Acute mitral insufficiency. Mitral valve chord avulsion treatment

The patient called an ambulance (the ECG was not taken). The condition was assessed as an attack of bronchial asthma. After the measures taken, the patient's condition improved. The next day the patient went to work. Behind medical care didn't apply. But from that time on, he began to notice shortness of breath with moderate physical activity (climbing 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: a round formation was noted, with clear contours, 2*2 cm in size, at the base of the anterior leaflet mitral valve(myxoma?)

The EMS team transported the patient to the hospital for examination and selection of therapy.

It is also known from the anamnesis that he has been working as a “tunneler” for 25 years. The work involves daily heavy physical labor (heavy lifting).

Objective examination data: general state patient medium degree gravity. Consciousness is clear. The skin is of normal color and normal moisture. Edema lower limbs No. The lymph nodes not enlarged. Breathing on auscultation is harsh, there are no wheezes. NPV 16 per minute. The heart area is not changed. The apex beat is not detected. On auscultation, heart sounds are muffled and arrhythmic. A systolic murmur is heard at the apex. Blood pressure 140/90 mm Hg. Heart rate=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, WS – 1.3 cm, EDV – 5.7 cm, ESR – 3.8 cm, LVMI 182.5 g/m2, IOT – 0.46, EDV – 130 ml, ESV – 55 ml, EF – 58%. No violations of local contractility were detected. RA 22 cm2, RV PSAX – 3.4 cm, basal diameter of the RV - 3.7 cm, free wall thickness 0.4 cm, TAPSE 2.4 cm. IVC 1.8 cm, collapse on inspiration< 50%.

The study was conducted against the background of atrial fibrillation. MPAP – 45 mm Hg.

In the LA cavity during systole, 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. Severance of the chord of the anterior leaflet of the mitral valve with the formation of severe insufficiency. Insufficiency of TC is not to a large extent. Signs of pulmonary hypertension.

Mitral valve prolapse

Mitral valve prolapse (MVP) is a clinical pathology in which one or two valve leaflets anatomical education prolapse, that is, they bend into the cavity of the left atrium during systole (heartbeat), which should not normally happen.

Diagnosis of MVP has become possible thanks to the use of ultrasound technology. Mitral valve 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 detected approximately four times more often. In adolescence, the ratio of girls to boys is 3:1, and for women to men it is 2:1. In older people, the difference in the incidence of MVP in both sexes is leveled out. This disease also occurs during pregnancy.

Anatomy

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

There are four valves in the heart:

Mitral. It separates the cavity of the left atrium and the ventricle and consists of two valves - anterior and posterior. Prolapse of the anterior valve leaflet is much more common than the posterior one. Special threads called chords are attached to each of the valves. They provide contact between the valve and muscle fibers, which are called papillary or papillary muscles. For the full functioning of this anatomical formation, the joint coordinated work of all components is necessary. During cardiac contraction - systole - the muscle cavity cardiac ventricle decreases, and accordingly the pressure in it increases. In this case, the papillary muscles are activated, which close the exit of blood back into the left atrium, from where it flows out of the pulmonary circulation, enriched with oxygen, and, accordingly, the blood enters the aorta and further, along arterial vessels, is delivered to all organs and tissues.
Tricuspid (three-leaf) valve. It consists of three doors. 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 is closed, which prevents blood from flowing back to the heart.
Valve pulmonary artery. It is located between the right ventricle and the pulmonary artery. Likewise aortic valve, it prevents blood from returning to the heart (right ventricle) during diastole.

Normally, the work of the heart can be imagined in the following way. 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 during systole it spreads through the aorta to all organs of the systemic circulation (liver, brain, limbs and others). Having transferred oxygen to the cells, the blood takes carbon dioxide and returns to the heart, this time in right atrium. From its cavity, fluid enters the right ventricle and, during systole, is expelled into the pulmonary artery and then into the lungs (pulmonary circulation). The cycle repeats.

What is prolapse and why is it dangerous? This is a state of inadequate functioning of the valve apparatus, in which, during muscle contraction, the blood outflow pathways are not completely closed, and, therefore, part of the blood returns back to the heart during systole. So, with mitral valve prolapse, the 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 pathology of the mitral valve, the changes are insignificant, so this condition is often considered as a normal variant.

Causes of mitral valve prolapse

There are two main reasons for the occurrence of this pathology. One of them is a congenital structural disorder connective tissue 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 hereditarily transmitted defect in the structure of connective tissue fibers, which serve as the basis of the valves. In this case, pathologists lengthen the threads (chords) connecting the valve to the muscle, and the valves themselves become softer, more pliable and more easily stretched, which explains their loose closure at the time of 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 may cause changes normal anatomy valves:
- Rheumatism (rheumatic carditis). As a rule, heart damage 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 musculoskeletal system, the process involves the heart valves, which are subject to much greater destructive effects of streptococcus.
- Coronary 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 to the papillary muscles. Chordal rupture may occur.
- Chest injuries. Strong impacts in the chest area can provoke a sharp separation of the valve chords, which leads to serious complications in case of failure to provide timely assistance.

