Features of the clinic, diagnosis and treatment of various variants of non-rheumatic mitral insufficiency. Mitral valve prolapse: symptoms, treatment of different degrees

Then it was noticed that in persons with an average systolic click and systolic murmur at the first point of auscultation during echocardiography, the leaflet (s) of the mitral valve sags into the cavity of the left atrium during systole.

Currently, primary (idiopathic) and secondary MVP are distinguished. The causes of secondary MVP are rheumatism, trauma chest, acute myocardial infarction and some other diseases. In all these cases, there is a detachment of the chords of the mitral valve, as a result of which the leaflet begins to sag into the atrial cavity. In patients with rheumatism, due to inflammatory changes affecting not only the cusps, but also the chords attached to them, the detachment of small chords of the 2nd and 3rd order was most often noted. According to modern views, in order to convincingly confirm the rheumatic etiology of MVP, it is necessary to show that the patient did not have this phenomenon before the onset of rheumatism and arose during the course of the disease. However, it is very difficult to do this in clinical practice. At the same time, in patients with mitral valve insufficiency referred for cardiac surgery, even without a clear indication of a history of rheumatism, in about half of the cases, morphological examination of the mitral valve cusps reveals inflammatory changes in both the cusps and chords.

Chest trauma is the cause of acute detachment of chords and the development of severe mitral insufficiency with a clinical picture of acute left ventricular failure. Often this is the cause of death of such patients. Acute posterior myocardial infarction involving the posterior papillary muscle also leads to avulsion of chordae and the development of posterior mitral leaflet prolapse.

The population frequency of MVP, according to different authors (from 1.8 to 38%), varies significantly depending on the diagnostic criteria used, but most authors believe that it is 1015%. At the same time, the share of secondary MVP accounts for no more than 5% of all cases. The prevalence of MVP fluctuates significantly with age after 40 years, the number of people with this phenomenon decreases sharply and in the age population over 50 years is only 13%. Therefore, MVP is a pathology of people of young working age.

In persons with MVP, according to the results of many researchers, an increased incidence of serious complications has been established: sudden death, life-threatening arrhythmias, bacterial endocarditis, stroke, severe mitral valve insufficiency. Their frequency is low up to 5%, however, given that these patients are of working, draft and childbearing age, the problem of identifying a subgroup of patients with an increased risk of complications among a huge number of people with MVP becomes extremely relevant.

Idiopathic (primary) MVP is currently the most common pathology of the valvular apparatus of the heart. According to the vast majority of authors, the basis of the pathogenesis of idiopathic MVP is genetically determined disorders of various components of the connective tissue, which leads to "weakness" of the connective tissue of the mitral valve leaflets and, therefore, their prolapse into the atrial cavity under blood pressure in systole. Since connective tissue dysplasia is considered to be the central pathogenetic link in the development of MVP, these patients should have signs of damage to the connective tissue from other systems, not just the heart. Indeed, many authors have described a complex of changes in the connective tissue of various organ systems in individuals with MVP. According to our data, these patients are significantly more likely to have an asthenic type of constitution, increased skin extensibility (more than 3 cm above the outer ends of the clavicles), funnel chest deformity, scoliosis, flat feet (longitudinal and transverse), myopia, increased joint hypermobility (3 or more joints), varicose veins veins (including varicocele in men), positive signs thumb(possibility to withdraw distal phalanx thumb behind the ulnar edge of the palm) and the wrist (the first and fifth fingers cross when grasping the wrist of the opposite hand). Since these signs are detected during a general examination, they are called phenotypic signs of connective tissue dysplasia. At the same time, at least 3 of the listed signs are simultaneously detected in persons with MVP (often 56 or even more). Therefore, in order to detect MVP, we recommend referring people with the simultaneous presence of 3 or more phenotypic traits connective tissue dysplasia.

We carried out a morphological study of skin biopsy specimens in persons with MVP using light-optical examination (histological and histochemical methods). A complex of morphological signs of skin pathology was identified: epidermal dystrophy, thinning and flattening of the papillary layer, destruction and disorganization of collagen and elastic fibers, changes in the biosynthetic activity of fibroblasts, and pathology of the vessels of the microvasculature, and some others. At the same time, no such changes were found in skin biopsies of the control group (without MVP). The revealed signs indicate the presence of dysplasia of the connective tissue of the skin in persons with MVP, and, consequently, the generalization of the process of "weakness" of the connective tissue.

Clinical picture

The clinical picture in MVP is very diverse and can be conditionally divided into 4 large syndromes of autonomic dystonia, vascular disorders, hemorrhagic and psychopathological. Autonomic dystonia syndrome (SVD) includes pain in the left side of the chest (stabbing, aching, not related to physical activity, lasting either a few seconds for stabbing pains, or hours for aching pains), hyperventilation syndrome (central symptom a feeling of lack of air, a desire to take a deep, full breath), a violation of the autonomic regulation of the activity of the heart (complaints about palpitations, a feeling of a rare heartbeat, a feeling of uneven beating, "fading" of the heart), violations of thermoregulation (a feeling of "chilling", long-term subfebrile condition after infections ), disorders of the gastrointestinal tract (irritable bowel syndrome, functional gastric dyspepsia, etc.), psychogenic dysuria (frequent or, on the contrary, rare urination in response to psycho-emotional stress), excessive sweating. Naturally, in such a situation, all possible organic causes that can cause similar symptoms should be excluded.

The syndrome of vascular disorders includes syncopal vasovagal conditions (fainting in stuffy rooms, with prolonged standing, etc.), orthostatic, as well as pre-fainting conditions under the same conditions, migraines, crawling sensation in the legs, cold to the touch distal extremities, morning and night headaches (which are based on venous stasis), dizziness, idiopathic pastosity or swelling. At present, the hypothesis of the arrhythmogenic nature of syncope in MVP has not been confirmed, and they are considered as vasovagal (i.e., a violation of the autonomic regulation of vascular tone).

Hemorrhagic syndrome combines complaints of light education bruising, frequent nosebleeds and bleeding from the gums, heavy and / or prolonged menstruation in women. The pathogenesis of these changes is complex and includes impaired collagen-induced platelet aggregation (due to collagen pathology in these patients) and/or thrombocytopathies, as well as vasculitis-type vascular pathology. In persons with MVP and hemorrhagic syndrome, thrombocytosis and an increase in platelet ADP aggregation are often found, which are regarded as reactive changes systems of hemostasis according to the type of hypercoagulability, as a compensatory reaction of this system to chronic hemorrhagic syndrome.

The syndrome of psychopathological disorders includes neurasthenia, anxiety-phobic disorders, mood disorders (most often in the form of its instability). An interesting fact is that the severity of clinical symptoms directly correlates with the number of phenotypic signs of "weakness" of the connective tissue from other organ systems and with the severity of morphological changes in the skin (see above).

