home→Suspensions→ Myxomatous degeneration of the mitral valve leaflets. Myxomatous degeneration of the mitral valve: what is it, symptoms of manifestation, how to treat

Myxomatous degeneration of the mitral valve leaflets. Myxomatous degeneration of the mitral valve: what is it, symptoms of manifestation, how to treat

For citation: Ostroumova O.D., Stepura O.B., Melnik O.O. Mitral valve prolapse - normal or pathological? // RMJ. 2002. No. 28. S. 1314

MGMSU them. ON THE. Semashko

P The term mitral valve prolapse (MVP) is understood sagging of one or both leaflets of the mitral valve into the cavity of the left atrium during systole . This phenomenon was described relatively recently - only in the second half of the 60s, when the echocardiography method appeared. 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. Causes secondary PMK 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 valves, 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 injury 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 , affecting the posterior papillary muscle, also leads to the separation of the chords and the development of prolapse of the posterior leaflet of the mitral valve.

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 10-15%. 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 1-3%. That's why 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 development serious complications: 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, military 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. connective tissue, which leads to "weakness" of the connective tissue of the mitral valve cusps 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 connective tissue damage 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, in these patients, compared with persons without MVP, the 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 hypermobility of the joints (3 or more joints), varicose veins (including varicocele in men), positive signs of the thumb (the ability to move the distal phalanx of the thumb beyond the ulnar edge of the palm) and wrists (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 (more often 5-6 and even more). Therefore, in order to detect MVP, we recommend that individuals be referred for echocardiography with the simultaneous presence of 3 or more phenotypic signs of 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 has been 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 big syndromes - vegetative dystonia, vascular disorders, hemorrhagic and psychopathological. Syndrome of vegetative dystonia (SVD) includes pain in the left half of the chest (stabbing, aching, not associated with physical activity, lasting either a few seconds for stabbing pains, or hours for aching pains), hyperventilation syndrome (the central symptom is a feeling of lack of air, a desire to take a deep , a full breath), violation of the autonomic regulation of the activity of the heart (complaints of palpitations, a feeling of a rare heartbeat, a feeling of uneven beating, "fading" of the heart), violations of thermoregulation (a feeling of "chilling", long-lasting subfebrile condition after infections), disorders of the gastrointestinal intestinal tract (irritable bowel syndrome, functional gastric dyspepsia, etc.), psychogenic dysuria (frequent or, conversely, 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.

Syndrome of vascular disorders includes syncopal conditions - vasovagal (fainting in stuffy rooms, with prolonged standing, etc.), orthostatic, as well as pre-fainting states in the same conditions, migraines, crawling in the legs, cold to the touch distal extremities, morning and night headaches (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 easy 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 detected, which are regarded as reactive changes in the hemostasis system by the type of hypercoagulation, as a compensatory response of this system to chronic hemorrhagic syndrome.

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, dysfunction sinus node, 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. In a 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 revealed 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 the phenotypic severity of 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 WHO-GFQ) was significantly higher than in the control group. Arterial hypertension was detected by us in approximately 1/3 of the examined young (18-40) persons with MVP, while in the control group (without MVP) it was only in 5%.

The functioning of the autonomic nervous system with MVP has an important clinical significance, since until recently it was believed that these patients were 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 - 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 is significantly reduced), 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

The main method for diagnosing MVP is still echocardiography . Currently, it is considered that only B-mode should be used, otherwise a large number of false positive results can be obtained. In our country, it is customary to divide PMK into 3 degrees, depending on the depth of prolapse (1st - up to 5 mm below the valve ring, 2nd - 6-10 mm and 3rd - more than 10 mm), although many domestic authors have established that that PMK depth up to 1 cm 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).

Under myxomatous degeneration understand the complex of morphological changes in the leaflets of the mitral valve, corresponding to the "weakness" of the connective tissue (see above the description of morphological changes in the skin) 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 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 from 4 clinical hospitals in Moscow over 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, it should be noted hypertension- 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. Myxomatically altered 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 of acute disorders cerebral circulation with MVP is bacterial endocarditis and bacterial emboli.

Treatment

The issues of treatment of these patients are practically not developed. In recent years, an increasing number of studies have been 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 content of RNA 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 doses.

After the use of Magnerot in patients with MVP, a significant decrease in the frequency of all symptoms of SVD was revealed. . Thus, the frequency of violations of the autonomic regulation of the heart rhythm decreased from 74.4 to 13.9%, violations of thermoregulation - from 55.8 to 18.6%, pain in the left half of the chest - from 95.3 to 13.9%, disorders gastrointestinal tract - from 69.8 to 27.9%. Before mild treatment the degree of 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 persons (7%) with a complete absence of these disorders, the number of patients with mild SVD increased by 5 times, while severe SVD was not found in any patient.

After therapy in patients with MVP, also the frequency and severity of vascular disorders significantly decreased: 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 with 88.4 to 44.2%, dizziness from 74.4 to 44.2%. If before treatment mild, moderate and severe were diagnosed in 30.2, 55.9 and 13.9% of persons, respectively, then after treatment in 16.3% of cases there were no vascular disorders, the number of patients with mild the degree of vascular disorders, while a severe degree was not detected in any of the examined after treatment with Magnerot.