Classification of mitral valve prolapse

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

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

Symptoms of mitral valve prolapse

As mentioned above, mitral valve prolapse in the vast majority of cases is practically asymptomatic and is diagnosed accidentally during a routine medical examination.

To the most frequent symptoms Mitral valve prolapse includes:

Cardialgia (pain in the heart area). This sign occurs in approximately 50% of MVP cases. The pain is usually localized in the left half of the chest. They can be either short-term or last 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 relieved by taking nitroglycerin, which happens with coronary disease hearts;
Feeling short of air. Patients have an irresistible desire to do deep breath“to the fullest”;
A feeling of interruptions in the functioning of the heart (either a very rare heartbeat, or, on the contrary, a rapid heartbeat (tachycardia);
Dizziness and fainting. They are caused by violations heart rate(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, a therapist or cardiologist diagnoses valve prolapses by auscultation (listening to the heart using a stethoscope), which they perform for each patient during routine medical examinations. Heart murmurs are caused by sound phenomena when the valves open and close. If a heart defect is suspected, the doctor will refer you 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 treatment tactics for mitral valve prolapse are 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 patients’ work and rest schedules and adherence to a daily routine. Be sure to pay attention to long (sufficient) sleep. The issue of physical education and sports should be decided individually by the attending physician after assessing physical fitness indicators. Patients, in the absence of severe regurgitation, are shown moderate physical activity and active image life without any restrictions. The most preferred are skiing, swimming, skating, and cycling. But activities related to the jerking 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 (calming) plants: valerian, motherwort, hawthorn, wild rosemary, sage, St. John's wort and others.

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

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

In case of severe regurgitation, as well as circulatory failure, surgery may be performed. 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 rheumatic lesions hearts. 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 case of development similar complication, valve replacement is indicated.
Attacks of angina and arrhythmia. This condition is accompanied by abnormal heart rhythm, weakness, dizziness, a feeling of interruptions in the heart, crawling “goosebumps” before the eyes, and fainting. This pathology requires serious drug treatment.
Infectious endocarditis. This disease causes inflammation of the heart valve.

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 if indicated) and others. Must undergo regular annual medical examinations treat in a timely manner colds, especially sore throat.

Mitral valve chord avulsion treatment

Key words: chorda tendineus, mitral regurgitation, echocardiography.

The patient, Hakobyan Artashes, 76 years old, was admitted to the department of liver surgery of the Erebuni Medical Center on June 7, 2004. on planned surgery about the left side inguinoscrotal hernia. From the anamnesis: 4 days ago, while working on a personal plot, I suddenly felt severe shortness of breath for the first time in my life.

Objective examination: forced position in bed – orthopnea, skin cyanotic, respiratory rate – 24 per minute. In the lungs, upon auscultation, breathing is weakened on the right side of the lower abdomen, there are isolated moist rales, on the left side there are no features. Heart rate – 80/min, blood pressure – 150/90 mmHg. Art. Heart sounds are rhythmic, clear, and a rough 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, protrudes from under the edge of the costal arch by 2 cm. Stool and diuresis are normal. Peripheral edema No.

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

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

Hyperkinesia is observed interventricular septum. Overall contractility is reduced due to pronounced mitral regurgitation. EF = 50–52%. Doppler: mitral regurgitation grade 3–4, tricuspid regurgitation grade 2.

To clarify the diagnosis and better visualization structural changes transesophageal echocardiography was performed on the mitral valve (June 9, 2004): visualization was satisfactory. Flotation of the anterior mitral valve leaflet is determined, and separation of one of the tendon chords is noted. Doppler: mitral regurgitation grade 3-4, tricusidal regurgitation grade 2. The regurgitant jet in the left atrium reaches the first pulmonary vein. Pulmonary artery pressure - 50 mm Hg. Left atrium dilatation: LA = 5 cm, RV = 3.2 cm.

The patient was transferred to the department emergency cardiology, received nitrates, ACE inhibitors, Ca 2+ channel blockers, diuretics. From surgical treatment categorically refused. During treatment with arteriolodilators, dynamic echocardiography was performed. There was a decrease in the degree of mitral regurgitation. He was discharged in satisfactory condition following therapy. Outpatient treatment and follow-up are recommended.

Features of the clinic, diagnosis and treatment of various types of non-rheumatic mitral regurgitation

Among the causes of non-rheumatic mitral regurgitation, the most common are mitral valve prolapse and papillary muscle dysfunction. Less common are chordae tendinous rupture and mitral annulus calcification.

Mitral valve prolapse is clinical syndrome, caused by pathology of one or both cusps of the mitral valve, most 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 are asymptomatic, being the most common valve defect. It is found predominantly in individuals, more often in women. Secondary mitral valve prolapse is observed in a number of heart diseases - rheumatism, including rheumatic defects (on average in 15% or more cases), in PS, especially secondary defect interatrial septum (20-40%), ischemic heart disease (16-32%), cardiomyopathies, etc.