ECG changes in MVP are most often detected with Holter monitoring. Significantly more often, these patients had negative T waves in leads V1,2, episodes of paroxysmal supraventricular tachycardia, sinus node dysfunction, prolongation of the QT interval, supraventricular and ventricular extrasystoles in the amount of more than 240 per day, horizontal depression of the ST segment (lasting more than 30 minutes per day ). Since ST segment depression is present in individuals with pain in the left half of the chest, other than angina pectoris, given also the young age of these patients, the absence of dyslipidemia and other risk factors for coronary artery disease, these changes are not interpreted as ischemic. They are based on uneven blood supply to the myocardium and / or sympathicotonia. Extrasystoles, especially ventricular ones, were mostly detected in the position of patients lying down. At the same time, during the exercise test, extrasystoles disappeared, which indicates their functional nature and the role of hyperparasympathicotonia in their genesis. At special study we noted the predominance of parasympathetic tone and / or a decrease in sympathetic influences in individuals with MVP and extrasystole.

When conducting a test with maximum physical activity, we established a high or very high physical performance of patients with MVP, which did not differ from that of the control group. However, these individuals showed violations of the hemodynamic provision of physical activity in the form of lower threshold values for heart rate (HR), systolic blood pressure (BP), double product and their lower increase per threshold load, which directly correlated with the severity of SVD and phenotypic severity. connective tissue dysplasia.

Usually in clinical practice, MVP is associated with the presence of arterial hypotension. According to our data, the frequency of arterial hypotension did not differ significantly in individuals with or without MVP, however, the frequency arterial hypertension(1 degree according to VVNOK) was significantly higher than in the control group. Arterial hypertension was detected by us in about 1/3 of the examined young (1840) persons with MVP, while in the control group (without MVP) only 5%.

The functioning of the autonomic nervous system in MVP is important clinical significance, because until recently it was believed that these patients are dominated by sympathetic influences therefore, b-blockers were the drugs of choice for treatment. However, at present, the point of view on this aspect has changed significantly: among these people there are individuals both with a predominance of the sympathetic tone, and with a predominance of the tone of the parasympathetic link of the autonomic nervous system. Moreover, the latter even predominate. According to our data, an increase in the tone of one or another link correlates more with clinical symptoms. So, sympathicotonia was noted in the presence of migraine, arterial hypertension, pain in the left half of the chest, paroxysmal supraventricular tachycardia, vagotonia in syncope, extrasystole.

The presence of SVD and the type of autonomic regulation in persons with MVP is directly related to the fourth syndrome of the clinical picture of psychopathological disorders. In the presence of these disorders, the incidence and severity of SVD, as well as the frequency of detection of hypersympathicotonia, increase. According to many authors, it is the psychopathological disorders in these individuals that are primary, and the symptoms of SVD are secondary, arising in response to these psychopathological features. Indirectly, the results of treatment of persons with MVP also testify in favor of this theory. So, the use of b-blockers, although it allows you to eliminate the objective signs of hypersympathicotonia (for example, heart rate significantly decreases), but all other complaints persist. On the other hand, the treatment of persons with MVP with anti-anxiety drugs led not only to the correction of psychopathological disorders, a significant improvement in the well-being of patients, but also to the disappearance of hypersympathicotonia (heart rate and blood pressure decreased, supraventricular extrasystoles and paroxysms of supraventricular tachycardia decreased or disappeared).

Diagnostics

Echocardiography is still the main method for diagnosing MVP. It is currently believed that only Vmode should be used, otherwise one can get a large number of false positive results. In our country, it is customary to divide PVP into 3 degrees depending on the depth of prolapse (1st up to 5 mm below the valve ring, 2nd 610 mm and 3rd more than 10 mm), although many domestic authors have found that PVP up to 1 cm deep is prognostically favorable. At the same time, persons with the 1st and 2nd degree of prolapse practically do not differ from each other in clinical symptoms and the frequency of complications. In other countries, it is customary to divide MVP into organic (in the presence of myxomatous degeneration) and functional (in the absence of echocardiographic criteria for myxomatous degeneration). In our opinion, such a division is more optimal, since the likelihood of complications depends on the presence of myxomatous degeneration (regardless of the depth of MVP).

Myxomatous degeneration is understood as a complex of morphological changes in the mitral valve cusps, corresponding to the "weakness" of the connective tissue (see the description of morphological changes in the skin above) and described by morphologists as a result of studying materials obtained during cardiac surgery(in persons with MVP and severe, hemodynamically significant, mitral regurgitation). In the early 90s, Japanese authors created echocardiographic criteria for myxomatous degeneration; their sensitivity and specificity is about 75%. These include leaflet thickening greater than 4 mm and its reduced echogenicity. Identification of individuals with myxomatous leaflet degeneration seems to be very important, since all complications of MVP (sudden death, severe mitral valve insufficiency requiring surgical treatment, bacterial endocarditis and strokes) in 95-100% of cases were noted only in the presence of myxomatous leaflet degeneration. According to some authors, such patients should be given antibiotic prophylaxis for bacterial endocarditis (for example, during tooth extraction). MVP with myxomatous degeneration is also considered one of the causes of stroke in young people with no generally accepted risk factors for stroke (primarily arterial hypertension). We studied the frequency of ischemic strokes and transient ischemic attacks in patients under the age of 40 years according to archival data 4 clinical hospitals Moscow for a 5-year period. The proportion of these conditions in people under 40 years of age averaged 1.4%. Of the causes of strokes in young people, hypertension should be noted in 20% of cases, however, in 2/3 of young people there were no generally accepted risk factors for the development of ischemic brain damage. Some of these patients (who agreed to participate in the study) underwent echocardiography, and in 93% of cases MVP with myxomatous degeneration of prolapsing leaflets was found. Myxomatous leaflets of the mitral valve can be the basis for the formation of micro and macrothrombi, since the loss of the endothelial layer with the appearance of small ulcerations due to increased mechanical stress is accompanied by the deposition of fibrin and platelets on them. Consequently, strokes in these patients are of thromboembolic origin, and therefore, a number of authors recommend daily intake of small doses of acetylsalicylic acid for persons with MVP and myxomatous degeneration. Another reason for the development acute disorders cerebral circulation with MVP is bacterial endocarditis and bacterial emboli.

The issues of treatment of these patients are practically not developed. In recent years, all large quantity research is devoted to the study of the effectiveness of oral magnesium preparations. This is due to the fact that magnesium ions are necessary for laying collagen fibers into a quaternary structure, therefore, magnesium deficiency in tissues causes the chaotic arrangement of collagen fibers, the main morphological sign of connective tissue dysplasia. It is also known that the biosynthesis of all matrix components in the connective tissue, as well as maintaining their structural stability, is a function of fibroblasts. From this point of view, the decrease in the RNA content in the cytoplasm of dermal fibroblasts revealed by us and other authors seems important, which indicates a decrease in the biosynthetic activity of the latter. Given the information about the role of magnesium deficiency in fibroblast dysfunction, it can be assumed that the described changes in the biosynthetic function of fibroblasts and the violation of the structure of the extracellular matrix are associated with magnesium deficiency in patients with MVP.

