral valve prolapse

As a rule, valve prolapse is diagnosed by a therapist or cardiologist during auscultation (listening to the heart with a stethophonendoscope), which they perform on each patient during routine medical examinations. Murmurs in the heart are caused by sound phenomena when the valves open and close. If a heart disease is suspected, the doctor gives a referral for ultrasound diagnostics (ultrasound), which allows you to visualize the valve, determine the presence of anatomical defects in it and the degree of regurgitation. Electrocardiography (ECG) does not reflect changes occurring in the heart with this pathology of the valve leaflets

Treatment and contraindications

The tactics of treatment of mitral valve prolapse is determined by the degree of prolapse of the valve leaflets and the volume of regurgitation, as well as the nature of psycho-emotional and cardiovascular disorders.

An important point in therapy is the normalization of work and rest regimes for patients, compliance with the daily routine. Be sure to pay attention to a long (sufficient) sleep. The issue of physical culture and sports should be decided individually by the attending physician after assessing the indicators of physical fitness. Patients, in the absence of severe regurgitation, are shown moderate physical activity and an active lifestyle without any restrictions. The most preferred skiing, swimming, skating, cycling. But activities related to the jerky type of movements are not recommended (boxing, jumping). In the case of severe mitral regurgitation, sports are contraindicated.

An important component in the treatment of mitral valve prolapse is herbal medicine, especially based on sedative (soothing) plants: valerian, motherwort, hawthorn, wild rosemary, sage, St. John's wort and others.

To prevent the development of rheumatoid lesions of the heart valves, tonsillectomy (removal of the tonsils) is indicated in case of chronic tonsillitis (tonsillitis).

Drug therapy for MVP is aimed at treating complications such as arrhythmia, heart failure, as well as symptomatic treatment of manifestations of prolapse (sedation).

In case of severe regurgitation, as well as the addition of circulatory failure, an operation is possible. As a rule, the affected mitral valve is sutured, that is, valvuloplasty is performed. If it is ineffective or unfeasible for a number of reasons, implantation of an artificial analogue is possible.

Complications of mitral valve prolapse

. This condition is a common complication of rheumatic heart disease. In this case, due to incomplete closure of the valves and their anatomical defect, there is a significant return of blood to the left atrium. The patient is worried about weakness, shortness of breath, cough and many others. In the event of the development of such a complication, valve replacement is indicated.
Attacks of angina pectoris and arrhythmias. This condition is accompanied by an abnormal heart rhythm, weakness, dizziness, a feeling of interruptions in the work of the heart, crawling "goosebumps" before the eyes, fainting. This pathology requires serious medical treatment.
Infective endocarditis. In this disease, inflammation of the heart valve occurs.

Prevention of mitral valve prolapse

First of all, to prevent this disease, it is necessary to sanitize all chronic foci of infection - carious teeth, tonsillitis (it is possible to remove the tonsils according to indications) and others. Be sure to undergo regular annual medical examinations in a timely manner to treat colds, especially sore throats.

Detachment of the chord of the mitral valve treatment

Keywords: chorda tendonus, mitral insufficiency, echocardiography.

The patient, Hakobyan Artashes, 76 years old, was admitted to the Department of Hepatic Surgery of the Medical Center Erebuni on June 7, 2004. for a planned operation for a left-sided inguinal-scrotal hernia. From the anamnesis: 4 days ago, while working on a personal plot, he suddenly felt severe shortness of breath for the first time in his life.

Objective examination: forced position in bed - orthopnea, cyanotic skin, respiratory rate - 24 per minute. In the lungs during auscultation - on the right in the n / o breathing is weakened, in the same place - single moist rales, on the left - without features. Heart rate - 80 per minute, blood pressure - 150/90 mm Hg. Art. Heart sounds are rhythmic, clear, coarse pansystolic murmur is heard at all points. The left border of the heart is expanded by 1.5–2 cm, the right border by 1–1.5 cm. The liver is enlarged, it bulges from under the edge of the costal arch by 2 cm. Stool and diuresis are normal. There are no peripheral edema.

On the ECG: signs of left ventricular hypertrophy, diffuse changes in the ventricular myocardium.

Echocardiography (June 18, 2004): dilatation of all cavities of the heart, LA = 4.8 cm, LVCD = 5.8 cm, RV = 3.2 cm. Myocardial hypertrophy in both ventricles. The aorta is sealed, in the ascending section is not expanded. AK: the leaves are sealed, the antiphase is not broken. MK: the anterior leaf, after its middle part, floats, moves asynchronously, in comparison with its base and middle part, the rear leaf is compacted, its opening amplitude is not reduced. There are no zones of local asynergies.

There is hyperkinesia of the interventricular septum. Overall contractility is reduced due to severe mitral regurgitation. EF = 50–52%. Doppler: mitral regurgitation of 3-4 degrees, tricuspid regurgitation of 2 degrees.

To clarify the diagnosis and better visualize the structural changes in the mitral valve, transesophageal echocardiography was performed (June 9, 2004): visualization is satisfactory. The flotation of the anterior leaflet of the mitral valve is determined, the detachment of one of the tendon chords is noted. Doppler: mitral regurgitation of 3-4 degrees, tricusidal regurgitation of 2 degrees. Regurgitant jet in the left atrium reaches the first pulmonary vein. Pressure in the pulmonary artery - 50 mm Hg. Dilatation of the left atrium: LA = 5 cm, RV = 3.2 cm.

The patient was transferred to the emergency cardiology department and received nitrates, ACE inhibitors, Ca 2+ tubular blockers, and diuretics. He categorically refused surgical treatment. Against the background of treatment with arteriolodilators, echocardiography was performed in dynamics. There was a decrease in the degree of mitral regurgitation. He was discharged in a satisfactory condition on the background of the therapy. Recommended outpatient treatment and follow-up.

Features of the clinic, diagnosis and treatment of various variants of non-rheumatic mitral insufficiency

Mitral valve prolapse and papillary muscle dysfunction are the most common causes of non-rheumatic mitral regurgitation. Rupture of tendinous cords and calcification of the mitral ring are less common.

Mitral valve prolapse is a clinical syndrome caused by the pathology of one or both leaflets of the mitral valve, more often the posterior one, with their bulging and prolapse into the cavity of the left atrium during ventricular systole. There are primary, or idiopathic, prolapse, which is an isolated heart disease, and secondary.