The etiology has not been established. With primary prolapse, there is a hereditary predisposition with an autosomal dominant type of transmission. Its morphological substrate is a nonspecific, so-called myxomatous degeneration valve leaflets with replacement of the spongy and fibrous layers by an accumulation of pathological acidic mucopolysaccharides, which contain fragmented collagen fibers. There are no elements of inflammation. Similar morphological changes are characteristic of Marfan syndrome. Some patients with mitral valve prolapse experience joint hypermobility, skeletal changes (thin long fingers, straight back syndrome, scoliosis), and occasionally dilatation of the aortic root. Prolapse of the tricuspid and aortic valves also occurs, sometimes in combination with a similar lesion of the mitral valve. These facts allowed us to suggest that the basis of the disease is a genetically determined pathology of connective tissue with isolated or predominant damage to the leaflets of the heart valves, most often the mitral valve.

Macroscopically, one or both valves are enlarged and thickened, and the chordae tendineae attached to them are thinned and elongated. As a result, the valves are domed into the cavity of the left atrium (parus) and their closure is more or less disrupted. The valve ring may 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, it may, however, increase. Due to an increase in the radius of curvature of the valve, the tension experienced by the chordae tendineae and intact papillary muscles increases, which aggravates the stretching of the chordae and can 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 increase regurgitation and cause arrhythmias.

In most cases of primary prolapse, the myocardium is not changed in morphological and functional terms, however, in a small proportion of symptomatic patients, causeless nonspecific myocardial dystrophy and fibrosis are described. These data serve as the basis for discussing the possibility of a connection between prolapse and myocardial damage of unknown etiology, that is, with cardiomyopathies.

Clinic. The presentation 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. Most patients remain asymptomatic throughout their lives.

Complaints are non-specific and include various types cardialgia, often persistent, not relieved by nitroglycerin, interruptions and heartbeats that occur periodically, mainly at rest, a feeling of shortness of breath with melancholy sighs, dizziness, fainting, general weakness and fatigue. A significant portion of these complaints are of functional, neurogenic origin.

Auscultation data are of utmost diagnostic importance. A mid- or late systolic click is characteristic, which may be the only manifestation of the pathology or, more often, accompanied by the so-called late systolic murmur. As phonocardiography data show, it is noted 0.14 s or more after the first sound and, apparently, is caused by a sharp tension of the sagging elongated chordae tendineae or the bulging valve leaflet. Late systolic murmur can be observed without a click and indicates mitral regurgitation. It is best heard above the apex of the heart, short, often quiet and musical. The click and noise shift to the beginning of systole, and the noise lengthens and intensifies as the filling of the left ventricle decreases, which aggravates the discrepancy between the dimensions 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 maneuver (straining), and inhalation of amyl nitrite. On the contrary, an increase in the EDV of the left ventricle during squatting and isometric load (compression of a hand dynamometer) or the administration of norepinephrine hydrotartrate causes a delay in the click and a shortening of the noise, until they disappear.

Diagnostics. Changes to ECG absent or non-specific. Most often, biphasic or negative waves are observed T in leads II, III and aVF, usually positive during the obsidan (inderal) test. Data radiography without features. Only in cases of severe regurgitation are changes characteristic of mitral insufficiency noted.

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

In my own way diagnostic value echocardiography is not inferior angiocardiography, in which bulging of the mitral valve leaflets into the left atrium with the throwing of contrast material from the left ventricle into it is also determined. Both methods, however, may give false results. positive results, and existing diagnostic signs require verification.

The course and prognosis are favorable in most cases. Patients usually lead normal image life, and the defect does not impair survival. Severe complications occur very rarely. As shown by the results of long-term (20 years or more) observations, their risk increases with 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 approximately 5% of patients and in some cases is associated with spontaneous rupture of the chord (2); 3) ventricular ectopic arrhythmias, which can cause palpitations, dizziness and fainting, and in isolated, extremely in rare cases, leading to ventricular fibrillation and sudden death; 4) infective endocarditis; 5) embolism of cerebral vessels due to thrombotic deposits, which can form on the altered valves. The last two complications are, however, so rare that they are not routinely prevented.

If the disease is asymptomatic, treatment is not required. For cardialgia, beta-blockers are quite effective, providing

to a certain extent empirical. In the presence of severe mitral regurgitation with signs of left ventricular failure, surgical treatment is indicated - plastic surgery or replacement of the mitral valve.

Recommendations for antibiotic prophylaxis for 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 is caused by ischemia, fibrosis, and less often inflammation. Its occurrence is facilitated by changes in the geometry of the left ventricle during its dilatation. It occurs quite often in acute and chronic forms IHD, cardiomyopathies and other myocardial diseases. Mitral regurgitation, as a rule, is small and manifests itself as a late systolic murmur due to a violation of the closure of the valve leaflets in the middle and end of systole, which is largely ensured by contraction of the papillary muscles. Rarely, with significant dysfunction, the murmur may be pansystolic. The course and treatment are determined by the underlying disease.