A number of researchers have reported tissue magnesium deficiency in individuals with MVP. We found a significant decrease in the level of magnesium in the hair in 3/4 of patients with MVP (on average, 60 or less mcg/g at a rate of 70-180 mcg/g).

We treated 43 patients with MVP aged 18 to 36 years for 6 months with Magnerot containing 500 mg of magnesium orotate (32.5 mg of elemental magnesium) at a dose of 3000 mg/day (196.8 mg of elemental magnesium), for 3 receptions.

After the use of Magnerot in patients with MVP, a significant decrease in the frequency of all SVD symptoms was revealed. Thus, the frequency of violations of autonomic regulation of the heart rhythm decreased from 74.4 to 13.9%, thermoregulation disorders from 55.8 to 18.6%, pain in the left side of the chest from 95.3 to 13.9%, disorders of the gastrointestinal tract from 69.8 to 27.9%. Before treatment mild degree SVD was diagnosed in 11.6%, moderate in 37.2%, severe in 51.2% of cases, i.e. patients with severe and moderate severity of vegetative dystonia syndrome prevailed. After treatment, a significant decrease in the severity of SVD was noted: there were faces (7%) with total absence of these disorders, the number of patients with mild SVD increased 5 times, while severe SVD was not detected in any patient.

After therapy, patients with MVP also significantly decreased the frequency and severity of vascular disorders: morning headache from 72.1 to 23.3%, syncope from 27.9 to 4.6%, presyncope from 62.8 to 13.9% , migraine from 27.9 to 7%, vascular disorders in the extremities from 88.4 to 44.2%, dizziness from 74.4 to 44.2%. If before mild treatment, moderate and severe degrees were diagnosed in 30.2, 55.9 and 13.9% of persons, respectively, then after treatment in 16.3% of cases vascular disorders were absent, the number of patients with a mild degree of vascular disorders increased by 2.5 times, while a severe degree was not detected in any of the examined patients after treatment with Magnerot.

A significant decrease in the frequency and severity of hemorrhagic disorders was also established: heavy and / or prolonged menstruation in women from 20.9 to 2.3%, nosebleeds from 30.2 to 13.9%, gum bleeding disappeared. The number of persons without hemorrhagic disorders increased from 7 to 51.2%, with an average severity hemorrhagic syndrome decreased from 27.9 to 2.3%, and a severe degree was not detected.

Finally, after treatment in patients with MVP, the frequency of neurasthenia (from 65.1 to 16.3%) and mood disorders (from 46.5 to 13.9%) significantly decreased, although the frequency of anxiety-phobic disorders did not change.

The severity of the clinical picture as a whole after treatment also significantly decreased. Therefore, it is not surprising that a highly significant improvement in the quality of life of these patients was noted. This concept means the subjective opinion of the patient about the level of his well-being in physical, psychological and social terms. Before treatment, on a self-assessment scale of general well-being, persons with MVP rated it worse than the control group (persons without MVP) by about 30%. After treatment, patients with MVP noted a significant improvement in the quality of life on this scale by an average of 40%. At the same time, the assessment of the quality of life on the scales "work", " social life" and "personal life" before treatment in persons with MVP also differed from the control: in the presence of MVP, patients rated their violations on these three scales as initial or moderate approximately equally, while healthy people noted the absence of violations. After treatment, patients with MVP showed a highly significant improvement in the quality of life by 4050% compared with the baseline.

According to Holter monitoring of the ECG after therapy with Magnerot, compared with the baseline, a significant decrease in the average heart rate (by 7.2%), the number of episodes of tachycardia (by 44.4%), the duration of the QT interval and the number of ventricular extrasystoles (by 40%) was established. Especially important is the positive effect of Magnerot in the treatment of ventricular extrasystole in this category of patients.

According to the daily monitoring of blood pressure revealed a significant decrease to normal values of the mean systolic and diastolic blood pressure, hypertensive load. These results confirm the previously established fact that there is an inverse relationship between the level of magnesium in tissues and the level of blood pressure, as well as the fact that magnesium deficiency is one of the pathogenetic links in the development of arterial hypertension.

After treatment, a decrease in the depth of mitral valve prolapse was revealed, a significant decrease in the number of patients with hypersympathicotonia, while the number of persons with an equal tone of both parts of the autonomic nervous system increased. Similar information is contained in the works of other authors devoted to the treatment of persons with MVP with oral magnesium preparations.

Finally, according to the morphological study of skin biopsy samples after therapy with Magnerot, the severity of morphological changes decreased by 2 times.

Thus, after a 6-month course of therapy with Magnerot in patients with idiopathic MVP, a significant improvement in objective and subjective symptoms was found with a complete or almost complete reduction in the manifestations of the disease in more than half of the patients. During the treatment, a decrease in the severity of the syndrome of autonomic dystonia, vascular, hemorrhagic and psychopathological disorders, cardiac arrhythmias, blood pressure levels, as well as an improvement in the quality of life of patients was noted. In addition, during treatment, the severity of morphological markers of connective tissue dysplasia significantly decreased according to skin biopsy data.

Literature:

1. Martynov A.I., Stepura O.B., Ostroumova O.D. et al. Mitral valve prolapse. Part I. Phenotypic features and clinical manifestations. // Cardiology. 1998, No. 1 P. 7280.

2. Martynov A.I., Stepura O.B., Ostroumova O.D. et al. Mitral valve prolapse. Part II. Rhythm disturbances and psychological status. // Cardiology. 1998, No. 2 P. 7481.

3. Stepura O.B., Ostroumova O.D. et al. The role of magnesium in the pathogenesis and development of clinical symptoms in patients with idiopathic mitral valve prolapse. // Russian Journal of Cardiology 1998, No. 3 S. 4547.

4. Stepura O.B., Melnik O.O., Shekhter A.B. et al. The results of the use of magnesium salt of orotic acid "Magnerot" in the treatment of patients with idiopathic mitral valve prolapse. // Russian Medical News 1999 No. 2 S.1216.