Primary mitral valve prolapse occurs in 5-8% of the population. The vast majority of patients have an asymptomatic course, being the most common valvular disease. It is found predominantly in individuals, more often in women. Secondary mitral valve prolapse is noted in a number of heart diseases - rheumatism, including rheumatic defects (on average in 15% or more cases), PS, especially secondary atrial septal defect (20-40%), coronary artery disease (16-32%), cardiomyopathies, etc.

The etiology has not been established. In primary prolapse, a hereditary predisposition with an autosomal dominant type of transmission is noted. Its morphological substrate is a nonspecific, so called myxomatous degeneration valve leaflets with the replacement of the spongy and fibrous layers with an accumulation of pathological acidic mucopolysaccharides, in which there are fragmented collagen fibers. There are no elements of inflammation. Similar morphological changes are characteristic of Marfan's syndrome. In some patients with mitral valve prolapse, hypermobility of the joints, skeletal changes (thin long fingers, straight back syndrome, scoliosis), and occasionally dilatation of the aortic root are noted. Prolapse of the tricuspid and aortic valves also occurs, sometimes in combination with a similar lesion of the mitral valve. These facts made it possible to suggest that the disease is based on a genetically determined pathology of the connective tissue with an isolated or predominant lesion of the cusps of the heart valves, more often the mitral one.

Macroscopically, one or both leaflets are enlarged and thickened, and the tendon chords attached to them are thinned and elongated. As a result, the valves dome-shaped invaginate into the cavity of the left atrium (sail) and their closure is more or less disturbed. The valve ring can stretch. In the vast majority of patients, mitral regurgitation is minimal and does not worsen over time, and there are no hemodynamic disturbances. In a small proportion of patients, however, it may increase. Due to the increase in the radius of curvature of the leaflet, the stress experienced by the tendinous chords and unchanged papillary muscles increases, which exacerbates the stretching of the chorchi and may contribute to their rupture. Tension of the papillary muscles can lead to dysfunction and ischemia of these muscles and the adjacent myocardium of the ventricular wall. This may contribute to increased regurgitation and arrhythmias.

In most cases of primary prolapse, the myocardium is morphologically and functionally unchanged, however, in a small part of symptomatic patients, causeless nonspecific myocardial dystrophy and fibrosis have been described. These data serve as the basis for discussing the possibility of prolapse being associated with myocardial damage of unknown etiology, that is, with cardiomyopathies.

Clinic. The manifestations and course of the disease are highly variable, and the clinical significance of mitral valve prolapse remains unclear. In a significant proportion of patients, pathology is detected only with careful auscultation or echocardiography. In most patients, the disease remains asymptomatic throughout life.

Complaints are nonspecific and include various types of cardialgia, often persistent, not stopped by nitroglycerin, interruptions and heartbeats that periodically occur, mainly at rest, a feeling of lack of air with dreary sighs, dizziness, fainting, general weakness and fatigue. A significant part of these complaints is of a functional, neurogenic, origin.

Auscultation data are of great diagnostic value. A mid- or late systolic click is characteristic, which may be the only manifestation of pathology or, more often, accompanied by the so-called late systolic murmur. As the data of phonocardiography show, it is observed 0.14 s or more after the first tone and, apparently, is due to a sharp tension of sagging elongated tendon chords or a protruding valve leaflet. Late systolic murmur may occur without a click and is indicative of mitral regurgitation. It is best heard over the apex of the heart, short, often quiet and musical. The click and murmur are shifted to the beginning of systole, and the murmur lengthens and intensifies with a decrease in left ventricular filling, which aggravates the discrepancy between the size of its cavity and the mitral valve apparatus. For these purposes, auscultation and phonocardiography are performed when the patient moves to a vertical position, the Valsalva test (straining), inhalation of amyl nitrite. On the contrary, an increase in the EDV of the left ventricle during squatting and isometric loading (compression of a manual dynamometer) or the administration of norepinephrine hydrotartrate causes a delay in the click and a shortening of the murmur, up to their disappearance.

Diagnostics. Changes to ECG absent or non-specific. Most often, biphasic or negative teeth are noted. T in leads II, III and aVF, usually positivized with an obzidan (enderal) test. Data radiography without features. Only in cases of severe regurgitation are changes characteristic of mitral insufficiency noted.

Diagnosis is made with echocardiography. When examining in M-mode, a sharp posterior displacement of the posterior or both leaflets of the mitral valve is determined in the middle or end of systole, which coincides with the click and the appearance of systolic murmur (Fig. 56). Two-dimensional scanning from the parasternal position clearly shows the systolic displacement of one or both valves into the left atrium. The presence and severity of concomitant mitral regurgitation is assessed using a Doppler study.

In its diagnostic value, echocardiography is not inferior to angiocardiography, which also determines the bulging of the mitral valve leaflets into the left atrium with the injection of a contrast agent from the left ventricle into it. Both methods, however, can give false positive results, and existing diagnostic features require verification.

The course and prognosis are favorable in most cases. Patients, as a rule, lead a normal life, and the defect does not impair survival. Severe complications are very rare. As shown by the results of long-term (20 years or more) observations, their risk increases with a significant thickening of the mitral valve leaflets according to echocardiography (A. Marks et al., 1989, etc.). Such patients are subject to medical supervision.

Complications of the disease include: 1) the development of significant mitral regurgitation. It is observed in about 5% of patients and in some cases is associated with spontaneous rupture of the notochord (2); 3) ventricular ectopic arrhythmias, which can cause palpitations, dizziness and fainting, and in isolated, extremely rare cases, lead to ventricular fibrillation and sudden death; 4) infective endocarditis; 5) embolism of cerebral vessels with thrombotic overlays, which can form on altered valves. The last two complications, however, are so rare that they are not routinely prevented.

In the asymptomatic course of the disease, treatment is not required. With cardialgia, p-blockers are quite effective, which

some degree of empirical. In the presence of severe mitral regurgitation with signs of left ventricular failure, surgical treatment is indicated - plastic or mitral valve replacement.

Recommendations for antibiotic prophylaxis of infective endocarditis are not generally accepted due to the significant prevalence of mitral valve prolapse, on the one hand, and the rarity of endocarditis in such patients, on the other.