Installed and a significant decrease in the frequency and severity of hemorrhagic disorders: heavy and / or prolonged menstruation in women from 20.9 to 2.3%, nosebleeds - from 30.2 to 13.9%, bleeding gums 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 significantly decreased the frequency of neurasthenia (from 65.1 to 16.3%) and mood disorders (from 46.5 to 13.9%), although the frequency of phobic anxiety disorders did not change.

The severity of the clinical picture as a whole after treatment also significantly decreased. Therefore, it is not surprising that it was noted highly significant improvement in the quality of life of these patients . 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 - 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 patients with MVP also differed from the control: in the presence of MVP, patients regarded their impairments 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 40-50% compared with the baseline.

According to ECG Holter monitoring after therapy with Magnerot, compared with the baseline, a significant decrease in the average heart rate (by 7.2%), the number of tachycardia episodes (by 44.4%), the duration of the QT interval and the number of ventricular extrasystoles (by 40%) was established. Particularly important is positive effect of Magnerot in the treatment of ventricular extrasystoles 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 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, there was a decrease in the severity of autonomic dystonia syndrome, vascular, hemorrhagic and psychopathological disorders, heart rhythm disturbances, blood pressure levels, as well as an improvement in the quality of life of patients. 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 - S.72-80.

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 - S.74-81.

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 - P. 45-47.

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 - P.12-16.

Depending on the cause, primary mitral valve prolapse (idiopathic, hereditary, congenital) is isolated, which is an independent pathology not associated with any disease and caused by genetic or congenital incompetence of the connective tissue. Mitral valve prolapse in differentiated STD (Marfan syndrome, Ehlers-Danlos syndrome (types I-III), osteogenesis imperfecta (types I and III), elastic pseudoxanthoma, increased skin extensibility (cutis laha)) is currently classified as a primary mitral valve prolapse .

Secondary mitral valve prolapse develops due to any disease and accounts for 5% of all cases of valve prolapse.

Causes of secondary mitral valve prolapse

Rheumatic diseases.
Cardiomyopathy.
Myocarditis
Coronary artery disease.
Primary pulmonary hypertension.
Aneurysm of the left ventricle.
Heart injury.
Hematological diseases (Willebrand disease, thrombocytopathy, sickle cell anemia).
Mix a of the left atrium.
Myasthenia.
thyrotoxicosis syndrome.
Sports heart.
Primary gynomastia.
Hereditary diseases (Klinefelter syndrome, Shereshevsky-Turner, Noonan).

According to the presence of structural changes in the leaflets of the mitral valve, there are:

classic mitral valve prolapse (cusp displacement >2 mm, leaflet thickness >5 mm);
non-classical PMK (leaf displacement > 2 mm, leaf thickness

According to the localization of mitral valve prolapse:

PMC front sash;
PMK rear sash;
PMK of both valves (total PMK).

According to the degree of prolapse:

prolapse of the I degree: leaf deflection by 3-5 mm;
prolapse II degree: leaf deflection by 6-9 mm;
prolapse III degree: leaf deflection more than 9 mm.

According to the degree of myxomatous degeneration of the valvular apparatus:

myxomatous degeneration of the 0th degree - there are no signs of myxomatous lesions of the mitral valve;
myxomatous degeneration I degree - minimal. Thickening of the mitral leaflets (3-5 mm), arcuate deformation of the mitral opening within 1-2 segments, no violation of the closure of the valves;
myxomatous degeneration II degree - moderate. Thickening of the mitral cusps (5-8 mm), elongation of the cusps, deformation of the contour of the mitral orifice over several segments. stretching of the chords (including single ruptures), moderate stretching of the mitral ring, violation of the closure of the valves;
myxomatous degeneration III degree - pronounced. Mitral leaflet thickening (>8 mm) and elongation, maximum depth of leaflet prolapse, multiple chordae ruptures, significant expansion of the mitral annulus, no leaflet closure (including significant systolic separation). Multivalvular prolapse and dilatation of the aortic root are possible.

According to the hemodynamic characteristics:

without mitral regurgitation;
with mitral regurgitation.

Causes of primary mitral valve prolapse

The occurrence of primary mitral valve prolapse is due to myxomatous degeneration of the mitral cusps, as well as other connective tissue structures of the mitral complex (annulus fibrosus, chords) - a genetically determined defect in collagen synthesis, leading to a violation of the architectonics of fibrillar collagen and elastic structures of the connective tissue with the accumulation of acid mucopolysaccharides ( hyaluronic acid and hopdroitin sulfate) without an inflammatory component. A specific gene and chromosomal defect that determines the development of MVP has not yet been found, however, three loci associated with MVP have been identified on chromosomes 16p, 11p, and 13q. Two types of inheritance of myxomatous degeneration of the valvular apparatus of the heart have been described: autosomal dominant (with MVP) and, more rarely, X-linked (Xq28). In the second case, myxomatous valvular heart disease develops (A-linked myxomatous valvular degeneration, sex-linked valvular dysplasia). In MVP, an increased expression of the Bw35 antigen of the HLA system was noted, which contributes to a decrease in interstitial magnesium and impaired collagen metabolism.