Cardiology and cardiac surgery

mk-31mm, area mitr. otv -9,4sm2

fibrosis ++, peak pressure gradient - 6.4 mm Hg

left ventricle: kdr-49mm, ksr-27mm, kdo-115mm, kso-26mm fv-77%,

right atrium-41/61 mm

The state of health is normal, sometimes it manifests itself as if there were failures in the work of the heart,

used to be more often, especially after drinking alcohol, now I don’t drink at all

for three months I have been walking and running in the morning for about 5 km, no shortness of breath

There is an intervertebral hernia of 4.2 mm

2 months ago another doctor prescribed medications:

Predctal, bisoprolol, xefocam, panangin

After taking bisoprolol 2.5 mg, the heart rate decreased to 49 at normal resting

BP dropped to 110, normal 125 discomfort like it's empty in my head

Stopped taking medication feeling fine

Please tell me if I need to do the operation and if so, how quickly

And will I be able to continue working after the operation, I am a sailor

Detachment of the chord of the mitral valve consequences

Rupture of the chords of the mitral valve is a condition that can develop as a complication of both congenital degeneration of the elements of the valvular apparatus, and most common diseases of the mitral valve, including rheumatic valvulitis, infective endocarditis, and also become a consequence of traumatic injury. One way or another, according to most authors, chord rupture rarely occurs without a provoking factor or predisposing pathology.

Quite characteristic this complication for patients with myxomatous degeneration of the mitral valve. As already mentioned, in this state, the cellular material is randomly arranged with breaks and fragmentation of collagen fibrils. Tendon chords are thinned and/or elongated.

Mechanisms of cardiac remodeling and hemodynamic shifts that develop in dowry pathology are similar to changes in patients with dysfunction and rupture of papillary muscles. Clinically, the main symptom of chord rupture is certainly progressive heart failure. In addition, various types of tachyarrhythmias are characteristic. Often the course of the disease is complicated by thromboembolism.

Studies have shown that on the atrial surface and in the zones of fixation to the myocardium of the chords of the posterior leaflet of the mitral valve, which, according to the literature, is involved in the process in more than half of the cases, platelet aggregation often occurs. The nature and prognostic significance of this phenomenon is not completely clear. It is hypothesized that the connective tissue organization of these platelet aggregations may be involved in altering the appearance of the valve.

A characteristic echocardiographic finding in patients with mitral valve chord rupture is an abnormally mobile mitral valve. In the domestic literature, the term “hammering mitral valve” or “hammering leaflet” is often used to define this phenomenon.

Pathology is best detected when performing a two-dimensional echocardiography, which shows the sagging of a part of the mitral valve leaflet in systole into the cavity of the left atrium. At the same time, an important feature that makes it possible to distinguish this standing from severe mitral valve prolapse is that the end of the "threshing leaflet" points to the left atrium. As a rule, in patients with a rupture of the chords of the mitral valve, there is also a lack of closure of the two leaflets of the mitral valve and their systolic flutter.

Finally, the third characteristic feature of this pathology is the chaotic diastolic movement of the valve leaflets, which is best seen in the short axis position. With the acute development of mitral insufficiency due to the detachment of chords, in addition, dilatation of the cavity of the left atrium develops quite quickly.

There is evidence that rupture of the chords in patients with acute rheumatic fever often disrupts the function of the anterior leaflet of the mitral valve, while the posterior leaflet is more often involved in the process in patients with "threshing leaflet".

Dopplerography reveals varying degrees of mitral regurgitation, the jet of which in patients with a pathologically mobile valve, as in mitral valve prolapse, is usually directed eccentrically, in the direction opposite to the leaflet involved in the process.

Treatment of rupture of the chords, which led to the formation of hemodynamically significant mitral valve insufficiency, should be surgical. Resolving the issue of reconstructive surgery on the valve should be taken in a timely manner.

Avulsion of the Chord of the Posterior Leaflet of the Mitral Valve

#1 LeonLime

3. Recovery period?

Thanks in advance for your reply.

#2 Nikolay_Kiselev

1. How urgent is the operation? How long can a person with such a diagnosis live with normal health (there is a slight shortness of breath during exertion)

2. How difficult and dangerous is the operation? Operation time?

3. Recovery period?

4. Are the consequences of the operation positive and negative?

Thanks in advance for your reply.

1. Age and general state human?

2. Depends on who will do it and where, in Europe such operations are put on stream. The duration of the operation is several hours

3. week - 10 days in the hospital, if everything is without complications. Then usually physiotherapy and rehabilitation from a month to 2-3, who cares

4. If everything is without complications, then only positive consequences

#3 LeonLime

Age 38, condition - if I had not gone to the hospital for a non-cardiac injury, I would have realized that there is such a problem, but High blood pressure was discovered 10 years ago, but was blocked by medication. (sitting on a tablet)

#4 Nikolai_Kiselev

Depending on each type of intervention at the moment, there are different recovery times, but in any case, given the age, the patient's condition improves dramatically

#5 LeonLime

#6 Nikolai_Kiselev

I can tell you from my own experience of accompanying these patients in Europe

#7 LeonLime

Of course, I would be interested to hear your opinion.

Rupture of chords of the mitral valve

The main cause of mitral regurgitation is rheumatic valvulitis. However, in the works of modern authors it has been shown that about half of the cases of mitral insufficiency are associated with such lesions as mitral valve prolapse, ischemia and myocardial infarction, endocarditis, congenital anomalies of the leaflets, dysfunction or rupture of the papillary muscles and tendon chords of the mitral valve.

Cases of severe mitral regurgitation as a result of rupture of chords without damage to the leaflets were rare findings for a long time and were described in single works. The reason for the rarity of this syndrome was the lack of a clear clinical picture, misdiagnosis, and the usually rapid course of the disease, often ending in death, before the diagnosis was made.

The widespread introduction of cardiopulmonary bypass into clinical practice and the possibility of performing open-heart operations have led to the appearance in the literature of an increasing number of reports on the development of mitral insufficiency as a result of rupture of the chords. In the works of modern authors, the pathogenesis, clinical signs, diagnosis and treatment of this condition are described in more detail. Chordal rupture has been shown to be a more common pathology than previously thought. So, according to different authors, chord rupture is found in 16-17% of patients operated on for mitral insufficiency.

The mitral valve apparatus has a complex structure, its function depends on the coordinated interaction of all its components. In the literature, many works are devoted to the anatomy and function of the mitral valve.

There are six main anatomical and functional components of the mitral apparatus:

wall of the left atrium
fibrous ring,
sash,
chords,
papillary muscles
wall of the left ventricle.

The force of contraction and relaxation of the posterior wall of the left atrium affects the "competence" of the mitral valve.

The mitral annulus is a solid circular connective tissue ligament that forms the basis for thin fibroelastic valve leaflets, acts as a sphincter during systole, reducing the size of the mitral orifice to 19-39%.

The "competence" of the valve depends on the density of the closure of the leaflets, which are often two: the anterior, also called the anteromedial or aortic, has a common fibrous skeleton with the left coronary and half of the non-coronary leaflet of the aortic valve. This valve is semicircular, triangular in shape, often has notches along the free edge. On its atrial surface, at a distance of 0.8-1 cm from the free edge, a ridge is clearly visible, which determines the line of valve closure.