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

In the most severe cases, severe recurrent, sometimes intractable, pulmonary edema due to high venous pulmonary hypertension and even cardiogenic shock are noted. In contrast to chronic rheumatic mitral regurgitation, even with significant left ventricular failure, patients retain 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 leaflet are ruptured, it is sometimes localized on the back, and in the anterior leaflet - 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.

X-ray examination reveals signs of pronounced venous congestion in the lungs, up to edema, with a relatively slight increase in the left ventricle and atrium. Over time, the chambers of the heart expand.

The diagnosis can be confirmed by echocardiography, which shows fragments of the valve leaflet and chord 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 regurgitant flow 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 condition of the left ventricular myocardium. Many patients die, and those who survive exhibit severe mitral regurgitation.

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

Mitral annulus 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 facilitated by increased load on the valve (prolapse, increased CVD in the left ventricle) and hypercalcemia, especially with hyperparathyroidism. Calcifications are not located in the ring itself, but in the area of the base of the valve leaflets, more posteriorly. Small calcium deposits do not affect hemodynamics, while large ones, causing immobilization of the mitral ring and chordae, lead to the development of mitral regurgitation, usually small or moderate. IN isolated cases it is accompanied by a narrowing of the mitral orifice (mitral stenosis). It is often combined with calcification of the aortic mouth, causing its stenosis.

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

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

In most cases, no special treatment is required. In case of significant regurgitation, mitral valve replacement is performed. Prevention of infective endocarditis is indicated.

Infectious endocarditis of the mitral valve

Mitral valve insufficiency

Etiology. Rheumatic fever, infective endocarditis, atherosclerosis, cardiac injury with avulsion of chordae, papillary muscles, myocardial infarction involving the papillary muscles. “Relative” mitral valve insufficiency (without significant deformation and shortening of the leaflets) occurs with mitral valve prolapse and dilatation of the left ventricular cavity caused by any reason.

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

The left ventricular impulse is strengthened, expanded, and shifted to the left. According to percussion data at the initial stages of the border relative stupidity the hearts are not changed, with myogenic dilatation of the heart there is a shift of the left border to the left, the top - upward,

On auscultation - a weakened 1st tone, a pathological 3rd tone at the apex of the heart, an accent 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 armpit.

X-ray examination. Enlargement of the left ventricular arch and left atrium. Deviation of the shadow of the contrasted esophagus along an arc of large radius (8-10 cm).

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

Phonocardiogram. A decrease in the amplitude of the 1st tone at the apex, there is also a pathological 3rd tone (low-frequency oscillations separated from the 2nd tone by a time interval of at least 0.13 seconds). The systolic murmur associated with the 1st sound is of a decreasing nature, occupying from 2/3 to the entire systole.

Echo cardiogram. Increase in the size of the cavity of the left atrium, left ventricle.

Mitral valve insufficiency and hypertrophic cardiomyopathy. At 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 likelihood 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 case of mitral insufficiency, the noise is carried out into the armpit. With cardiomyopathy, the noise increases when standing up, when performing the Valsalva maneuver. Diagnostic doubts are resolved by echocardiography, which reveals important sign hypertrophic cardiomyopathy - asymmetric hypertrophy of the interventricular septum.

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

With dilated cardiomyopathy, mitral valve insufficiency (relative, without anatomical damage to the leaflets) is present in the vast majority of patients. The consequence of this is regurgitation of blood from the left ventricle into 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 sound at the apex of the heart.

ECG changes may be identical in dilated cardiomyopathy and organic mitral valve insufficiency, as well as the results of a FCG study. The method of choice in differentiating the diseases under consideration is echocardiography. 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 aortic mouth occurs, as a rule, with a systolic murmur at the apex of the heart. However, this noise is also heard at the base of the heart and is carried out not in the armpit, but in the carotid arteries.

Insufficiency of the tricuspid valve with sharp hypertrophy and dilation of the right ventricle can lead to the fact that in the area usual localization The left ventricular impulse turns out to be the right ventricular impulse. Diagnostic difficulties are resolved by the Rivero-Corvallo test: at the height of inspiration, the sound of tricuspid valve insufficiency intensifies. Tricuspid valve insufficiency is characterized by symptoms of isolated right ventricular heart failure, while bicuspid valve insufficiency is characterized by left ventricular or biventricular heart failure.

Mitral valve insufficiency and congenital heart disease - septal defect. Typical for a septal defect are: systolic cardiac tremors at the site of attachment of the 3-4th ribs to the sternum on the left; rough systolic murmur in the same zone and at the apex, having a ribbon-like shape on the phonocardiogram; According to radiography and ECG, there are signs of hypertrophy of both ventricles. Active search and detection of these symptoms makes the doctor 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, cardiac aneurysm, arterial hypertension with dilatation of the left ventricular cavity. When resolving issues of differential diagnosis, it is taken into account clinical picture the disease in general and the characteristics of the noise (its amplitude, volume ratio with the 1st tone, connection with it, conduction). Significant assistance in difficult cases Echocardiography provides evidence of the absence of changes in the mitral valve leaflets.