The pathogenesis of mitral valve prolapse

In the development of mitral valve prolapse, the leading role is played by structural changes in the cusps, annulus fibrosus, chords associated with myxomatous degeneration, followed by a violation of their size and relative position. With myxomatous degeneration, the loose spongy layer of the mitral cusp thickens due to the accumulation of acid mucopolysaccharides with thinning and fragmentation of the fibrous layer, reducing its mechanical strength. Elastic replacement fibrous tissue valve leaflet on a weak and inelastic spongy structure leads to bulging of the leaflet under blood pressure into the cavity of the left atrium during left ventricular systole. In a third of cases, myxomatous degeneration extends to the fibrous ring, leading to its expansion, and chords, followed by their lengthening and thinning. The main role in the occurrence of mitral regurgitation with mitral valve prolapse is given to the constant traumatic effect of the turbulent flow of regurgitation on the altered leaflets and dilatation of the mitral annulus. Expansion of the mitral annulus fibrosus more than 30 mm in diameter is characteristic of myxomatous degeneration and is a risk factor for mitral regurgitation occurring in 68-85% of persons with MVP. The rate of progression of mitral regurgitation is determined by the severity of the initial structural and functional disorders of the components of the mitral valve apparatus. In the case of slight prolapse of unchanged or slightly changed mitral valve leaflets, a significant increase in the degree of mitral regurgitation may not be observed for a long time, while in the presence of sufficiently pronounced changes in the leaflets, including tendon chords and papillary muscles, the development of mitral regurgitation is progressive. The risk of developing hemodynamically significant mitral regurgitation within 10 years among persons with MVP with a practically unchanged structure is only 0-1%, while an increase in the area and thickening of the mitral valve leaflet > 5 mm increases the risk of mitral regurgitation to 10-15%. Myxomatous degeneration of chords can lead to their ruptures with the formation of "floating" acute mitral regurgitation.

The degree of prolapse of the mitral leaflet also depends on some hemodynamic parameters: heart rate and left ventricular EDV. With an increase in heart rate and a decrease in EDV, the mitral valve leaflets converge, the diameter of the valve ring and the tension of the chords decrease, leading to an increase in the prolapse of the leaflets. An increase in the EDV of the left ventricle reduces the severity of mitral valve prolapse.

It's important to know!

Mitral valve prolapse - flexion of the mitral valve leaflets into the left atrium during systole. The most common cause is idiopathic myxomatous degeneration. Mitral valve prolapse is usually benign, but complications include mitral regurgitation, endocarditis, valve rupture, and possible thromboembolism.

In recent years, the number of patients suffering from pathologies of the cardiovascular system has increased. Mitral valve myxomatosis is a progressive condition that has a significant impact on the functioning of the valve leaflets in people of all ages.

In addition, such a pathology is accompanied by a violation of the structure of the connective tissue and this is expressed in mitral valve prolapse. To date, experts have not been able to identify the causes of the development of this in the human body, but it is believed that the development of such a problem is due to a hereditary fact.

Mitral valve myxomatosis is a common heart disease, which is diagnosed in people of different age categories. IN modern medicine several names for this pathology are used, and most often specialists use terms such as valve prolapse and degeneration.

Prolapse is a bulging or bending of the cusps of the heart valve in the direction of the proximal chamber of the organ. In the event that we are talking about mitral valve prolapse, then such a pathology is accompanied by bulging of the leaflets towards the left atrium.

P rolapse is one of the most common pathologies that can be detected in patients of absolutely any age.

Myxomatosis of the mitral valve can develop for various reasons, and experts distinguish between primary and secondary prolapse:

Primary valve prolapse refers to a pathology, the development of which is in no way associated with any known pathology or malformations.
secondary prolapse progresses against the background of many and pathological changes

Experts say that the development of both primary and secondary prolapse can occur during adolescence.

More information about mitral valve prolapse can be found in the video.

During puberty, the development of such a pathology can occur against the background of:

rheumatic endocarditis
myocarditis
Marfan syndrome

The development of secondary mitral valve prolapse usually occurs as a result of the progression of inflammatory or coronary diseases in the patient's body, resulting in dysfunction of the valves and papillary muscles. In the event that systemic lesions of the connective tissue are observed, then valve prolapse becomes one of the characteristic symptoms of such a disorder.

Degrees of the disease

Experts identify several stages in the development of this, and it is on them that the prognosis and possible therapy depend:

When diagnosing a first-degree disease in a patient, the valve leaflets thicken up to 3-5 mm. As a result of such changes, there is no violation of their closure, therefore, a person does not have a pronounced one. Usually, doctors do not worry about such a pathological state of appetite and they recommend that he undergo preventive examinations at least several times a year, as well as lead a healthy lifestyle.
The second degree of pathology is characterized by stretched and more thickened valves, the size of which is 5-8 mm. This pathological condition is supplemented by a change in the contour of the mitral orifice and even the appearance of single ruptures of the chords. In addition, with the second degree of myxomatosis of the mitral valve, there is a violation of the closure of the valves.
In the third degree of pathology, the mitral cusps become very thick, and their thickness reaches 8 mm. In addition, there is a deformation of the mitral ring, which ends with stretching and rupture of the chords. characteristic symptom this degree of the disease is the complete absence of closure of the valves.

Medical practice shows that the first stage of the disease is not considered dangerous, since it does not cause abnormalities and malfunctions in the functioning of the heart. At stages 2 and 3, a return of a certain volume is observed, since the process of closing the valves is disrupted.Such a pathological condition requires mandatory attention, since the risk of developing various diseases increases.

Valve leaflet degeneration can progress with age, which can lead to the development of various abnormalities.