Distal to the crest is the so-called rough zone, which, at the moment of closing the valve, comes into contact with a similar zone of the posterior leaflet. The posterior leaflet, also called the lesser, ventricular, mural, or posterolateral, has a larger base at the annulus fibrosus. On its free edge there are notches that form "bowls". At the annulus fibrosus, the lateral edges of both valves are fastened by the anterior and posterior lateral commissures. The area of the valves is 2 1/2 times the size of the opening they are supposed to cover. Normally, the mitral opening passes two fingers, the distance between the commissures is 2.5-4 cm, and the anteroposterior opening size is on average 1.5 cm. The inner, free edge of the valves is movable, they should open only towards the cavity of the left ventricle.

Tendon chords are attached to the ventricular surface of the valves, which keep the valves from prolapse into the atrial cavity during ventricular systole. The number of chords, their branching, the place of attachment to the valves, papillary muscles and the wall of the left ventricle, their length, thickness are very diverse.

There are three groups of chords of the mitral valve: chords extending from the anterolateral papillary muscle in a single trunk, then radially diverging and attaching to both valves in the region of the anterolateral commissure; chords extending from the posteromedial papillary muscle and attached to the valves in the region of the posterolateral commissure; the so-called basal chords, which depart from the wall of the left ventricle or the tops of small trabeculae and join the ventricular surface only at the base of the posterior leaflet.

In functional terms, there are true cords that are attached to the sashes, and false chords connecting various sections muscular wall of the left ventricle. In total, there are from 25 to 120 chords of the mitral valve. There are a number of classifications of chords in the literature. Ranganathan's classification of chords is useful, as it allows one to define functional value tendon filaments: Type I - chords that penetrate into the "rough" zone of the valves, of which two chords of the anterior leaflet are thick and are called supporting, the zone of their introduction is called critical; Type II - basal chords attached to the base of the posterior valve; III type- chords attached to the crevices of the rear leaf.

The two main papillary muscles, from the tops of which the chords extend, and the wall of the left ventricle are two muscular components of the mitral valve, and their functions are interrelated. With various lesions of the papillary muscles, the connection between them and the wall of the left ventricle may be interrupted (with rupture of the papillary muscles) or weakened (with ischemia or fibrosis of the papillary muscles). Blood circulation in the papillary muscles is carried out by the coronary arteries. The anterolateral papillary muscle is supplied with blood by branches of the circumflex and anterior descending branches of the left coronary artery. The blood supply to the posterior median papillary muscle is poorer and more variable: from the terminal branches of the right coronary artery or the circumflex branch of the left coronary artery, depending on which blood supply dominates the back of the heart. According to some authors, it is the worse blood supply to the posterior median papillary muscle that explains the more frequent ruptures of the chords of the posterior mitral leaflet.

The mechanism for closing the mitral valve is carried out in the following way: at the beginning of the systole of the left ventricle, the subvalvular pressure increases rapidly, the papillary muscles tighten and exert appropriate pressure on the chords. The anterior cusp unfolds around the aortic root backward, the posterior cusp forward. This rotation of the valves occurs until the apical and commissural margins of both valves are closed. From this point on, the valve is closed, but unstable. As blood fills and arterial pressure rises in the left ventricle, the pressure on the contacting surfaces of the valves increases. The thin mobile triangle of the anterior sash protrudes upwards and shifts backwards towards the concave surface of the base of the posterior sash.

The mobile base of the rear sash resists the pressure of the front sash, resulting in their complete closing. Thus, the mechanism of mitral valve closure consists in gradually advancing contact of the surfaces of the leaflets from the tops towards the base of the leaflets. Such a “rolling” valve closing mechanism is an important factor to protect the leaflets from damage as a result of high intraventricular pressure.

Violation of the function of any of the above structures of the valve leads to a violation of its closing function and to mitral regurgitation. This review considers the literature data relating only to mitral regurgitation as a result of ruptured chords and measures to eliminate it.

The reasons for the rupture of the chords or the separation of their tops of the papillary muscles can be very diverse, and in some cases the cause cannot be established. Rupture of the chords is facilitated by rheumatic heart disease, bacterial endocarditis, Marfan's syndrome, in which not only the structure of the valves is disturbed, but also the chords shorten, thicken or fuse and become more prone to rupture. Rupture of the chords can be the result of trauma, including surgical, as well as closed injuries, in which the rupture of the chords may not be clinically manifested at first, but with age there is a "spontaneous" rupture of the chords.

Among other etiological factors, the authors point to myxomatous degeneration of the chordopapillary apparatus and the associated valve prolapse syndrome. With this syndrome, a characteristic histological picture is found: the valve leaflets are thinned, their edges are twisted and sag into the cavity of the left ventricle, the mitral opening is expanded.

In 46% of cases with such a pathology, there is a rupture of chords or papillary muscles. Microscopically, tissue hyalinization, an increase in the content of the main substance and a violation of the architectonics of the collagen substance are detected. The cause of myxomatous degeneration is unclear. This may be a congenital disease such as an erased form of Marfan's syndrome or an acquired degenerative process, for example, under the influence of a blood stream directed at the valve. So, in diseases of the aortic valve, the regurgitant jet is directed to the mitral valve, which can cause secondary lesions of the latter.

In connection with a more detailed study of the pathogenesis of chord rupture syndrome, the number of so-called spontaneous cases is decreasing all the time. In the works of recent years, a closer relationship of this syndrome with hypertension and coronary heart disease has been shown. If the ischemic zone of the myocardium extends to the zone of the base of the papillary muscle, then as a result of a violation of its blood supply, deterioration of function and untimely contraction, a detachment of the chord from the top of the papillary muscle may occur. Other authors believe that the rupture of the chord cannot be due to ischemic lesion the notochord itself, since it consists of collagen, fibrocytes and elastin and is covered with a single-layer epithelium. blood vessels not in chords. Obviously, the rupture of the chords or their separation from the papillary muscles is due to fibrosis of the latter, which is often observed in coronary heart disease. One of the common causes of chord rupture is myocardial infarction and subsequent dysfunction of the papillary muscles. The enlarged cavity of the left ventricle and post-infarction aneurysms lead to displacement of the papillary muscles, violation of the geometric relationships of the valve components and rupture of the chords.

According to Caufield, in all cases of "spontaneous" rupture of the chords, microscopic examination reveals focal destruction of the elastic substance, the disappearance of fibrocytes and a disorderly arrangement of collagen fibers. The author believes that such a change in the connective tissue elements is caused by enzymatic processes, and the source advanced level elastase can be infectious diseases(pneumonia, abscess, etc.). The process of destruction and liquefaction of collagen does not necessarily end with a rupture of the chord, since the process of replacing the affected area of the chord with fibroblasts of the connective tissue occurs quite quickly. However, such a chord is largely weakened and at risk of rupture.