Dysfunction of the papillary muscles due to their ischemia, fibrosis, rarely inflammation. Its occurrence is facilitated by a change in the geometry of the left ventricle during its dilatation. It is quite common in acute and chronic forms of coronary artery disease, cardiomyopathies and other myocardial diseases. Mitral regurgitation, as a rule, is small and manifests itself as a late systolic murmur due to impaired closure of the valve leaflets in the middle and end of systole, which is largely provided by contraction of the papillary muscles. Occasionally, with significant dysfunction, the murmur may be pansystolic. The course and treatment are determined by the underlying disease.

Rupture of the chorda tendon or chordae may be spontaneous or associated with trauma, acute rheumatic or infective endocarditis, and myxomatous degeneration of the mitral valve. It leads to acute onset of mitral insufficiency, often significant, which causes a sharp volume overload of the left ventricle and the development of its insufficiency. The left atrium and pulmonary veins do not have time to expand, as a result of which the pressure in the pulmonary circulation rises significantly, which can lead to ventricular failure.

In the most severe cases, there is severe recurrent, sometimes not stopping, pulmonary edema due to high venous pulmonary hypertension and even cardiogenic shock. Unlike chronic rheumatic mitral regurgitation, even with significant left ventricular failure, patients maintain sinus rhythm. The murmur is loud, often pansystolic, but sometimes ends before the end of systole due to equalization of pressure in the left ventricle and atrium and may have an atypical epicenter. When the chords of the posterior valve are ruptured, it is sometimes localized on the back, and the anterior valve is at the base of the heart and is carried out to the vessels of the neck. In addition to the III tone, the IV tone is noted.

An x-ray examination is characterized by signs of pronounced venous congestion in the lungs, up to edema, with a relatively small increase in the left ventricle and atrium. Over time, the cavity of the heart expands.

Echocardiography allows confirming the diagnosis, in which fragments of the leaflet and chord of the valve are visible in the cavity of the left atrium during systole and other signs. In contrast to rheumatic disease, the valve leaflets are thin, there is no calcification, and the flow of regurgitation is located eccentrically on Doppler examination.

Cardiac catheterization is usually not required to confirm the diagnosis. A feature of her data is high pulmonary hypertension.

The course and outcome of the disease depend on the state of the myocardium of the left ventricle. Many patients die, and the survivors have a picture of severe mitral regurgitation.

Treatment includes conventional therapy for severe heart failure. Particular attention should be paid to reducing afterload with the help of peripheral vasodilators, which can reduce regurgitation and blood stasis in the pulmonary circulation, and increase MOS. After stabilization of the condition, surgical correction of the defect is performed.

Mitral annular calcification is a disease of the elderly, more often women, the cause of which is unknown. It is caused by degenerative changes in the fibrous tissue of the valve, the development of which is promoted by an increased load on the valve (prolapse, increased KDD in the left ventricle) and hypercalcemia, especially in hyperparathyroidism. Calcifications are located not in the annulus itself, but in the region of the base of the valve leaflets, larger than the posterior one. Small calcium deposits do not affect hemodynamics, while significant ones, causing immobilization of the mitral ring and chords, lead to the development of mitral regurgitation, usually mild or moderate. In isolated cases, it is accompanied by narrowing of the mitral orifice (mitral stenosis). Often combined with calcification of the aortic orifice, causing its stenosis.

The disease is usually asymptomatic and is detected when a gross systolic murmur or calcium deposits are detected in the projection of the mitral valve on an x-ray. Most patients have heart failure, mainly due to concomitant myocardial damage. The disease can be complicated by impaired intraventricular conduction due to calcium deposits in the interventricular septum, infective endocarditis, and rarely cause embolism or thromboembolism, more often cerebral vessels.

The diagnosis is made on the basis of echocardiography data. Valve calcification in the form of a band of intense echo signals is determined between the posterior leaflet of the valve and the posterior wall of the left ventricle and moves parallel to the posterior wall.

In most cases, no special treatment is required. With significant regurgitation, mitral valve replacement is performed. Prevention of infective endocarditis has been shown.

mitral valve infective endocarditis

mitral valve insufficiency

Etiology. Rheumatic fever, infective endocarditis, atherosclerosis, heart injury with detachment of chords, papillary muscles, myocardial infarction involving the papillary muscles. "Relative" insufficiency of the mitral valve (without its significant deformation and shortening of the valves) occurs with mitral valve prolapse and dilatation of the left ventricular cavity caused by any reasons.

Clinic, diagnostics. In the stage of defect compensation, the patient does not complain. In the stage of decompensation, shortness of breath appears, initially during physical exertion, palpitations, and sometimes cardialgia. At later stages, the addition of shortness of breath at rest and nocturnal attacks of cardiac asthma, pain in the right hypochondrium due to an enlarged liver, and edema of the lower extremities are characteristic.

The left ventricular impulse is enhanced, expanded, shifted to the left. According to percussion, at the initial stages, the boundaries of relative dullness of the heart are not changed, with myogenic dilatation of the heart, there is a shift of the left border to the left, the upper one - up,

On auscultation - weakened 1st tone, pathological 3rd tone at the apex of the heart, emphasis of the 2nd tone on the pulmonary artery. Systolic murmur with a maximum at the apex of the heart, often decreasing in nature, is carried out to the left axillary cavity.

X-ray study. An increase in the arch of the left ventricle and left atrium. Deviation of the shade of the contrasted esophagus along a large radius arc (8-10 cm).

Electrocardiogram. Signs of hypertrophy of the left ventricle, left atrium (expansion and splitting of the tooth in the 1st 2nd standard leads).

Phonocardiogram. Reducing the amplitude of the 1st tone at the apex, in the same place - a pathological 3rd tone (low-frequency oscillations separated from the 2nd tone by a time interval of at least 0.13 seconds). Systolic murmur associated with the 1st tone, decreasing in nature, occupying from 2/3 to the entire systole.

Echo cardiogram. Enlargement of the cavity of the left atrium, left ventricle.