Most often, the patient develops complications in the form of:

stroke
mitral valve insufficiency
lethal outcome

With such a pathology, the prognosis can be disappointing, so timely illness plays an important role. When detecting myxomatosis of the mitral valve, it is important to prescribe an effective one as soon as possible, which will avoid the development of many complications.

Symptoms

The initial stage of myxomatosis of the mitral valve is usually accompanied by the absence of characteristic symptoms and this is explained by the fact that there is no violation of the circulatory process, and there is also no regurgitation at all.

In the event that the pathology passes to the next stage of its development, then this causes the following symptoms:

the patient's performance is noticeably reduced, and any minimal load causes rapid fatigue and weakness
often there is shortness of breath with any kind of exertion and is accompanied by a constant feeling of lack of air
periodically appear pain in the region of the heart in the form of tingling, but they are of a short duration
there are frequent dizziness that cause arrhythmia and the result of this is perhaps a pre-syncope state
an additional sign of the disease is the appearance of a cough, which is initially dry, but is gradually accompanied by sputum discharge and, in some cases, with blood streaks

During the conduction, the specialist will notice a violation of the functioning of the cardiovascular system while listening to the heart. The doctor draws attention to the noise that occurs as a result of the backflow of blood to the ventricle. With such pathological condition of the body, the patient needs a more thorough examination, the appointment of the necessary and the study of the anamnesis.

Treatments

In the event that the patient has the first stage of mitral valve prolapse, it is usually not performed. In this case, a periodic visit to a cardiologist is prescribed in order to control the progression of the pathology and its intensity.

The appearance of complaints of heart palpitations and pain in the chest area requires certain treatment which is carried out with the use of beta-blockers. In the event that it is complicated by rhythm disturbances of a stable nature, then specialists can prescribe thinning drugs.

Their main task is to prevent the formation of blood clots and most effective means this group are:

warfarin
Aspirin

With severe mitral valve insufficiency, treatment can be carried out using surgical treatment in the form of catheterization. In the event that there are indications for surgical intervention or a suspicion of rupture of the subvalvular chords, the patient is placed in a hospital.

The most common type of surgery for mitral valve prolapse is its plastic surgery, during which the risk of death is low and the prognosis is favorable.

Patients with such a pathology need the obligatory observation of a cardiologist and a therapist. In addition, it is important to observe a certain mode of work and rest, and engage in exercise possible only after expert evaluation.

Kazan State

University of Technology

abstract

"Mitral valve myxomatosis"

Completed:

student gr.41-91-42

Khismiev Rishat

Checked:

Senior Lecturer

Khusnutdinova R. G.

Kazan 2009

myxomatosis mitral valve

1. Preface

2. Etiology and pathogenesis

3. Classification

4. Clinical picture

5. Treatment

6. Prevention

7. Forecast

References

1. Preface

Mitral valve prolapse - bending of one or both leaflets of the mitral valve into the cavity of the left atrium during left ventricular systole. This is one of the most common forms of violation of the valvular apparatus of the heart. Mitral valve prolapse may be accompanied by prolapse of other valves or be combined with other minor anomalies of the heart.

2. Etiology and pathogenesis

By origin, primary (idiopathic) and secondary mitral valve prolapse are isolated. Primary mitral valve prolapse is associated with connective tissue dysplasia, which is also manifested by other microanomalies in the structure of the valve apparatus (changes in the structure of the valve and papillary muscles, impaired distribution, improper attachment, shortening or lengthening of the chords, the appearance of additional chords, etc.). Connective tissue dysplasia is formed under the influence of various pathological factors affecting the fetus during its intrauterine development (preeclampsia, acute respiratory viral infections and occupational hazards in the mother, unfavorable environmental conditions, etc.). In 10-20% of cases, mitral valve prolapse is maternally inherited. At the same time, relatives with signs of connective tissue dysplasia and/or psychosomatic diseases are detected in 1/3 of proband families. Connective tissue dysplasia may also present with myxomatous transformation of the valve leaflets associated with a hereditary disorder of the collagen structure, especially type III. At the same time, due to the excessive accumulation of acid mucopolysaccharides, the cusp tissue (sometimes also the valve ring and chords) proliferates, which causes the effect of prolapse.

Secondary mitral valve prolapse accompanies or complicates various diseases. In secondary mitral valve prolapse, as in primary, the initial inferiority of the connective tissue is of great importance. So, he often accompanies some hereditary syndromes(Marfan syndrome, Ehlers-Danlo-Chernogubov syndrome, congenital contracture arachnodactyly, osteogenesis imperfecta, pseudoxanthoma elastic), as well as congenital heart defects, rheumatism and other rheumatic diseases, non-rheumatic carditis, cardiomyopathy, some forms of arrhythmia, autonomic dystonia syndrome, endocrine pathology ( hyperthyroidism), etc. Mitral valve prolapse may be the result of acquired myxomatosis, inflammatory damage to valvular structures, impaired contractility of the myocardium and papillary muscles, valve-ventricular disproportion, asynchronous activity of various parts of the heart, which is often observed in congenital and acquired diseases of the latter. Dysfunction of the autonomic nervous system undoubtedly takes part in the formation of the clinical picture of mitral valve prolapse. In addition, metabolic disorders and micronutrient deficiencies, in particular magnesium ions, are important.

