Spine

The main causes of the mix of the valve. Myxomatous Degeneration of Mitral Valve Mixomatosis Heart

28.06.2020

Kazan State

University of Technology

abstract

"Mitral valve mixture"

Performed:

student G.41-91-42

Hismi'ev Rishat

Checked:

senior Lecturer

Husnutdinova R. G.

Kazan 2009

mitroxatosis Mitral valve

1. Preface

2. Etiology and pathogenesis

3. Classification

4. Clinical picture

5. Treatment

6. Prevention

7. Forecast

References

1. Preface

The prolapse of the mitral valve is the bending of one or both of the mitral valve flaps into the left atrium cavity during the left ventricular systole. This is one of the most frequent forms of violation of the valve apparatus of the heart. The prolapse of the mitral valve may be accompanied by the proportion of other valves or combine with other small heart development anomalies.

2. Etiology and pathogenesis

By origin, the primary (idiopathic) and secondary prolapse of the mitral valve is isolated. The primary prolapse of the mitral valve is associated with the connective tissue dysplasia, which is also manifested by other microanomalines for the structure of the valve apparatus (changing the structure of the valve and nipple muscles, disrupting the distribution, improper attachment, shortening or elongation of chord, the appearance of additional chord, etc.). The dysplasia of the connective tissue is formed under the influence of various pathological factors acting on the fetus during its intrauterine development (gestosis, ORVI and professional harmfulness of the mother, unfavorable ecological situation, etc.). In 10-20% of cases of the mitral valve prolapse, it is inherited by the maternal line. At the same time, in 1/3 families of the samples, relatives reveal with signs of connective tissue dysplasia and / or psychosomatic diseases. The connective tissue dysplasia can also appear by the mixture transformation of the valve sesters associated with the hereditary due to the disorder of the collagen structure, especially type III. At the same time, due to the excess accumulation of acidular mucopolysaccharides, the flap fabric is proliferated (sometimes the valve ring and chord), which causes the splashing effect.

Secondary prolapse of the mitral valve accompanies or complicates various diseases. In the secondary prolapse of the mitral valve, as in the primary, the initial inferiority of the connective tissue is of great importance. So, he often accompanies some hereditary syndromes (Marfan Syndrome, Elessa Dano-Chernogubov syndrome, congenital contracturated Arahanodactilia, imperfect osteogenesis, Elastic pseudochantom), as well as congenital heart defects, rheumatism and other rheumatic diseases, irrematic cardits, cardiomyopathy, some forms of arrhythmias, vegetative dystonia syndrome, endocrine pathology (hyperthyroidism) and others. The mitral valve prolapse may be due to the acquired mixomatosis, inflammatory damage to the valve structures, disorders of the contraction of myocardium and nipple muscles, valve-ventricular disproportions, asynchronous activities of various parts of the heart, which is often observed with innate and acquired diseases of the latter. In the formation of a clinical picture of the mitral valve prolapse, undoubtedly takes part the dysfunction of the autonomic nervous system. In addition, the importance of metabolic disorders and a shortage of trace elements, in particular magnesium ions.

The structural and functional inferiority of the valve apparatus of the heart leads to the fact that during the left ventricular systole period, the flaps of the mitral valve in the cavity of the left atrium occurs. Upon prolapse of the free part of the sash, accompanied by their incomplete closure in systole, auscultation is recorded insulated mesoismic clips associated with excessive tension of chord. A loose contact of the valve flaps or their discrepancy in Systole determines the appearance of systolic noise of various intensity, indicating the development of mitral regurgitation. Changes in the sublinking apparatus (chord lengthening, reduction of the precision ability of nobble muscles) also create conditions for the occurrence or enhancement of mitral regurgitation.

3. Classification

There is no generally accepted classification of the mitral valve prolapse. In addition to the separation of the mitral valve prolapse by origin (primary or secondary), it is customary to allocate auscultative and "dumb" forms, indicate the location localization (front, rear, both sash), degree of its severity (I degree - from 3 to 6 mm, II degree - from 6 to 9 mm, III degree - more than 9 mm), time of occurrence with respect to systole (early, late, holositolic), the presence and severity of mitral regurgitation. The state of the autonomic nervous system is also evaluated, the type of flow of the mitral valve prolapse is determined, possible complications and outcomes are taken into account.

4. Clinical picture

The prolapse of the mitral valve is characterized by a variety of symptoms, depending first of all from the severity of connective tissue dysplasia and vegetative shifts.

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

In most cases, in the prolapse of the mitral valve, various manifestations of connective tissue dysplasia are found: asthenic physique, high growth, reduced body weight, increased skin elasticity, weak muscles development, hypermobility of joints, dysfunction, scoliosis, deformation chest, Wildorded blades, flatfoot, myopia. You can detect hypertelectricism of the eyes and nipples, a kind of structure own sinks, Gothic packed, sandalwood slot and other small developmental abnormalities. The visceral manifestations of the dysplasia of the connective tissue include nephroptosis, an anomalies of the structure of the raging bubble, etc.