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 of asthenic constitution. These noises are not loud, are not combined with a weakening of the 1st tone, and are not carried into the armpit. The boundaries of the heart, according to percussion and x-ray data, are not changed. According to the FKG data, innocent noises are not associated with the 1st tone and are variable. Occupies 1/3-1/2 systole.

“Pure” mitral valve insufficiency of rheumatic etiology is a rare defect. The statement of G.F. is correct. Langa, S.S. Zimnitsky that the “rheumatic sign” is a combined mitral valve disease. For diagnostics rheumatic fever The generally accepted Jones criteria are used in various modifications.

At infective endocarditis more typical is damage to the aortic valve with the formation of its insufficiency. The mitral valve is affected much less frequently, and this lesion is naturally combined with endocarditis of the aortic valve. The criteria for the diagnosis of infective endocarditis are described in detail in the corresponding chapter.

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

Atherosclerotic lesion of the aorta occurs with systolic murmur, induration and calcification of the aorta, according to X-ray data.

Mitral valve insufficiency during myocardial infarction occurs due to damage to the papillary muscles and separation of the chordae. Symptoms (systolic murmur with typical irradiation into the axilla, increase or appearance of left ventricular heart failure) develop acutely, usually on the 5-11th day of illness.

Traumatic mitral valve insufficiency is characterized by an appropriate history. In fact, a traumatic iatrogenic defect is mitral valve insufficiency as a result of mitral commissurotomy (post-commissurotomy mitral insufficiency).

Mitral valve prolapse often occurs in older women with low body weight.

Contrary to the generally accepted point of view, the classic auscultatory picture of mitral valve prolapse - a 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. Depending on 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. According to echocardiography and the human method, we should talk about prolapse of the first degree 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). If regurgitation is present, its severity is assessed semi-quantitatively, in points from 1 to 4.

The course of the disease can be asymptomatic, mild, moderate or severe. Mild course characterized by complaints of predominantly asthenic type (weakness, fatigue, headache, uncertain painful sensations in the heart area), spontaneous fluctuations in blood pressure, nonspecific ECG changes (depression S-T interval in 2, 3 standard leads, lead aVF, left chest leads, T wave inversion). The course of moderate severity is characterized by complaints of pain in the heart, palpitations, interruptions, non-systemic dizziness, and fainting. The ECG, along with nonspecific changes, shows rhythm and conduction disturbances. Mitral regurgitation is mildly expressed. ABOUT severe course should be spoken when to a large extent 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 condition of the myocardium. If mitral insufficiency is mild, the patient remains able to work for a long time. Mitral insufficiency with large regurgitation of blood into the left atrium is severe; sometimes in these patients decompensation develops faster than with mitral stenosis. After a few months or years, left ventricular failure is accompanied by symptoms of right heart failure.

Complications. Arrhythmias. Acute left heart failure. Thromboembolism of the renal, mesenteric arteries, and 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 leaflets, subvalvular structures, dilatation of the fibrous ring or disruption 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 disturbances of intracardiac hemodynamics are accompanied by a decrease in minute volume of blood circulation and the development of pulmonary hypertension syndrome.

The causes of mitral insufficiency are presented in Table 1.

Acute mitral regurgitation

Damage to the mitral annulus

Infectious endocarditis (abscess formation)
Trauma (from valve surgery)
Paraprosthetic fistula due to suture cutting or infective endocarditis

Damage to the mitral valve leaflets

Infective endocarditis (perforation or destruction of the leaflet (Fig. 7).)
Injury
Tumors (atrial myxoma)
Myxomatous degeneration of the leaflets
Systemic lupus erythematosus (Libman-Sachs lesion)

Rupture of chordae tendineae

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

Perforation of the bioprosthetic leaflet due to infective endocarditis
Degenerative changes in bioprosthetic valves
Mechanical damage (rupture of the bioprosthetic leaflet)
Jamming of the locking element (disc or ball) of a mechanical prosthesis

Chronic mitral insufficiency

Inflammatory changes

Myxomatous degeneration of the mitral valve leaflets (“click syndrome”, Barlow syndrome, prolapsed leaflet, mitral valve prolapse
Marfan syndrome
Ehlers-Danlos syndrome
Pseudoxanthoma
Calcification of the mitral valve annulus

Infective endocarditis developing on normal, altered or prosthetic valves

Rupture of chordae tendineae (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 mitral valve annulus and left ventricular cavity (cardiomyopathy, aneurysmal dilatation of the left ventricle)
Hypertrophic cardiomyopathy
Paraprosthetic fistula due to cutting of sutures

Splitting or fenestration of the mitral valve leaflet
Formation of a “parachute-shaped” mitral valve due to:
Disturbances in the fusion of endocardial cushions (mitral valve rudiments)
Endocardial fibroelastosis
Transposition of the great vessels
Abnormal formation of the left coronary artery