Structural and functional inferiority of the valvular apparatus of the heart leads to the fact that during the period of left ventricular systole there is a deflection of the mitral valve leaflets into the cavity of the left atrium. With prolapse of the free part of the valves, accompanied by their incomplete closure in systole, isolated mesosystolic clicks associated with excessive tension of the chords are auscultated. Loose contact of the valve leaflets or their divergence in systole determines the appearance of systolic murmur of varying intensity, indicating the development of mitral regurgitation. Changes in the subvalvular apparatus (elongation of the chords, a decrease in the contractile ability of the papillary muscles) also create conditions for the onset or intensification of mitral regurgitation.

3. Classification

There is no generally accepted classification of mitral valve prolapse. In addition to distinguishing between mitral valve prolapse by origin (primary or secondary), it is customary to distinguish between auscultatory and “silent” forms, indicate the location of prolapse (anterior, posterior, both leaflets), its severity (I degree - from 3 to 6 mm, II degree - from 6 to 9 mm, III degree - more than 9 mm), the time of occurrence in relation to systole (early, late, holosystolic), the presence and severity of mitral regurgitation. The state of the autonomic nervous system is also assessed, the type of flow of mitral valve prolapse is determined, and possible complications and outcomes.

4. Clinical picture

Mitral valve prolapse is characterized by a variety of symptoms, depending primarily on the severity of connective tissue dysplasia and autonomic changes.

Complaints in children with mitral valve prolapse are very diverse: increased fatigue, headaches, dizziness, fainting, shortness of breath, pain in the heart, palpitations, a feeling of interruptions in the work of the heart. Characterized by reduced physical performance, psycho-emotional lability, increased excitability, irritability, anxiety, depressive and hypochondriacal reactions.

In most cases, with mitral valve prolapse, various manifestations of connective tissue dysplasia are found: asthenic physique, tall stature, reduced body weight, increased skin elasticity, poor muscle development, joint hypermobility, posture disorder, scoliosis, chest deformity, pterygoid scapulae, flat feet, myopia . You can find hypertelorism of the eyes and nipples, the peculiar structure of the auricles, the gothic palate, the sandal-shaped gap and other minor developmental anomalies. Visceral manifestations of connective tissue dysplasia include nephroptosis, anomalies in the structure gallbladder and etc.

Often, with mitral valve prolapse, a change in heart rate and blood pressure is observed, mainly due to hypersympathicotonia. The borders of the heart are usually not expanded. Auscultatory data are the most informative: isolated clicks or their combination with late systolic murmur are more often heard, less often - isolated late systolic or holosystolic murmur. Clicks are recorded in the middle or end of systole, usually at the apex or at the fifth point of auscultation of the heart. They are not conducted outside the region of the heart and do not exceed the second tone in volume, can be transient or permanent, appear or increase in intensity in vertical position and during physical activity. Isolated late systolic murmur (rough, "scratching") is heard at the apex of the heart (better in the position on the left side); it is carried out in the axillary region and is enhanced in an upright position. Holosystolic murmur, reflecting the presence of mitral regurgitation, occupies the entire systole, is stable. In some patients, a "squeak" of chords is heard, associated with the vibration of valvular structures. In some cases (with a "silent" variant of mitral valve prolapse), auscultatory symptoms are absent. The symptoms of secondary mitral valve prolapse are similar to those of the primary one and are combined with manifestations characteristic of a concomitant disease (Marfan's syndrome, congenital heart defects, rheumatic heart disease, etc.). Mitral valve prolapse must be differentiated primarily from congenital or acquired mitral valve insufficiency, systolic murmurs caused by other variants of minor anomalies in the development of the heart, or valvular dysfunction. Echocardiography is the most informative, contributing to the correct assessment of the detected cardiac changes.

5. Treatment

Treatment for mitral valve prolapse depends on its form, severity clinical symptoms, including the nature of cardiovascular and vegetative changes, as well as the characteristics of the underlying disease.

With the "silent" form, treatment is limited to general measures aimed at normalizing the vegetative and psycho-emotional status of children, without reducing physical activity.

In the auscultatory variant, children who satisfactorily tolerate physical activity and not having noticeable ECG abnormalities, can do physical education in a group. The only exception is exercise associated with sudden movements, running, jumping. In some cases, exemption from participation in competitions is necessary.

When mitral regurgitation, pronounced violations of repolarization processes on the ECG, distinct arrhythmias are detected, a significant limitation of physical activity with an individual selection of the exercise therapy complex is necessary.

In the treatment of children with mitral valve prolapse, the correction of autonomic disorders, both non-drug and drug, is of great importance. In case of violations of ventricular repolarization (according to ECG), agents are used that improve myocardial metabolism [potassium orotate, inosine (for example, riboxin), vitamins B5, B15, levocarnitine, etc.]. Effective drugs that correct magnesium metabolism, in particular orotic acid, magnesium salt (magnerot). In some cases (with persistent tachycardia, frequent ventricular extrasystoles, the presence of an extended Q-T interval, persistent violations of repolarization processes), the appointment of R-blockers (propranolol), if necessary, antiarrhythmic drugs of other classes, is justified. With pronounced changes in the valvular apparatus, prophylactic courses of antibiotic therapy are indicated (especially in connection with surgical intervention) in order to prevent the development of infective endocarditis. Necessarily conservative or surgical treatment of foci of chronic infection.

With mitral insufficiency, accompanied by severe, treatment-resistant cardiac decompensation, as well as with the addition of infective endocarditis and other serious complications (pronounced arrhythmias), surgical correction of mitral valve prolapse (restorative surgery or mitral valve replacement) is possible.