Mitral valve insufficiency and hypertrophic cardiomyopathy. With hypertrophic cardiomyopathy, a systolic murmur is heard at the apex of the heart, which, with a superficial examination of the patient, can serve as a reason for diagnosing mitral valve insufficiency. The probability of a diagnostic error increases if the systolic murmur in a patient with hypertrophic cardiomyopathy is combined with a weakening of the 1st tone and extratones. As with mitral valve insufficiency, the epicenter of the murmur can be located at the apex of the heart and in the Botkin zone. However, in mitral insufficiency, the murmur is conducted into the armpit. With cardiomyopathy, the noise increases when standing up, during the Valsalva test. Diagnostic doubts are resolved by echocardiography, which reveals an important sign of hypertrophic cardiomyopathy - asymmetric hypertrophy of the interventricular septum.

Mitral valve insufficiency and dilated cardiomyopathy. Differential diagnostic difficulties arise if mitral valve insufficiency is pronounced. The defect of the valves and their shortening are so significant that it leads to a large regurgitation of blood from the left ventricle into the left atrium. Such patients develop early cardiomegaly, arrhythmias, total heart failure.

With dilated cardiomyopathy, mitral valve insufficiency (relative, without anatomical damage to the valves) is present in the vast majority of patients. The consequence of this is the regurgitation of blood from the left ventricle to the left atrium and systolic murmur, and the absence of a period of closed valves and weakening of systole lead to a decrease in the sonority of the 1st tone at the apex of the heart.

ECG changes can be identical in dilated cardiomyopathy and organic mitral valve insufficiency, as well as the results of a FCG study. The method of choice in the differentiation of the diseases under consideration is cardiographic echo. It proves the absence of anatomical changes in the valve in dilated cardiomyopathy and their presence in organic mitral valve insufficiency.

Mitral valve insufficiency and other acquired heart defects. Stenosis of the mouth of the aorta proceeds, as a rule, with a systolic murmur at the apex of the heart. However, this noise is also heard on the basis of the heart, it is carried out not into the armpit, but to the carotid arteries.

Insufficiency of the tricuspid valve with a sharp hypertrophy and dilatation of the right ventricle can lead to the fact that in the area of \u200b\u200bnormal localization of the left ventricular impulse, there is a right ventricular impulse. Diagnostic difficulties are resolved by the Rivero-Corvallo test: at the height of inspiration, the noise of tricuspid valve insufficiency increases. Tricuspid valve insufficiency is characterized by symptoms of isolated right ventricular failure, for bicuspid valve insufficiency - left ventricular or biventricular heart failure.

Mitral valve insufficiency and congenital heart disease - septal defect. Typical for a septal defect are: systolic heart trembling at the site of attachment of the 3rd-4th ribs to the sternum on the left; coarse systolic murmur in the same area and at the apex, having a ribbon-like shape on the phonocardiogram; according to X-ray and ECG signs of hypertrophy of both ventricles. Active search and detection of these symptoms leads the doctor to suspect a septal defect and refer the patient to a specialized center.

Mitral valve insufficiency and functional systolic murmur. Functional systolic murmur at the apex of the heart is heard in diseases of the heart muscle, aneurysm of the heart, arterial hypertension with dilatation of the cavity of the left ventricle. When addressing issues of differential diagnosis, the clinical picture of the disease as a whole and the characteristics of the noise (its amplitude, loudness ratio with the 1st tone, connection with it, conduction) are taken into account. Significant assistance in difficult cases is provided by echocardiography, which proves the absence of changes in the mitral valve cusps.

Mitral valve insufficiency and innocent heart murmurs. Innocent (random, accidental) systolic murmurs are heard at the apex of the heart, in the Botkin zone in healthy children and adolescents, sometimes in young people with asthenic constitution. These noises are not loud, they are not combined with the weakening of the 1st tone, they are not conducted into the armpit. The borders of the heart, according to percussion and x-ray method, are not changed. According to the FCG, innocent noises are not associated with the 1st tone, they are changeable. Occupy 1/3-1/2 systole.

"Pure" insufficiency of the mitral valve of rheumatic etiology is a rare defect. The statement of G.F. Langa, S.S. Zimnitsky that the "rheumatic seal" is a combined mitral defect. For the diagnosis of rheumatic fever, the generally accepted Jones criteria in various modifications are used.

In infective endocarditis, aortic valve damage is more typical with the formation of its insufficiency. The mitral valve is affected much less frequently, and this lesion is naturally combined with aortic valve endocarditis. Criteria for the diagnosis of infective endocarditis are detailed in the appropriate chapter.

Atherosclerotic mitral valve insufficiency is usually diagnosed in elderly people with signs of coronary artery disease, hypertension.

Atherosclerotic lesion of the aorta proceeds with systolic murmur, thickening and calcification of the aorta, according to the X-ray method.

Mitral valve insufficiency in myocardial infarction occurs due to damage to the papillary muscles and detachment of the chords. Symptoms (systolic murmur with typical irradiation to the armpit, increase or appearance of left ventricular heart failure) develops acutely, usually on the 5-11th day of illness.

Traumatic mitral valve insufficiency is characterized by an appropriate history. In fact, traumatic iatrogenic defect is mitral valve insufficiency in the outcome of mitral commissurotomy (post-commissurotomy mitral insufficiency).

Mitral valve prolapse is common in older women with low body weight.

Contrary to the generally accepted point of view, the classic auscultatory picture of mitral valve prolapse - systolic click and late systolic murmur - occurs only in 25-30% of patients. In other cases, a variable systolic murmur is heard at the apex of the heart. According to the number of affected valves, variants with changes in one (anterior, posterior) or both valves are possible. According to the time of occurrence, valve prolapse can be early, late and pansystolic. Prolapse of the first degree should be said, according to the echo cardiograph and the chess method, if it is 3-6 mm, in the second it is 6-9 mm, in the third it exceeds 9 mm. Hemodynamic disturbances may be absent (prolapse without regurgitation). In the presence of regurgitation, its severity is assessed semi-quantitatively, in points from 1 to 4.

The course of the disease can be asymptomatic, mild, moderate or severe. A mild course is characterized by complaints of a predominantly asthenic type (weakness, fatigue, headache, vague pain in the heart area), spontaneous fluctuations in blood pressure, nonspecific ECG changes (depression of the S-T interval in 2, 3 standard leads, lead aVF, left chest leads, inversion T wave). The course of moderate severity is characterized by complaints of pain in the region of the heart, palpitations, interruptions, non-systemic dizziness, fainting. On the ECG, along with nonspecific changes, rhythm and conduction disturbances. Mitral regurgitation is expressed unsharply. A severe course should be discussed with a significant degree of mitral regurgitation, which leads to left ventricular, and then total heart failure.