The main clinical signs of rupture of the chord are the sudden development of symptoms of overload and insufficiency of the left ventricle, shortness of breath. During the physical examination of the patient, a loud apical pansystolic murmur is determined, resembling a systolic ejection murmur. With the most frequently observed rupture of the chords of the posterior leaflet, a regurgitant jet of great force is directed to the septal wall of the left atrium adjacent to the aortic bulb, which causes irradiation of noise to the upper right corner of the sternum and simulation of aortic defect. If the anterior leaflet becomes "incompetent", the regurgitant blood stream will be directed posteriorly and laterally, to the free wall of the left atrium, which creates noise irradiation to the left axillary region and the chest wall behind.

Chordal rupture is characterized by the absence of cardiomegaly and an enlarged left atrium on x-ray, sinus rhythm, and an unusually high V wave on the curve of left atrial pressure and pulmonary capillary pressure. In contrast to rheumatic disease, with chord rupture, there is a significantly lower volume of end-diastolic pressure in the left ventricle. In 60% of patients, the mitral ring is dilated.

Diagnosis of the syndrome is quite difficult. In all patients with apical holosystolic murmur and acutely developing pulmonary edema mitral valve chord rupture should be suspected. ECG has no characteristic features. With the help of echocardiography, chord rupture can be diagnosed in 60% of cases. When the chords of the anterior valve are ruptured, the range of its movement is noted with an amplitude of up to 38 mm. with simultaneous chaotic flutter of the leaflet echo during diastole and multiple echoes during systole. When the chords of the posterior leaflet are ruptured, a paradoxical range of its mobility is observed during systole and diastole. There is also an echo of the left atrium during systole and an additional echo between the two leaflets of the mitral valve. During cardiac catheterization in the left ventricle, normal systolic pressure with increased end-diastolic pressure is determined. Significantly increased pressure in the left atrium. If a chord rupture is suspected, it is necessary to perform coronary angiography, since if a patient has coronary disease, its elimination may be a necessary factor in the treatment of chord rupture.

The severity of mitral regurgitation depends on the number and location of ruptured chords. One chord breaks rarely, more often - a whole group of chords. Most often (up to 80% of cases) there is a rupture of the chords of the posterior valve. In 9% of cases, there is a rupture of the chords of both valves. The spectrum of clinical conditions ranges from mild regurgitation resulting from a rupture of a single chord to catastrophic irreversible regurgitation caused by a rupture of multiple chords.

In the first case, the disease can progress slowly over 1 year or more, in the second case, death occurs very quickly, within 1 week. 17.6 months. In most cases, regurgitation caused by rupture of the chords is malignant, leading to myxomatous degeneration and prolapse of the valve leaflets, and expansion of the mitral annulus.

Chordal rupture is characterized by rapid clinical deterioration despite drug treatment. Therefore, surgical treatment is indicated for all patients with this pathology. If symptoms persist for less than 2 years, the left atrium is enlarged, the V wave on the left atrial pressure curve reaches 40 mm. rt. Art., then such patients need urgent surgical treatment.

There is no consensus regarding the tactics of surgical treatment for ruptured chords. The total number of operations performed for this pathology barely exceeds 200. Depending on the severity of the lesion, the duration of the symptoms, the presence concomitant diseases make prosthetics or valve-preserving reconstructive interventions. Most authors currently prefer to replace the valve with an artificial prosthesis, since prosthetics are an "easier" solution for the surgeon. However, when replacing the mitral valve due to a ruptured chord, paravalvular fistulas quite often (in 10% of cases) occur, since the sutures on the unaffected tender tissue of the annulus are held with difficulty.

The fact that when the chords are ruptured, the mitral valve cusps do not have significant fibrous thickening and other signs that accompany rheumatic damage, such as adhesion of the chords, calcification of the valves, and the expansion of the fibrous ring is insignificant, makes understandable the desire of surgeons to preserve the patient's own valve. In 20-25% of patients with rupture of the chords of the mitral valve, it is necessary to perform clalan-preserving interventions.

Reconstructive surgery should be aimed at restoring the “competence” of the valve, achieved by good closure of its leaflets. One of the most effective and commonly used recovery operations is the plicgia of the valves. The method of operation, proposed in I960 by McGoon, is that the "floating" or "dangling" segment of the valve is immersed in the direction of the left ventricle, and the tissue of this segment approaches the intact chords. Gerbode proposed a modification of this operation, which consists in the fact that the plication sutures are extended to the base of the leaflet and fixed here on the annulus and the wall of the left atrium with mattress sutures. According to A. Zeltser et al., the operation of plicating the posterior leaflet by this method in terms of trauma and prognosis gives better results than valve replacement.

Good results are obtained by combining leaflet plication with annuloplasty. Thus, Hessel reported in a review article that 54 patients who underwent such a combined intervention for chordal rupture in 9 surgical centers had no serious complications for more than 5 years of follow-up. Good results were achieved in 92% of cases.

In some cases, only a reduction in the size of the mitral orifice by annuloplasty can achieve convergence of the edges of the leaflets and restore valve function.

The literature describes cases of direct stitching of a ruptured chord, stitching it to the papillary muscle. In the works of a number of authors, the replacement of chords with clear or dacron threads, as well as ribbons or twists of marceline, teflon, dacron, was described. According to some authors, such reconstructive surgeries are effective, according to others, they are often accompanied by eruption of sutures, thrombosis, and gradual weakening of the artificial material. During the operation, it is difficult to determine the required length of the chord prosthesis, in addition, after the elimination of regurgitation, the size of the left ventricle decreases and the chord prosthesis becomes longer than necessary, which leads to prolapse of the valves into the left atrium.

It should be noted that, despite the good results of reconstructive operations performed by a number of surgeons for ruptured mitral valve chords, the majority still prefer valve replacement. The results of operations are better, the shorter the duration of the disease, the left atrium and the greater the V wave on the pressure curve in the left atrium.

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 and 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, every 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. Attached to each of the wings special threads called chords. They provide valve contact with muscle fibers, which are called papillary or papillary muscles. For full-fledged work 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. 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 outflow tracts of blood are not completely closed, and, therefore, part of the blood during systole 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 not pronounced, 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 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 disease that can cause changes normal anatomy 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 musculoskeletal system, heart valves are involved in the process, which are exposed 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 valve chords, which leads to serious complications in case of untimely assistance.

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.

To the most common symptoms 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 may 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. physical fitness. Patients, in the absence of severe regurgitation, are shown moderate physical activity and active image life 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 (calming) plants: valerian, motherwort, hawthorn, ledum, 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(angina).

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

Mitral valve insufficiency. This state is frequent complication 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, for the prevention of 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. Mandatory to pass regular annual medical examinations timely treat colds, especially sore throats.