6. Prevention

Prevention is aimed mainly at preventing the progression of existing valvular disease and the occurrence of complications. For this purpose, an individual selection of physical activity and the necessary medical and recreational activities, adequate treatment of other existing pathologies (with secondary mitral valve prolapse) are carried out. Children with mitral valve prolapse are subject to dispensary observation with regular examinations (ECG, echocardiography, etc.).

7. Forecast

The prognosis for mitral valve prolapse in children depends on its origin, the severity of morphological changes in the mitral valve, the degree of regurgitation, the presence or absence of complications. IN childhood mitral valve prolapse usually proceeds favorably. Complications of mitral valve prolapse in children are rare. Perhaps the development of acute (due to detachment of chords, with pulmonary venous hypertension) or chronic mitral insufficiency, infective endocarditis, severe forms of arrhythmias, thromboembolism, syndrome sudden death, most often having arrhythmogenic character. The development of complications, the progression of valvular disorders and mitral regurgitation adversely affect the prognosis. Mitral valve prolapse that occurs in a child can lead to difficult-to-correct disorders at a more mature age. In this regard, timely diagnosis, accurate implementation of the necessary medical and preventive measures just in childhood.

References

1. Children's diseases. Baranov A.A. // 2002.

Features of the development of myxomatosis of the mitral valve and methods of its treatment

In recent years, the number of patients suffering from pathologies of the cardiovascular system has increased. Mitral valve myxomatosis is a progressive condition that has a significant impact on the functioning of the valve leaflets in people of all ages.

In addition, such a pathology is accompanied by a violation of the structure of the connective tissue and this is expressed in mitral valve prolapse. To date, experts have not been able to identify the causes of the development of such a disease in the human body, but it is believed that the development of such a problem is due to a hereditary fact.

Diseases of the cardiovascular system

Mitral valve myxomatosis refers to a common heart disease that is diagnosed in people of different age groups. In modern medicine, several names for such a pathology are used, and most often specialists use terms such as valve prolapse and degeneration.

P rolapse is one of the most common pathologies that can be detected in patients of absolutely any age.

Myxomatosis of the mitral valve can develop for various reasons, and experts distinguish between primary and secondary prolapse:

Primary valve prolapse refers to a pathology, the development of which is in no way associated with any known pathology or malformations.
secondary prolapse progresses against the background of many diseases and pathological changes

Experts say that the development of both primary and secondary prolapse can occur during adolescence.

More information about mitral valve prolapse can be found in the video.

Degrees of the disease

Characteristics of the degrees of myxomatosis of the mitral valve

Experts identify several stages in the development of such a disease, and it is on them that the prognosis and possible therapy depend:

When diagnosing a first-degree disease in a patient, the valve leaflets thicken up to 3-5 mm. As a result of such changes, there is no violation of their closure, so the person does not have pronounced symptoms. Usually, doctors do not worry about such a pathological state of appetite and they recommend that he undergo preventive examinations at least several times a year, as well as lead a healthy lifestyle.
The second degree of pathology is characterized by stretched and more thickened valves, the size of which is 5-8 mm. This pathological condition is supplemented by a change in the contour of the mitral orifice and even the appearance of single ruptures of the chords. In addition, with the second degree of myxomatosis of the mitral valve, there is a violation of the closure of the valves.
In the third degree of pathology, the mitral cusps become very thick, and their thickness reaches 8 mm. In addition, there is a deformation of the mitral ring, which ends with stretching and rupture of the chords. A characteristic symptom of this degree of the disease is the complete absence of closure of the valves.

Medical practice shows that the first stage of the disease is not considered dangerous, since it does not cause abnormalities and malfunctions in the functioning of the heart. At stages 2 and 3, there is a return of a certain volume of blood back, since the process of closing the valves is disrupted. Such a pathological condition requires mandatory attention, since the risk of developing various complications increases.

Valve leaflet degeneration can progress with age, which can lead to the development of various abnormalities.

Most often, the patient develops complications in the form of:

stroke
mitral valve insufficiency
lethal outcome

With such a pathology, the prognosis can be disappointing, so timely diagnosis of the disease plays an important role. If myxomatosis of the mitral valve is detected, it is important to prescribe as early as possible effective treatment which will avoid the development of many complications.

Symptoms

In the event that the pathology passes to the next stage of its development, then this causes the following symptoms:

the patient's performance is noticeably reduced, and any minimal load causes rapid fatigue and weakness
often there is shortness of breath with any kind of exertion and is accompanied by a constant feeling of lack of air
periodically there are pain sensations in the region of the heart in the form of tingling, but they are of a short duration
there are frequent dizziness that cause arrhythmia and the result of this is perhaps a pre-syncope state
an additional sign of the disease is the appearance of a cough, which is initially dry, but is gradually accompanied by sputum discharge and, in some cases, with blood streaks

During the examination, the specialist will notice a violation of the functioning of the cardiovascular system while listening to the heart. The doctor draws attention to the noise that occurs as a result of the backflow of blood to the ventricle. With such a pathological condition of the body, the patient needs a more thorough examination, the appointment of the necessary studies and the study of the anamnesis.

Symptoms

Myxomatous degeneration of the mitral valve is a gradually progressive condition that affects the anatomy and function of the valve leaflets in middle-aged and senile people.

The exact causes of the disease have not been determined, but it is known that a similar problem is associated with heredity.