Surgery or drug treatment for mitral valve infection

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

Deciding on the feasibility and hemodynamic effectiveness of a particular option reconstructive surgery in patients with infective endocarditis is taken taking into account the location of the lesion, its prevalence and how long it has existed. Any infectious process is accompanied by tissue swelling and infiltration, and in advanced cases, destruction. This fully applies to intracardiac structures. When assessing the possibility of preserving valve structures, it is important to understand that sutures placed on swollen, inflamed tissues high probability will erupt, which will lead to 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 a “cold” period, against the background of remission of the infectious process. However, this is not always possible or advisable. In such cases, it is advisable to excise all the affected tissue on the one hand radically, on the other - as sparingly as possible. Sutures should be placed on unchanged tissue and, if possible, pads should be used (optimally from autopericardium). When using non-implantation techniques, it is still desirable to strengthen the plastic area in one way or another. You can use the same autopericardium strips for this. Some surgeons pre-treat them for 9 minutes in a glutaraldehyde solution (De La Zerda D.J. et al. 2007).

From a practical point of view, it is important to know what time frame a surgeon should use when deciding to operate on a patient with active infective endocarditis. It is clear that there is not and cannot be a single standard recipe. Everything is determined by virulence pathogenic microorganism, the peculiarities of its relationship with the macroorganism and the nature of the therapy performed. But some starting data must be taken into account. Classic experimental studies by Durack D.T. et al. (1970, 1973) and our work on angiogenic sepsis in rabbits (Shikhverdiev N.N. 1984) it was shown 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 that has passed since the onset of the disease. Specifically, we observed a patient who developed infective endocarditis affecting all four valves within 3–4 days. According to our ideas, the formation of a lesion requiring surgical sanitation takes from 2 to 5 days. As an example, we present a photograph of the mitral valve of a patient in whom 12 days 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 on within this time frame. Moreover, patients undergo surgery very rarely during such periods.

Firstly, 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 conservative therapy within 2 weeks (previously considered 4 - 6 weeks).

Secondly, the location of the lesion is of great importance. When destroyed infectious process aortic valve, surgical treatment can be said to be inevitable, and the sooner it is performed, the better for the patient. For the mitral and especially tricuspid valves, the development time of circulatory decompensation is longer. Of course, experience is needed in order to take the 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 active position.

For comparison, we present a resected mitral valve in a patient who was treated conservatively for too long (for 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.

Many people scare themselves and others with heartbreak, saying that such a nuisance can easily happen from fear or extreme 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 tissue can not. Unfortunately, not only mechanical damage to the main “engine” in the body can lead to 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

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

Rupture of the heart muscle usually occurs 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 partial rupture myocardium. It is believed that the greatest danger regarding heart rupture is the first heart attack. After it, if the patient managed to survive, a hypoxia-resistant scar tissue, 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% are damage to the interventricular septum, 5% are damage to the chords heart valve and papillary muscles, as a result of which acute mitral regurgitation develops. As the body ages, the likelihood of heart rupture after a heart attack increases greatly. So, if up to 50 years it is 4%, then after 60 years it increases to over 30%, becoming especially significant in the case of an extensive anterior transmural infarction with a 20% area of damage to the left ventricle.

More often, tearing of fibers is observed during a heart attack in women, the elderly due to slow scarring of the myocardium, in people with low body weight, and with exhaustion. There are other risk factors that are recognized to seriously increase the danger acute pathology myocardium:

arterial hypertension;
diabetes;
maintaining physical activity during acute phase heart attack, or within a week from the moment of its development;
late hospitalization and untimely initiation of treatment for heart attack;
lack of use of thrombolytic drugs during the most early dates after thrombosis of coronary vessels;
the first heart attack ending in infarction, with previously absent ischemic heart disease, angina pectoris, or vascular disease;
the presence of early post-infarction angina;
taking NSAIDs, hormones that prevent scar tissue from quickly forming.

Others possible reasons Myocardial rupture, which are much less common, can be:

traumatic heart injury;
tumors of the heart muscle;
endocarditis;
infiltrative organ damage during sarcoidosis, amyloidosis, hemochromatosis;
congenital structural abnormalities of the heart.

Heartbreak despite achievements modern medicine, is a little-studied pathology. Many experts consider it a hopeless condition, the only chance of survival in which is emergency and successfully performed surgical treatment. Unfortunately, the speed with which the disease develops leaves almost no opportunity to organize surgical intervention, especially when the person is not in a specialized cardiac surgery department. That is why experts note the importance preventive measures and identifying risk factors, which will help prevent such a dangerous complication of myocardial infarction.

Types of heart rupture

Depending on the location of the damage, it can be internal or external. Internal ruptures include ruptures of the interventricular septum, which separates the left and right ventricles. It leads to rapid violation blood flow, a drop in pressure and the death of a person. Also included in the group of internal ruptures are damage to the papillary muscles of the heart, which move the valves. Death in this case develops due to pulmonary edema against the background stagnation. It is these patients who can be saved through emergency surgical treatment, since they are able to survive several days before death. External ruptures cause blood to leak into the pericardium (the sac around the heart), which puts the heart under compression and it stops working.