The course of mitral valve insufficiency is variable, it is determined by the severity of regurgitation and the state of the myocardium. If mitral insufficiency is mild, for a long time the patient remains able to work. Mitral insufficiency with large blood regurgitation into the left atrium is difficult, sometimes in these patients decompensation develops faster than with mitral stenosis. Symptoms of insufficiency of the right parts of the heart join left ventricular failure after a few months or years.

Complications. Arrhythmias. Acute left ventricular heart failure. Thromboembolism of the renal, mesenteric arteries, cerebral vessels.

mitral valve insufficiency

The essence of this defect is a violation of the closing function of the valve due to fibrous deformation of the cusps, subvalvular structures, dilatation of the fibrous ring or a violation of the integrity of the elements of the mitral valve, which causes the return of part of the blood from the left ventricle to the atrium. These disorders of intracardiac hemodynamics are accompanied by a decrease in the minute volume of blood circulation, the development of pulmonary hypertension syndrome.

The causes of mitral insufficiency are presented in Table 1.

Acute mitral insufficiency

Mitral annulus injury

Infective endocarditis (abscess formation)
Trauma (during valve surgery)
Paraprosthetic fistula due to ruptured sutures or infective endocarditis

Mitral valve injury

Infective endocarditis (perforation or destruction of the leaflet (Fig. 7).)
Injury
Tumors (Atrial Myxoma)
Myxomatous leaflet degeneration
Systemic lupus erythematosus (Libmann-Sachs lesion)

Rupture of tendon chords

Idiopathic, i.e. spontaneous
Myxomatous degeneration (mitral valve prolapse, Marfn syndrome, Ehlers-Danlos)
Infective endocarditis
Rheumatism
Injury

Damage or dysfunction of the papillary muscles

Cardiac ischemia
Acute left ventricular failure
amyloidosis, sarcoidosis
Injury

Dysfunction of the mitral valve prosthesis (in patients who have previously undergone surgery)

Bioprosthesis leaflet perforation due to infective endocarditis
Degenerative changes in bioprosthesis leaflets
Mechanical damage (rupture of the bioprosthesis leaflet)
Jamming of the locking element (disk or ball) of a mechanical prosthesis

Chronic mitral insufficiency

Inflammatory changes

Myxomatous degeneration of the mitral valve leaflets (“click syndrome”, Barlow's syndrome, prolapsing leaflet, mitral valve prolapse
Marfan syndrome
Ehlers-Danlos syndrome
Pseudoxanthoma
Mitral annulus calcification

Infective endocarditis on normal, altered, or prosthetic valves

Rupture of tendon cords (spontaneous or secondary due to myocardial infarction, trauma, mitral valve prolapse, endocarditis)
Rupture or dysfunction of the papillary muscles (due to ischemia or myocardial infarction)
Dilatation of the fibrous ring of the mitral valve and the cavity of the left ventricle (cardiomyopathy, aneurysmal dilatation of the left ventricle)
Hypertrophic cardiomyopathy
Paraprosthetic fistula due to eruption of sutures

Splitting or fenestration of the mitral valve leaflet
The formation of a "parachute" mitral valve due to:
Disorders of fusion of endocardial cushions (rudiments of the mitral valve)
Fibroelastosis of the endocardium
Transpositions of the great vessels
Abnormal formation of the left coronary artery

Surgery or medication for mitral valve infection

In surgery, it is customary to subdivide infective endocarditis into primary, secondary, and prosthetic valve endocarditis (“prosthetic”). Primary refers to the development of an infectious process on previously unchanged, so-called native valves. With a secondary infection, it complicates heart defects already formed due to a rheumatic or sclerotic process. In itself, the presence of an infection in the heart is not a contraindication for performing reconstructive interventions.

The decision on the possibility and hemodynamic efficiency of a certain variant of reconstructive surgery in patients with infective endocarditis is made taking into account the localization of the lesion, its prevalence and duration of existence. Any infectious process is accompanied by tissue edema and infiltration, and in advanced cases, destruction. This fully applies to intracardiac structures. When evaluating the possibility of preserving valve structures, it is important to understand that the sutures placed on edematous, inflamed tissues are likely to cut through, which will lead to an undesirable result - valve failure. Therefore, many surgeons have long and rightly noted that operations performed against the background of active infective endocarditis are accompanied by a significantly greater number of complications.

Naturally, it is better to operate in the "cold" period, against the background of remission of the infectious process. However, this is not always possible and appropriate. In such cases, it is desirable to excise all the affected tissues on the one hand radically, on the other - as economically as possible. Stitches should be placed on intact tissues and, if possible, pads should be used (optimally - from the autopericardium). When using implant-free techniques, it is still desirable to strengthen the plastic area in one way or another. You can use the same strips from the autopericardium for this. Some surgeons pretreat them for 9 minutes in a solution of glutaraldehyde (De La Zerda D.J. et al. 2007).

From a practical point of view, it is important to know what terms the surgeon should be guided by when deciding on surgery in a patient with active infective endocarditis. It is clear that there is no single standard recipe and cannot be. Everything is determined by the virulence of the pathogenic microorganism, the peculiarities of its relationship with the macroorganism and the nature of the therapy being carried out. But some starting data must be taken into account. The classic experimental studies of Durack D.T. et al. (1970, 1973) and our work on angiogenic sepsis in rabbits (Shikhverdiev N.N. 1984) showed that the formation of an active focus of infective endocarditis is possible within 2–3 days after infection against the background of endocardial trauma (for example, with a catheter). There are also very clear clinical examples. For primary infective endocarditis, it is often possible to determine the exact date (and sometimes even the exact time) of infection and then correlate the nature of pathomorphological changes with the period elapsed from the onset of the disease. In particular, we observed a patient who developed infective endocarditis involving all four valves within 3–4 days. According to our ideas, it takes 2 to 5 days to form a focus that requires surgical sanitation. As an example, we give a photograph of the mitral valve of a patient in whom 12 days have passed from the moment of infection to the complete destruction of the mitral valve.

Complete destruction of the mitral valve in primary infective endocarditis with a disease duration of 12 days. Vegetations, perforations, opened abscesses.