Acute mitral insufficiency (AMN) is a sudden onset of valve regurgitation leading to left ventricular heart failure with pulmonary edema and pulmonary hypertension.
Causes of acute mitral regurgitation in children and adolescents

In children and adolescents, the causes of OMN are usually blunt chest trauma, rheumatism, and infective endocarditis, and, less commonly, myxomatous degeneration and cardiac tumors. The causes of OMN are listed below, depending on the anatomical structures of the valvular apparatus.

Mitral annulus injury:
infective endocarditis (abscess formation);
trauma (valve surgery);
paravalvular failure due to suture separation (surgical technical problem, infective endocarditis).

Mitral valve injury:
- infective endocarditis (perforation of the leaflet or due to blockage of the leaflet by vegetation);
- Trauma (leaflet rupture during percutaneous mitral balloon valvotomy, penetrating chest trauma);
- tumors (atrial myxoma);
- myxomatous degeneration;
- systemic lupus erythematosus (Libman-Sachs endocarditis).

Tendon chord rupture:
- idiopathic (spontaneous);
- myxomatous degeneration (mitral valve prolapse, Marfan syndrome, Ehlers-Danlos syndrome);
- infective endocarditis;
- acute rheumatic fever;
- trauma (percutaneous balloon valvuloplasty, closed chest trauma)

Papillary muscle damage:
- diseases of the coronary arteries, leading to dysfunction and less often to the separation of the papillary muscle;
- acute global dysfunction of the left ventricle;
- infiltrative diseases (amyloidosis, sarcoidosis);
- trauma.

Children have the most common cause acute mitral insufficiency is a threshing or dangling leaflet (flail mitral leaflet).

Unlike prolapse of the MV, the tip of the torn part is displaced into the atrium more than the valve body (Fig. 6.1). The dangling leaf syndrome occurs as a result of a rupture of part of the leaflet, chords or papillary muscles, which is far from always possible to differentiate. This rupture usually occurs with closed blunt chest trauma (especially in children with myxomatous MVP), less often as a complication of infective endocarditis.

Hemodynamics
OMN, which usually occurs secondary to a detachment of the mitral valve chords, leads to a sudden overload of the left ventricle and left atrium. Overloading the volume of the left ventricle is accompanied by a significant increase in its work. An increase in the filling pressure of the left ventricle, combined with a shunt of blood from the left ventricle into the left atrium during systole, leads to an increase in pressure in the left atrium. In turn, an increase in pressure in the left atrium leads to a sharp increase in pressure in the lungs, which results in acute edema lungs and respiratory failure.

Clinical picture
In the event of acute mitral regurgitation, the clinical picture is mainly determined by the symptoms of pulmonary edema and acute left ventricular failure.

The size of the heart, as a rule, remains normal.

auscultatory signs
Acute mitral insufficiency is characterized by the appearance of the following sound symptoms.

A systolic tremor or a coarse systolic murmur is heard. It can be heard even from the back, near the vertebrae, closer to the neck. Noise can be carried out in the axillary region, on the back or along the left edge of the sternum.

There is a murmur of systolic regurgitation in the xiphoid process (that is, in the projection of the tricuspid valve) due to the rapid development of pulmonary hypertension and acute right ventricular overload.

The maximum systolic murmur is heard not in the region of the apex of the heart, but along the left edge of the sternum and at the base of the heart (this is observed with dysfunction of the subvalvular structures of the anterior leaflet of the mitral valve, which leads to the medial direction of the flow of regurgitant blood).

The systolic murmur ends before the aortic component of the II tone (due to the limitation of left atrial distensibility and the drop in the pressure gradient between the left ventricle and the left atrium at the end of systole).

There is no III tone, despite severe heart failure.

A pathological IV tone appears, which is better heard in the region of the apex of the heart in the position of the child on the left side (usually IV tone is heard with mitral regurgitation, secondary to dysfunction of the papillary muscles, and also with OMN caused by rupture of tendon chords).

An accent of the II tone quickly arises and its splitting over the pulmonary artery.

Symptoms of acute pulmonary edema:
- shortness of breath, more often inspiratory, less often mixed;
- cough with sputum;
- orthopnea;
- profuse cold sweat;
- cyanosis of the mucous membranes of the skin;
- a lot of wheezing in the lungs;
- tachycardia, gallop rhythm, accent II tone over the pulmonary artery.

Clinically conventionally isolated 4 stages of acute pulmonary edema:
I - dyspnoetic: characterized by dyspnea, an increase in dry wheezing, which is associated with the onset of edema of the lung (mainly interstitial) tissue; there are few wet rales;

II - orthopnea: moist rales appear, the number of which prevails over dry ones;

III - advanced clinical symptoms: wheezing is heard at a distance, pronounced orthopnea;

IV - extremely severe: a lot of different-sized wheezing, foaming, profuse cold sweat, progression of diffuse cyanosis. This stage is called the boiling samovar syndrome.

There are interstitial and alveolar pulmonary edema.
With interstitial pulmonary edema, which corresponds to the clinical picture of cardiac asthma, fluid infiltration occurs throughout the lung tissue, including perivascular and peribronchial spaces. This sharply worsens the conditions for the exchange of oxygen and carbon dioxide between the air of the alveoli and the blood, and contributes to an increase in pulmonary, vascular and bronchial resistance.

Further flow of fluid from the interstitium into the cavity of the alveoli leads to alveolar pulmonary edema with the destruction of the surfactant, the collapse of the alveoli, and their flooding with transudate containing not only blood proteins, cholesterol, but also formed elements. This stage is characterized by the formation of an extremely persistent protein foam that blocks the lumen of the bronchioles and bronchi, which in turn leads to fatal hypoxemia and hypoxia (like asphyxia during drowning). An attack of cardiac asthma usually develops at night, the patient wakes up from a feeling of lack of air, takes a forced sitting position, tends to go to the window, excited, fear of death appears, answers questions with difficulty, sometimes with a nod of the head, is not distracted by anything, completely surrendering to the struggle for air. The duration of an attack of cardiac asthma is from several minutes to several hours.

On auscultation of the lungs, early signs interstitial edema, you can listen to weakened breathing in the lower sections, dry rales, indicating swelling of the bronchial mucosa.

Acute alveolar pulmonary edema is a more severe form of left ventricular failure. Bubbling breathing is characteristic with the release of flakes of white or pink foam (due to the admixture of erythrocytes). Its quantity can reach several liters. In this case, oxygenation of the blood is especially sharply disturbed and asphyxia may occur. The transition from interstitial pulmonary edema to alveolar edema sometimes occurs very quickly, within a few minutes. The detailed clinical picture of alveolar pulmonary edema is so bright that it does not cause diagnostic difficulties. As a rule, against the background of the above-described clinical picture of interstitial pulmonary edema in the lower, and then in the middle sections and over the entire surface of the lungs, a significant amount of different-sized wet rales appears. In some cases, along with wet rales, dry rales are heard, and then differential diagnosis with an attack of bronchial asthma is necessary. Like cardiac asthma, alveolar pulmonary edema is more common at night. Sometimes it is short-term and goes away on its own, in some cases it lasts for several hours. With strong foaming, death from asphyxia can occur very quickly, in the next few minutes after the onset of clinical manifestations.