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

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

The duration of the pathology may vary. Simultaneous ruptures lead to instant death due to cardiac tamponade, slowly flowing over several hours or days, causing circulatory disorders and human death. A complete rupture damages the muscle to its full depth, an incomplete rupture damages it partially, followed by the formation of a bulge (aneurysm) of the heart.

Signs of manifestation

Most often, a serious complication occurs 1-4 days after a myocardial infarction occurs. Sometimes the danger persists until the end of the 3rd week after a heart attack. The 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 heart area, which radiates to the area between the shoulder blades and is not relieved by taking medications;
drop in blood pressure;
fainting;
dizziness;
weak pulse;
cold, clammy sweat;
enlargement of the liver.

The rupture period itself in 90% of cases proceeds sharply, suddenly, and only in 10% of cases develops slowly. As a rule, cardiac tamponade occurs and 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, the pressure and pulse disappear, then breathing stops, the pupils dilate.

Slow ruptures can last several hours or days, since they are characteristic of a small amount of myocardial damage. It happens relatively favorable course a disease when slowly flowing blood becomes a blood clot that clogs the hole that appears. The symptoms of the pathology are as follows:

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

The prognosis for cardiac rupture depends on the size of the organ damage, the severity of shock phenomena, and the speed of conduction. surgical treatment. The operation performed within 48 hours for partial heart tears is especially successful.

Complications of pathology

This disease itself is so severe that it almost always leads to death. Any patient who does not receive surgical treatment dies. Even with a small rupture, when the latter is closed by a blood clot, death occurs no later than 2 months without heart surgery. At quality treatment up to 50% of patients die during surgery, since the sutures in the area of \u200b\u200bthe rupture can cut through.

Carrying out diagnostics

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

A patient with suspected cardiac rupture undergoes an ECG. If the study was done in the pre-rupture period, a rise in the S-T interval and the appearance of a pathological QS wave in several leads are recorded. This means expansion of the infarction zone and subsequent rupture. If a rupture has already occurred, it is first noted wrong rhythm heart, and then it stops - asystole. If it is possible to perform ECHO-CG, then the location of the rupture or tear, the size of the lesion, the presence of blood in the pericardium, and 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 a wait. Sometimes, before preparing a person for a long and serious operation, he undergoes a minimally invasive intervention to stabilize hemodynamics - intra-aortic balloon counterpulsation. The patient may also be indicated for pericardiocentesis - pumping out fluid from the pericardium and stopping cardiac tamponade. Additionally to maintain vital functions Nitrates are administered to reduce vascular resistance.

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

Preventive measures

This disease can be prevented 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;
be as active as possible;
treat hypertension, ischemic heart disease and atherosclerosis in a timely manner;
Seek immediate medical attention if you suspect unusual heart pain or other abnormal symptoms;
in case of a heart attack - do not move, go straight to the intensive care unit.

Acute Mitral Valve Insufficiency- The most common causes of acute mitral regurgitation are rupture of the chordae tendineae of the valve apparatus and infective endocarditis. Mitral valve insufficiency may also be a consequence of the operation “closed” commissurotomine when the indications for it are expanded.

Rupture of the chordae tendineae may be caused by previous endocarditis, rheumatic lesions, sclerosis, or trauma. In some cases, the cause of this complication is quite difficult to establish.

As a rule, the chords attached to the posterior leaflet of the mitral valve are subject to rupture. The section of the valve separated from the chord sags during ventricular systole into the cavity of the left atrium, which leads to an increase in the load on the adjacent chords, their elongation 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 failure mitral valve characterized by shortness of breath, tachycardia, weakness. A rough systolic murmur suddenly appears (or increases significantly against the background of a chronic defect), occupying the entire systole. It is often carried out along the right edge of the sternum, it is typically of aortic localization, however, as a rule, it is well heard at the apex and is carried out in axillary area. With its occurrence, symptoms of circulatory failure quickly progress: tachycardia, shortness of breath, congestion in the pulmonary circulation.

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

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

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

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

The development of acute mitral regurgitation in infective endocarditis is usually caused not only by rupture of the chordae tendineae, but also by destruction of the valve leaflets.

Clinic. The onset is subacute. The course gradually progresses and does not differ significantly from that described above. The intensity of the systolic murmur may gradually increase.

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

Treatment is only surgical. The operation involves replacing the mitral valve.

The prognosis largely depends on active symptomatic treatment and massive antibiotic therapy.
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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 (heartbeat), which should not normally happen.