But this does not mean that all patients should be operated within these terms. Moreover, in such terms, patients are operated on very rarely.

First, as already mentioned, do not underestimate conservative therapy, in particular antibiotic therapy: it is always better to operate against the background of a stopped septic process. According to modern concepts, one of the indications for surgical treatment of infective endocarditis is the ineffectiveness of conservative therapy for 2 weeks (previously it was considered 4-6 weeks).

Secondly, the localization of the lesion is of great importance. When the aortic valve is destroyed by an infectious process, surgical treatment can be said to be inevitable, and the sooner it is performed, the better for the patient. For mitral and especially tricuspid valves, the timing of the development of circulatory decompensation is longer. Of course, experience is needed in order to take a patient for surgery in the most favorable status, and on the other hand, to prevent significant destruction of intracardiac structures, which will not allow saving one's own valve. In this regard, reconstructive surgery requires a more proactive approach.

For comparison, we present an excised mitral valve in a patient who was treated conservatively for too long (within 6 months). With such long-term conservative therapy, the valve leaflets thicken, fibrosis occurs, and ultimately the valve becomes unsuitable for reconstruction, and the only option for the patient is mitral valve replacement.

With a broken heart, many scare themselves and those around them, saying that such a nuisance can easily happen from fear or severe stress. But, if you think about it, in order for a heart rupture to occur, an injury must occur - a knife wound, a blow, because strong muscle tissues cannot tear on their own. Unfortunately, not only mechanical damage to the main "engine" in the body can lead to a serious illness. A complication of some diseases of the cardiovascular system can also be a tear of the heart muscle, which in the vast majority of cases leads to the death of the patient.

Causes of the disease

A very severe, almost always fatal consequence of myocardial infarction, which occurs in 2-8% of patients, is a heart rupture. It is a violation of the integrity of the organ wall, or, in other words, the formation of a through defect on the heart wall in transmural myocardial infarction.

Rupture of the heart muscle occurs, as a rule, 5-7 days after the onset of myocardial infarction. It is the third most common cause of death in patients, second only to pulmonary edema and cardiogenic shock, which, however, can develop against the background of partial myocardial rupture. It is believed that the greatest danger regarding the rupture of the heart is the first heart attack. After it, if the patient managed to survive, scar tissue resistant to hypoxia is formed, so repeated heart attacks are much less likely to lead to heart rupture.

According to statistics, 80% of all ruptures are damage to the free wall of the heart, 15% - damage to the interventricular septum, 5% - the chord of the heart valve and papillary muscles, resulting in acute mitral regurgitation. As the body ages, the likelihood of a heart rupture after a heart attack increases greatly. So, if up to 50 years it is 4%, then after 60 years it rises already in excess of 30%, while becoming especially significant in anterior extensive transmural infarction with a 20% left ventricular lesion.

More often, fiber tear is observed during a heart attack in women, the elderly due to slow scarring of the myocardium, in people with low body weight, with exhaustion. There are other risk factors that are recognized as seriously increasing the risk of acute myocardial pathology:

arterial hypertension;
diabetes;
preservation of motor activity during the acute phase of a heart attack, or within a week from the moment of its development;
late hospitalization and untimely initiation of treatment for a heart attack;
the absence of the use of thrombolytic drugs in the earliest periods after thrombosis of the coronary vessels;
the first heart attack that ended in a heart attack, with previously absent coronary artery disease, angina pectoris, vascular disease;
the presence of early postinfarction angina pectoris;
taking NSAIDs, hormones that prevent the formation of scar tissue quickly.

Other possible causes of myocardial rupture, which are much less common, can be:

traumatic injury to the heart;
tumors of the heart muscle;
endocarditis;
infiltrative damage to the organ during sarcoidosis, amyloidosis, hemochromatosis;
anomalies in the structure of the heart of a congenital type.

Rupture of the heart, despite the achievements of modern medicine, is a poorly understood pathology. Many experts consider it a hopeless condition, the only chance to survive in which is an emergency and successfully performed surgical treatment. Unfortunately, the speed with which the disease develops leaves almost no possibility for organizing surgical intervention, especially when a person is not in a specialized cardiac surgery department. That is why experts note the importance of preventive measures and the identification of risk factors, which will prevent such a formidable complication of myocardial infarction.

Varieties of heart rupture

According to the localization of damage, it can be internal, external. Internal ruptures include ventricular septum, which separates the left and right ventricles. This leads to a rapid disruption of blood flow, a drop in pressure and death. Also, the group of internal ruptures includes damage to the papillary muscles of the heart, which move the valves. Death in this case develops due to pulmonary edema against the background of congestion. It is these patients who can be saved by emergency surgical treatment, as they are able to live for several days before death. External tears cause blood to leak into the pericardium (the pericardial sac), which puts the heart under compression and stops working.

According to the timing of the appearance of the pathology is as follows:

early rupture - occurs within 72 hours after a heart attack or other disease;
late rupture - observed after 72 hours and later after a heart attack.

The duration of the pathology may be different. Instantaneous ruptures lead to instant death due to cardiac tamponade, slowly flowing for several hours, days cause circulatory disorders and death of a person. A complete rupture damages the muscle to its full depth, an incomplete one partially damages it, followed by the formation of a bulging (aneurysm) of the heart.

Signs of manifestation

Most often, a formidable complication occurs 1-4 days after the occurrence of myocardial infarction. Sometimes the danger persists until the end of the 3rd week after a heart attack. Symptoms of the disease are acute, sudden, but sometimes there is a so-called pre-rupture period, which also has its own clinical signs:

severe pain in the region of the heart, which radiates to the area between the shoulder blades and is not confused by taking medications;
drop in blood pressure;
fainting;
dizziness;
weakness of the pulse;
cold, clammy sweat;
enlargement of the liver.

Actually, the gap period in 90% of cases proceeds abruptly, suddenly, and only in 10% of cases develops slowly. As a rule, cardiac tamponade occurs, blood circulation stops. The patient loses consciousness, his skin becomes gray-bluish, which is especially noticeable on the face and the entire upper body. A person's neck swells and grows in size due to overfilling of the neck veins with blood. First, pressure and pulse disappear, then breathing stops, the pupils dilate.