The radiological picture in alveolar pulmonary edema in typical cases is due to symmetrical impregnation of the transudate of both lungs.

Instrumental Research
Electrocardiography
On the electrocardiogram in the event of acute mitral insufficiency, signs of overload of the right parts of the heart quickly develop. Tall, pointed, normal-length P waves are usually recorded in leads II and III. Tachycardia, a change in the end part of the QT complex in the form of a decrease in the ST segment are noted.

Radiography
In cases of hypervolemia of the pulmonary circulation from additional methods research for the diagnosis of interstitial pulmonary edema is of greatest importance radiological. At the same time, a number of characteristic features are noted:
- Kerley septal lines A and B, reflecting the swelling of the interlobular septa;
strengthening of the lung pattern due to edematous infiltration of perivascular and peribronchial interstitial tissues, especially pronounced in the root zones due to the presence lymphatic spaces and the abundance of tissue in these areas;
- subpleural edema in the form of a seal along the interlobar fissure.

In acute alveolar edema, the radiograph reveals a typical picture of pulmonary edema with predominant localization of edema in the basal and basal regions.

echocardiography
Typical echocardiographic manifestations of acute mitral regurgitation are:
- sudden appearance of a wide jet of regurgitation penetrating deep into the left atrium;

Throssing leaf at rupture of the chord or papillary muscle;

Excessive movement of the mitral valve leaflets;

Lack of dilatation of the left atrium or its slight expansion;

Systolic hyperkinesia of the walls of the myocardium of the left ventricle.

Treatment
Therapeutic measures are primarily aimed at the main mechanism of edema development with a decrease in venous return to the heart, a decrease in afterload, an increase in the propulsive function of the left ventricle and a decrease in increased hydrostatic pressure in the vessels of the pulmonary circulation. With alveolar pulmonary edema, additional measures are taken to destroy the foam, as well as to more vigorously correct secondary disorders.

In the treatment of pulmonary edema, the following tasks are solved.
A. Reduce hypertension in the pulmonary circulation by:
- decrease in venous return to the heart;
- decrease in the volume of circulating blood (BCC);
- dehydration of the lungs;
- normalization of blood pressure;
- anesthesia.

B. Increase the contractility of the left ventricular myocardium with:
- inotropic agents;
- antiarrhythmic drugs(if necessary).

B. Normalize acid-base balance blood gases.

D. Conduct support activities.

The main therapeutic measures for acute pulmonary edema
- Assign oxygen inhalation through nasal cannulas or a mask at a concentration sufficient to maintain arterial blood pO2 more than 60 mm Hg. (possible through alcohol vapor).

A special place in the treatment of pulmonary edema is occupied by the use of the narcotic analgesic morphine hydrochloride (children over 2 years old - 0.001-0.005 g per dose). Morphine relieves psycho-emotional arousal, reduces shortness of breath, has a vasodilating effect, reduces pressure in the pulmonary artery. It should not be administered with low blood pressure and respiratory distress. When signs of oppression appear respiratory center opiate antagonists are administered - naloxone (0.3-0.7 mg intravenously).

In order to reduce congestion in the lungs and provide a powerful venodilating effect that occurs after 5-8 minutes, furosemide is administered infusion at a dose of 0.1-1.0 mg (kg × h) under the control of diuresis.

In case of refractory pulmonary edema, when the administration of saluretics is ineffective, they are combined with an osmotic diuretic (mannitol - 10-20% solution at a dose of 0.5-1.5 g/kg of body weight intravenously 1 time per day).

At high blood pressure, sodium nitroprusside is prescribed, which reduces pre- and afterload. The initial dose is 0.5-10.0 mcg / min. The dose is selected individually until the normalization of blood pressure.

Eufillin (with concomitant bronchospasm) is administered intravenously slowly at a dose of 160-820 mg, and then 50-60 mg every hour.

Dobutamine is administered at a dose rate of 2-20 µg (kg×min), maximum - 40 µg (kg×min) intravenously.

Amrinon is administered by infusion, the starting dose is 50 μg/kg of body weight over 15 minutes; a maintenance dose at a rate of 0.1-1 μg (kg × min) continues to be administered until a persistent increase in blood pressure.

In severe hypoxemia, hypercapnia, artificial lung ventilation (ALV) is effective.

Breathing should be under constant positive pressure (spontaneous breathing with constant positive pressure - SD PPD).

Contraindications to the use of SD PPD are:
- disturbances in the regulation of breathing - bradypnea or Cheyne-Stokes breathing with long periods of apnea (over 15-20 s), when mechanical ventilation is indicated;
- a stormy picture of alveolar pulmonary edema with abundant foamy secretions in the oropharynx and nasopharynx, requiring the removal of foam and intratracheal administration of active defoamers;
- severe violations of the contractile function of the right ventricle.

Forecast
Acute pulmonary edema and cardiogenic shock are often a complication of acute mitral regurgitation. Mortality during surgical interventions in acute mitral insufficiency reaches 80%.

When the condition stabilizes, acute mitral insufficiency passes into the chronic stage - chronic mitral insufficiency (CMI) occurs.

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. Behind medical care did not apply. 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”. The work is connected with everyday hard physical labor(weight lifting).

Objective examination data: general condition of the patient of moderate severity. Consciousness is clear. Integuments of normal coloring, normal humidity. Edema lower extremities No. The lymph nodes 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

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

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 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 exposed 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

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.

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

. 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, for the prevention of 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. peripheral edema No.

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.

For more accurate diagnosis and better visualization structural changes 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 nonrheumatic mitral insufficiency. 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, changes in the skeleton (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 tendinous 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 non-specific and include various types cardialgia, often persistent, not stopped by nitroglycerin, interruptions and heartbeats that periodically occur, mostly 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 the filling of the left ventricle, which aggravates the discrepancy between the size of its cavity and the mitral valve apparatus. For these purposes, auscultation and phonocardiography are carried out 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 occur very rarely. 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 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 special treatment not 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 causes.

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 armpit.

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 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. Substantial assistance in difficult cases provides echocardiography, proving 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 diagnostics rheumatic fever 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) develop 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. easy current characterized by complaints of predominantly asthenic type (weakness, fatigue, headache, indefinite pain in the region of the heart), spontaneous fluctuations in blood pressure, non-specific ECG changes (depression of the 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 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. ABOUT severe course it should be said 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 valvular structures, it is important to understand that the sutures placed on edematous, inflamed tissues are likely to cut through, 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 significant a large number 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. Classic experimental studies 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 exact time) 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 destroyed infectious process of the aortic valve, 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.

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

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 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 exposed 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

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.

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

First of all, for the prevention of 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.