As a rule, at an early or middle stage of the disease, heart murmurs are determined, which do not show symptoms for several years or a lifetime.

In the later stages of the disease, complications are possible, manifested in arrhythmias, heart failure, and sudden death in severe cases.

Myxomatous degeneration of the mitral valve is a common cardiac pathology. This disease has many names (degeneration, endocardiosis or valve prolapse). Such a disease is associated with the mitral valve, which separates the left atrium and left ventricle. All names are descriptions of age-related degeneration of the structural parts of the heart valves, which is manifested by stretching and thickening of the valve leaflets.

In this case, the closure of the valves is disturbed and regurgitation (reverse blood flow) appears through one or a pair of valves with audible heart murmurs. Subsequently, degenerative changes and an increase in reverse blood flow intensify, the sections of the heart expand. Other complications may appear (cardiac arrhythmia, insufficiency and other dangerous conditions).

Symptoms

Signs of MD

The period of incubation of the virus in the body of a rabbit is from 5 to 14 days, depending on the specific strain of the disease. At the beginning of the development of the disease, signs can be noticed only upon careful examination. Red spots appear on the body of the rabbit.

Gradually, additional symptoms begin to appear.

There are a number of characteristic manifestations of infection with myxomatosis:

Eye damage. The mucosa turns red and begins to secrete milky mucus. My eyes are starting to swell.
Inhibited, slow movements.
Body temperature 42 degrees.
Deterioration of the structure of the coat. To the touch, the coat becomes stiff, begins to fall out in tufts.

With myxomatosis, the rabbit's eyes swell, small bumps appear on the body.

There are two types of myxomatosis: edematous and nodular.

Specific symptoms of myxomatosis depend on its form:

Edema. It develops very quickly and most often causes the death of a rabbit. This form of myxomatosis is practically incurable. Symptoms of the disease are swelling of the eyes, nasal cavity of the rabbit. They exude pus. Gradually, tumors cover the entire body of the animal. Often develop diseases of the genital organs of rabbits. Ears droop. The rabbit refuses food. Death occurs after 10 days.
Nodular. A lethal outcome in this form of the disease is rare, since the virus is amenable to therapy. Symptoms of nodular myxomatosis are small bumps (nodules) that form throughout the body. Most of the bumps are formed on the rabbit's head. They are mainly localized around the ears and eyes. In the second stage of the disease, conjunctivitis develops. The eyes are swollen with pus, breathing becomes difficult, a flow from the nose appears.

Rabbit owners often do not pay attention to the first signs of pet infection. The animal can spend 2 weeks in this state. When the disease becomes severe, the rabbit is completely immobilized. It is impossible to get the animal out of this state.

In the photo, the rabbit shows vivid symptoms of myxomatosis.

Myxomatosis can cause the development of comorbidities in the animal that worsen its condition. Most often, pneumonia develops, which definitely becomes the cause of death of the rabbit.

The source of infection with myxomatosis are sick animals. The virus persists in secretions from the eyes and nose, as well as in the subcutaneous tissue and parenchymal organs. In nature, carriers of the virus are wild hares (find out the differences between a hare and a rabbit).

Rabbit breeders have noticed that the most destructive spread of the disease manifests itself during the mass departure of mosquitoes. On the glands of all blood-sucking insects, the virus can survive for several months.

The myxomatosis virus is transmitted through secretions from the eyes and nose.

The virus does not die even when the dead animal is buried in the ground. Under such conditions, myxoma lives for 2 years! The virus enters the rabbit's body in all possible ways: through Airways, blood, genitals during mating, in utero.

Myxomatosis in rabbits

Causes and ways of infection
Symptoms and forms of the disease
Features of treatment
Prevention of myxomatosis

Myxomatosis in rabbits is a rather complex serious disease. It is characterized by the fact that the animal has a certain number of bumps. The causative agent is a virus, which is why if one animal falls ill, then literally the next day all the rest will fall ill.

Myxomatosis virus in rabbits spreads very quickly to all individuals in the rabbitry.

This disease affects both wild and domestic rabbits equally. And you should be extremely careful owners who breed animals for meat. After all, if the treatment is not carried out in time, then the meat can become completely unfit for consumption.

On the initial stage any signs will be absent, because, as in this case, the circulation is not disturbed, regurgitation is completely absent. But, with the transition of the disease to a more serious stage, a person will feel the following symptoms:

decreased performance, general weakness, fatigue even with minimal exertion;
shortness of breath that appears with minimal physical or emotional stress, a feeling of lack of air;
pain in the heart, which most often manifests itself in the form of tingling. Occur periodically, have a short duration;
dizziness, accompanied by arrhythmia, often leading a person to a pre-fainting state;
cough, it should be considered as an additional symptom that may not appear. At first it is dry, then it is accompanied by sputum, which may contain streaks of blood.

When visiting a doctor, signs of a malfunction of the cardiac system will first of all be noticed when listening to the heart. The doctor will hear the noises that accompany the backflow of blood to the ventricle. This can already be the reason for a more detailed examination, including the collection of anamnesis, laboratory tests, electrocardiography, echocardiography.

If electrocardiography shows only the presence of a violation, its stage, then ultrasound of the heart will be able to provide more complete information, because it will allow you to determine the size of the valves, the features of their deformation, in other words, everything pathological changes taking place in this case.