Slow ruptures can last several hours or days, as they are characteristic of a small amount of myocardial damage. There is also a relatively favorable course of the disease, when slowly flowing blood becomes a blood clot that clogs the hole that has appeared. Symptoms of pathology are as follows:

pain in the heart that is difficult to reduce with drugs, periodically increasing and weakening;
arrhythmia;
weakness of systolic pressure, while diastolic can generally tend to zero (during thrombosis, pressure returns to normal);
tenderness of the liver on palpation;
swelling of the legs, feet.

The prognosis for a heart rupture depends on the size of the organ lesion, on the severity of shock events, and on the speed of surgical treatment. Particularly successful is the operation performed within 48 hours with partial tears of the heart.

Complications of pathology

The disease itself is so severe that it almost always leads to death. Any patient who has not received surgical treatment dies. Even with a small gap when closing the last thrombus, death occurs no later than 2 months without heart surgery. With high-quality treatment, up to 50% of patients die during the operation, since the sutures in the rupture area can erupt.

Carrying out diagnostics

Usually a patient with myocardial infarction is already in the hospital for treatment, so that an experienced doctor will immediately determine the signs of a developing complication even according to a physical examination. The presence of edema of the extremities, grayness of the skin, a drop in pressure and pulse, as well as other characteristic symptoms, suggest the approach of a rupture. When listening to heart sounds, a coarse systolic murmur is determined, which appears suddenly during systole and is located at the apex of the heart, behind the sternum, between the shoulder blades.

An ECG is performed on a patient with suspected cardiac rupture. If the study was done in the prerupture period, an increase in the S-T interval, the appearance of a pathological QS wave in several leads are recorded. This means an expansion of the infarct zone and subsequent rupture. With a rupture that has already occurred, an irregular heart rhythm is first noted, and then it stops - asystole. If it is possible to perform an ECHO-KG, then the place of the rupture or tear, the size of the lesion, the presence of blood in the pericardium, and the disruption of the valves are revealed.

Treatment Methods

Treatment can only be surgical, no conservative measures can save a person. Much more successful are those operations that are performed outside the acute phase, but with this pathology, the patient does not have time for such an expectation. Sometimes, before preparing a person for a long and serious operation, a minimally invasive intervention is performed to stabilize hemodynamics - intra-aortic balloon counterpulsation. Also, the patient may be shown pericardiocentesis - pumping fluid from the pericardium and stopping cardiac tamponade. Additionally, to maintain vital functions, nitrate preparations are administered to reduce vascular resistance.

Among the methods of surgical intervention, open suturing of the rupture site or the placement of a prosthesis (patch) at the site of myocardial or valve damage, intravascular operations that are effective for tearing the interventricular septum, can bring positive results. If a tear with a thrombus is located at the apex of the heart, its partial amputation can be done. In the presence of a donor heart, an organ transplant is performed.

Preventive measures

It is possible to prevent such a disease by preventing myocardial infarction. To this end, you must follow these tips:

stop eating fatty foods, normalize cholesterol levels;
normalize your weight;
eliminate bad habits;
observe feasible activity;
timely treat hypertension, coronary artery disease and atherosclerosis;
Seek immediate medical attention if you suspect unusual heart pain or other abnormal symptoms.
in case of a heart attack - do not move, immediately go to the intensive care unit.

Acute Mitral Valve Insufficiency- The most common causes of acute mitral regurgitation are rupture of the tendon chords of the valvular apparatus and infective endocarditis. mitral valve insufficiency may also be a consequence of the operation of "closed" commissurotomine with the expansion of indications for it.

Rupture of tendon chords may be due to previous endocarditis, rheumatic lesions and sclerosis, trauma. In some cases, the cause of this complication is difficult to establish.

As a rule, the chords attached to the posterior leaflet of the mitral valve are ruptured. The portion of the leaflet detached from the chord sags during ventricular systole into the cavity of the left atrium, which leads to an increase in the load on neighboring chords, their lengthening and gradual stretching of the fibrous ring of the valve. All this significantly aggravates the pathological discharge of blood into the left atrium.

Clinic. Acute mitral valve insufficiency characterized by shortness of breath, tachycardia, weakness. Suddenly, a rough systolic murmur appears (or is significantly enhanced against the background of a chronic defect), occupying the entire systole. Often it is carried out along the right edge of the sternum, it is typical of aortic localization, however, as a rule, it is well heard at the apex and is carried out in the axillary region. With its occurrence, symptoms of circulatory insufficiency rapidly progress: tachycardia, shortness of breath, stagnation in the pulmonary circulation.

The diagnosis is established on the basis of anamnesis data (absence of rheumatism), X-ray examination (normal parts of the heart, increased pulmonary pattern), phonocardiography (systolic murmur, occupying the entire systole). These patients usually remain in sinus rhythm.

Echocardiography and left-sided ventriculography provide very valuable information in the diagnosis and clarification of the degree of regurgitation.

Treatment is only surgical. The operation is indicated immediately after the diagnosis is established and consists in the plastic reconstruction of the valve or its replacement under conditions of cardiopulmonary bypass, cold pharmacolegia and general hypothermia.

The prognosis for timely operation is favorable in more than 85% of patients. Without surgery, the average life expectancy is about 10 months.

The development of acute mitral insufficiency in infective endocarditis is caused, as a rule, not only by rupture of the tendon chords, but also by the destruction of the valve leaflets.

Clinic. The beginning is subacute. The course gradually progresses and does not differ significantly from that described above. Intensity of systolic noise at the same time can gradually increase.

The diagnosis is based on the confirmation of the underlying disease (bacterial endocarditis) and the signs of severe mitral regurgitation described above.

Treatment is only surgical. The operation is to replace the mitral valve.

The prognosis largely depends on active symptomatic treatment and massive antibiotic therapy.
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Anatomy

There are four valves in the heart:

Mitral. It separates the cavity of the left atrium and ventricle and consists of two valves - anterior and posterior. Anterior leaflet prolapse is much more common than the posterior leaflet. Special threads, called chords, are attached to each of the valves. They provide valve contact with muscle fibers, which are called papillary or papillary muscles. For the full-fledged work of this anatomical formation, joint coordinated work of all components is necessary. During cardiac contraction - systole - the cavity of the muscular cardiac ventricle decreases, and accordingly the pressure in it increases. At the same time, the papillary muscles are included in the work, which close the exit of blood back to the left atrium, from where it poured out from the pulmonary circulation, enriched with oxygen, and, accordingly, the blood enters the aorta and further, through the arterial vessels, is delivered to all organs and tissues.
Tricuspid (tricuspid) valve. It consists of three wings. Located between the right atrium and ventricle.
aortic valve. As described above, it is located between the left ventricle and the aorta and does not allow blood to return to the left ventricle. During systole, it opens, releasing arterial blood into the aorta under high pressure, and during diastole, it closes, which prevents back flow of blood to the heart.
Pulmonary valve. It lies between the right ventricle and the pulmonary artery. Similar to the aortic valve, it prevents blood from returning to the heart (right ventricle) during diastole.