Anatomy

There are four valves in the heart:

Mitral. It separates the cavity of the left atrium and the ventricle and consists of two valves - anterior and posterior. Prolapse of the anterior valve leaflet is much more common than the posterior one. Special threads called chords are attached to each of the valves. They provide contact between the valve and muscle fibers, which are called papillary or papillary muscles. For the full functioning of this anatomical formation, the 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. In this case, the papillary muscles are activated, which close the exit of blood back into the left atrium, from where it flows out of the pulmonary circulation, enriched with oxygen, and, accordingly, the blood enters the aorta and then, through arterial vessels, is delivered to all organs and tissues.
Tricuspid (three-leaf) valve. It consists of three doors. 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 is closed, which prevents blood from flowing back to the heart.
Pulmonary valve. It is located 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 during systole it spreads through the aorta to all organs of the systemic circulation (liver, brain, limbs and others). Having transferred oxygen to the cells, the blood takes up carbon dioxide and returns to the heart, this time to the right atrium. From its cavity, fluid enters the right ventricle and, during systole, is expelled into the pulmonary artery and then into the lungs (pulmonary circulation). The cycle repeats.

Causes of mitral valve prolapse

There are two main reasons for the occurrence of this pathology. One of them is a congenital disorder of 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 hereditarily transmitted defect in the structure of connective tissue fibers, which serve as the basis of the valves. In this case, pathologists lengthen the threads (chords) connecting the valve to the muscle, and the valves themselves become softer, more pliable and more easily stretched, which explains their loose closure at the time of 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 carditis). As a rule, heart damage 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, the process involves the heart valves, which are subject to a much greater destructive effect of streptococcus.
- Coronary 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 to the papillary muscles. Chordal rupture may occur.
- Chest injuries. Strong blows to the chest area can provoke a sharp separation of the valve chords, which leads to serious complications if assistance is not provided in a timely manner.

Classification of mitral valve prolapse

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

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

Symptoms of mitral valve prolapse

As mentioned above, mitral valve prolapse in the vast majority of cases is practically asymptomatic and is diagnosed accidentally during a routine medical examination.

The most common symptoms of mitral valve prolapse include:

Cardialgia (pain in the heart area). This sign occurs in approximately 50% of MVP cases. The pain is usually localized in the left half of the chest. They can be either short-term or last for several hours. Pain can also occur at rest or during 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 relieved by taking nitroglycerin, which happens with coronary heart disease;
Feeling short of air. Patients have an irresistible desire to take a deep breath “deeply”;
A feeling of interruptions in the functioning of the heart (either a very rare heartbeat, or, on the contrary, a rapid heartbeat (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

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

To prevent the development of rheumatoid damage to the heart valves, tonsillectomy (removal of the tonsils) is indicated in the 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 prolapse manifestations (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. If such a complication develops, valve replacement is indicated.
Attacks of angina and arrhythmia. This condition is accompanied by abnormal heart rhythm, weakness, dizziness, a feeling of interruptions in the heart, crawling “goosebumps” before the eyes, and fainting. This pathology requires serious drug treatment.
Infectious endocarditis. This disease causes inflammation of the heart valve.

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 if indicated) and others. Be sure to undergo regular annual medical examinations and promptly treat colds, especially sore throats.

Key words: chorda tendineus, mitral regurgitation, echocardiography.

The patient, Hakobyan Artashes, 76 years old, was admitted to the department of liver surgery of the Erebuni Medical Center 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, I suddenly felt severe shortness of breath for the first time in my life.

Objective examination: forced position in bed - orthopnea, cyanotic skin, respiratory rate - 24 per minute. In the lungs, upon auscultation, breathing is weakened on the right side of the lower abdomen, there are isolated moist rales, on the left side there are no features. Heart rate - 80 per minute, blood pressure - 150/90 mm Hg. Art. Heart sounds are rhythmic, clear, and a rough 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, protrudes from under the edge of the costal arch by 2 cm. Stool and diuresis are normal. There is no peripheral edema.

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, LV EDP = 5.8 cm, RV = 3.2 cm. Myocardial hypertrophy of both ventricles. The aorta is compacted and not dilated in the ascending section. AK: the valves are sealed, the antiphase is not broken. MK: front valve, after its middle part floats , moves asynchronously, in comparison with its base and middle part, the rear valve is compacted, the amplitude of its opening is not reduced. There are no zones of local asynergies.

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Hyperkinesia of the interventricular septum is observed. Overall contractility is reduced due to pronounced mitral regurgitation. EF = 50-52%. Doppler: mitral regurgitation grade 3-4, tricuspid regurgitation grade 2.

To clarify the diagnosis and better visualize structural changes in the mitral valve, transesophageal echocardiography was performed (June 9, 2004): visualization was satisfactory. Determined flotation anterior leaflet of the mitral valve, there is a separation of one of the chordae tendineae. Doppler: mitral regurgitation grade 3-4, tricusidal regurgitation grade 2. The regurgitant jet in the left atrium reaches the first pulmonary vein. Pulmonary artery pressure - 50 mm Hg. Left atrium dilatation: LA = 5 cm, RV = 3.2 cm.

The patient was transferred to the emergency cardiology department and received nitrates, ACE inhibitors, Ca 2+ channel blockers, and diuretics. He categorically refused surgical treatment. During treatment with arteriolodilators, dynamic echocardiography was performed. There was a decrease in the degree of mitral regurgitation. He was discharged in satisfactory condition following therapy. Outpatient treatment and follow-up are recommended.