One of the anomalies of cardiac development is mitral valve prolapse (MVP). It is characterized by the fact that its valves are pressed into the left atrial cavity at the moment when the left ventricle contracts (systole). This pathology has another name - Barlow's syndrome, named after the doctor who was the first to determine the cause of the late systolic apical murmur that accompanies MVP.

The significance of this heart defect is still not well understood. But most medical luminaries believe that it does not pose a particular threat to human life. Usually this pathology does not have pronounced clinical manifestations. It does not require drug therapy. The need for treatment arises when, as a result of MVP, a violation of cardiac activity (for example, arrhythmia) develops, which is accompanied by certain clinical manifestations.

To understand this, it is necessary to imagine how the heart works. Oxygen-enriched blood from the lung enters the left atrial cavity, which serves as a kind of storage (reservoir) for it. From there it enters the left ventricle. Its purpose is to push out with force all the incoming blood into the aortic mouth, for distribution to the organs located in the zone of the main blood circulation (large circle).

The blood flow again rushes to the heart, but already in the right atrium, and then into the cavity of the right ventricle. In this case, oxygen is used up, and the blood is saturated with carbon dioxide. The pancreas (right ventricle) throws it into the pulmonary circulation (pulmonary artery), where it is enriched with oxygen again.

During normal cardiac activity, at the time of the onset of atrial systole, the atria are completely freed from blood, and the mitral valve closes the entrance to the atria, there is no backflow of blood. Prolapse does not allow sagging, stretched valves to close completely. Therefore, not all blood enters the aortic ostium during cardiac output. Part of it returns back to the cavity of the left atrium.

The process of retrograde blood flow is called regurgitation. Prolapse, accompanied by a deflection of less than 3 mm, develops without regurgitation.

PMK classification

Diagnosis and treatment methods

Myxomatosis of the mitral valve is determined by the results of several studies:

assessment of patient complaints;
history data;
objective examination;
additional examination methods.

During the examination, the characteristic auscultatory signs of pathology are:

systolic click;
midsystolic murmur;
holosystolic murmur.

A distinctive feature of the auscultatory picture in myxomatous degeneration is its variability (the ability to change from visit to visit).

From an additional examination, the doctor appoints:

Holter monitoring;
Ultrasound of the heart (transthoracic, transesophageal) is the only method that allows you to visualize pathological changes;
tests with dosed physical activity;
radiography of the lungs;
MSCT;
electrophysiological study.

Such extensive diagnostics is needed to determine further tactics for managing the patient and monitoring ongoing therapy.

Diagnosis of myxomatous degeneration of the mitral valve

Pathology is determined while listening to the heart. The doctor hears systolic murmurs in the mitral valve.

For the final diagnosis, the physiological state of a person is examined and an echocardiogram is prescribed ( ultrasound diagnostics hearts). An echocardiogram allows you to determine the maneuvering of the valves, their structure and the functioning of the heart muscle. For examination, one-dimensional and two-dimensional modes are used. This research method allows you to determine the following pathological factors:

the anterior, posterior, or both flaps thicken by more than five millimeters in relation to the mitral annulus;
enlarged left atrium and ventricle;
contraction of the left ventricle is accompanied by sagging of the valve leaflets to the atrium;
the mitral ring expands;
tendinous filaments are lengthened.

An electrocardiogram is mandatory. ECG registers all kinds of failures of cardiac rhythm.

Additional diagnostic methods include chest x-ray.

The presence of pathology is indicated by systolic murmurs in the heart, which the doctor can hear during auscultation (listening). To confirm the diagnosis, prescribe:

electrocardiogram;
echocardiography (ultrasound of the heart);
chest x-ray.

On the initial stage when myxomatous degeneration of the mitral valve leaflets does not interfere with the work of the heart and does not affect general state organism, active treatment, and even more so, surgical intervention, is not required. However, the patient must be registered with a cardiologist, and regularly undergo examinations.

To date, there are no effective drugs that could completely stop and eliminate this pathological disease. Therefore, with the progression of the pathology, those medications are prescribed that help eliminate the symptoms and significantly slow down the dangerous process. These drugs include those that remove excess accumulated fluid from the body, are aimed at maintaining the working capacity of the heart muscle and improving blood circulation, and regulating the heart rate.

In the case when the pathology has led to mitral insufficiency and blood regurgitation, surgery may be indicated (you can watch the video on the Internet resource), in which it is possible:

preservation of the valve with plastic leaflets or their replacement;
prosthetics (the affected mitral valve is removed, and a biological or artificial prosthesis is put in its place).

Mitral valve prolapse is usually asymptomatic, although some patients experience chest pain, dyspnea, and manifestations of sympathicotonia (eg, palpitations, dizziness, presyncope, migraines, restlessness). Symptoms include a clear mid-systole click followed by a systolic murmur in the presence of regurgitation.

Mitral valve prolapse is a common condition. The prevalence is 1-5% among healthy people. Women and men are equally affected. Mitral valve prolapse usually follows a juvenile growth spurt.

A presumptive diagnosis is made clinically and confirmed by two-dimensional echocardiography. Holosystolic displacement 3 mm or late systolic displacement

Myxomatous degeneration of the mitral valve leaflets. Myxomatous degeneration of the mitral valve: what is it, symptoms of manifestation, how to treat

Causes of secondary mitral valve prolapse

Causes of primary mitral valve prolapse

The pathogenesis of mitral valve prolapse

It's important to know!

Degrees of the disease

Symptoms

Treatments

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