Causes of mitral valve prolapse

Congenital mitral valve prolapse is quite common and is associated with a hereditary defect in the structure of the connective tissue fibers that serve as the basis of the valves. With this pathology, the threads (chords) connecting the valve with the muscle are lengthened, and the valves themselves become softer, more pliable and more easily stretched, which explains their loose closure at the time of the heart systole. In most cases, congenital MVP proceeds favorably, without causing complications and heart failure, therefore, it is most often considered a feature of the body, and not a disease.
Heart diseases that can cause changes in the normal anatomy of the valves:
- Rheumatism (rheumatic heart disease). As a rule, a heart attack is preceded by a sore throat, a couple of weeks after which an attack of rheumatism (joint damage) occurs. However, in addition to the visible inflammation of the elements of the musculoskeletal system, heart valves are involved in the process, which are subjected to a much greater destructive effect of streptococcus.
- Ischemic heart disease, myocardial infarction (heart muscle). With these diseases, there is a deterioration in blood supply or its complete cessation (in the case of myocardial infarction), including the papillary muscles. Chord breaks may occur.
- Chest injury. Strong blows in the chest area can provoke a sharp separation of the valvular chords, which leads to serious complications if assistance is not provided in a timely manner.

Mitral valve prolapse classification

There is a classification of mitral valve prolapse depending on the severity of regurgitation.

I degree is characterized by a deflection of the sash from three to six millimeters;
II degree is characterized by an increase in the amplitude of the deflection up to nine millimeters;
III degree is characterized by the severity of the deflection of more than nine millimeters.

Mitral valve prolapse symptoms

As mentioned above, mitral valve prolapse in the vast majority of cases is almost asymptomatic and is diagnosed by chance during a preventive medical examination.

The most common symptoms of mitral valve prolapse include:

Cardialgia (pain in the region of the heart). This symptom occurs in about 50% of cases of MVP. Pain is usually localized in the region of the left half of the chest. They can be both short-term in nature and stretch for several hours. Pain can also occur at rest or with severe emotional stress. However, it is often not possible to associate the occurrence of a cardialgic symptom with any provoking factor. It is important to note that the pain is not stopped by taking nitroglycerin, which happens with coronary heart disease;
Feeling short of breath. Patients have an irresistible desire to take a deep breath "full chest";
Feeling of interruptions in the work of the heart (either a very rare heartbeat, or, on the contrary, rapid (tachycardia);
Dizziness and fainting. They are caused by heart rhythm disturbances (with a short-term decrease in blood flow to the brain);
Headaches in the morning and at night;
An increase in temperature, without any reason.

Diagnosis of mitral valve prolapse

To prevent the development of rheumatoid lesions of the heart valves, tonsillectomy (removal of the tonsils) is indicated in case of chronic tonsillitis (tonsillitis).

Drug therapy for MVP is aimed at treating complications such as arrhythmia, heart failure, as well as symptomatic treatment of manifestations of prolapse (sedation).

Complications of mitral valve prolapse

Mitral valve insufficiency. This condition is a common complication of rheumatic heart disease. In this case, due to incomplete closure of the valves and their anatomical defect, there is a significant return of blood to the left atrium. The patient is worried about weakness, shortness of breath, cough and many others. In the event of the development of such a complication, valve replacement is indicated.
Attacks of angina pectoris and arrhythmias. This condition is accompanied by an abnormal heart rhythm, weakness, dizziness, a feeling of interruptions in the work of the heart, crawling "goosebumps" before the eyes, fainting. This pathology requires serious medical treatment.
Infective endocarditis. In this disease, inflammation of the heart valve occurs.

Prevention of mitral valve prolapse

Keywords: chorda tendonus, mitral insufficiency, echocardiography.

Objective examination: forced position in bed - orthopnea, cyanotic skin, respiratory rate - 24 per minute. In the lungs during auscultation - on the right in the n / o breathing is weakened, in the same place - single moist rales, on the left - without features. Heart rate - 80 per minute, blood pressure - 150/90 mm Hg. Art. Heart sounds are rhythmic, clear, coarse pansystolic murmur is heard at all points. The left border of the heart is expanded by 1.5-2 cm, the right border - by 1-1.5 cm. The liver is enlarged, swells from under the edge of the costal arch by 2 cm. Stool and diuresis are normal. There are no peripheral edema.

On the ECG: signs of left ventricular hypertrophy, diffuse changes in the ventricular myocardium.

Echocardiography (June 18, 2004): dilatation of all cavities of the heart, LA = 4.8 cm, LVCD = 5.8 cm, RV = 3.2 cm. Myocardial hypertrophy in both ventricles. The aorta is sealed, in the ascending section is not expanded. AK: the leaves are sealed, the antiphase is not broken. MK: front leaf, after its middle part floats , moves asynchronously, in comparison with its base and middle part, the rear leaf is sealed, the amplitude of its opening is not reduced. There are no zones of local asynergies.

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There is hyperkinesia of the interventricular septum. Overall contractility is reduced due to severe mitral regurgitation. EF = 50-52%. Doppler: mitral regurgitation of 3-4 degrees, tricuspid regurgitation of 2 degrees.

To clarify the diagnosis and better visualize the structural changes in the mitral valve, transesophageal echocardiography was performed (June 9, 2004): visualization is satisfactory. Defined flotation anterior leaflet of the mitral valve, there is a detachment of one of the tendon chords. Doppler: mitral regurgitation of 3-4 degrees, tricusidal regurgitation of 2 degrees. Regurgitant jet in the left atrium reaches the first pulmonary vein. Pressure in the pulmonary artery - 50 mm Hg. Dilatation of the left atrium: LA = 5 cm, RV = 3.2 cm.