Often, during the prolapse of the mitral valve, there is a change in heart rate and blood pressure, mainly due to hypersympathicotone. Heart boundaries are usually not expanded. The most informative auscultative data: more often listened to insulated clicks or their combination with late-systemic noise, less often - isolated lateish systemic or nasicistal noise. Clicks are fixed in the middle or end of systole, usually at the top or in the fifth point of auscultation of the heart. They are not beyond the heart of the heart and do not exceed the volume of the second tone, they may be transient or permanent, appear or increase in the intensity in the vertical position and during exercise. Isolated lateral systemic noise (rough, "scraping") listened on the top of the heart (better in the position on the left side); It is carried out in the axillary region and is intensified in a vertical position. The nasicistal noise reflecting the presence of mitral regurgitation occupies the entire systole, is distinguished by stability. Part of the patients listened to the "peak" chord associated with the vibration of valve structures. In some cases (with a "sam" version of the Mitral Valve Prolapse), there is no auscultative symptomatic. The symptoms of the secondary prolapse of the mitral valve is similar to that in primary and combined with manifestations characteristic of the concomitant disease (marfan syndrome, congenital heart defects, rheumlock, etc.). The prolapse of the mitral valve must be differentiated primarily with the congenital or acquired deficiency of the mitral valve, systolic noises caused by other variants of small heart development anomalies or the valve dysfunction. The most informative EchoCG contributing to the correct assessment of the identified heartfill.

5. Treatment

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

With a "dumb" form, treatment is limited to general measures aimed at the normalization of the vegetative and psycho-emotional status of children, without a decrease in exercise.

In the auscultative version, children satisfactorily carry physical exertion and not having noticeable violations according to ECG data can do physical education in general group . Exclude only exercises, associated with sharp movements, running, jump. In some cases, it is necessary to exemption from participation in competitions.

When identifying mitral regurgitation, expressed violations of repolarization processes on ECG, reinforced arrhythmias, it is necessary to significantly limit the physical activity with the individual selection of the complex of the FFC.

In the treatment of children with the prolapse of the mitral valve, the correction is of great importance vegetative violationslike non-drug and medicated. In case of violations of ventricular repolarization (according to ECG), agents that improve myocardial metabolism [potassium orotat, inosine (for example, riboxin), Vitamins B5, B15, Levokarnitin, etc.] are used. Effective preparations that corrective magnesium exchanges, in particular orothic acid, magnesium salt (magnesot). In some cases (with a rack of tachycardia, frequent ventricular extrasystoles, the presence of an elongated Q-T interval, persistent violations of repolarization processes) justified the purpose of I-adrenobloclars (propranolol), if necessary, antiarrhythmic drugs of other classes. In pronounced changes in the valve apparatus, preventive antibiotic treatment courses are shown (especially in connection with surgery) in order to prevent the development of infectious endocarditis. Necessarily conservative or operational treatment of chronic infection foci.

In mitral insufficiency, accompanied by a pronounced, treatment-resistant cardiac decompensation, as well as with the addition of infectious endocarditis and other serious complications (pronounced arrhythmias), it is possible to conduct surgical correction of the mitral valve prolapse (rehabilitation operations or the prosthetics of the mitral valve).

6. Prevention

Prevention is directed mainly to preventing the progression of the existing valve vice and the occurrence of complications. To this end, the individual selection of physical exertion and the necessary medical and recreational activities, adequate treatment of other existing pathology (with secondary prolapse of the mitral valve). Children with a mitral valve prolapse are subject to dispensary observation with regular Necessia (ECG, ECCG, etc.).

7. Forecast

The forecast for the prolapse of the mitral valve in children depends on its origin, the severity of morphological changes of the mitral valve, the degree of regurgitation, the presence or absence of complications. IN childhood The prolapse of the mitral valve, as a rule, proceeds favorably. Complications in the prolapse of the mitral valve in children arise quite rarely. It is possible to develop acute (due to the separation of chord, with light venous hypertension) or chronic mitral insufficiency, infectious endocarditis, heavy forms of arrhythmias, thromboembolism, sudden death syndrome, which often has arrhythmogenic character. The development of complications, progression of valve violations and mitral regurgitation adversely affect the forecast. The prolapse of the mitral valve arising from the child is able to lead to difficult cultivated violations in more adulthood. In this regard, we need timely diagnosis, clearly carrying out the necessary medical and preventive measures in childhood.

References

1. Child disease. Baranov A.A. // 2002.

3 pathogenesis of the development of the disease

Thickening of mitral valve

Stretching and thickening of mitral valve sash causes a disruption of the latter closure, which contributes (due to higher pressure in the left ventricle than in the left atrium) inverse blood casting in the left atrium cavity. This in turn causes hyperfunction with subsequent hypertrophy of the left atrium and the relative failure of the pulmonary veins valves, and in the subsequent and hypertension in a small circle of blood circulation, which causes most of the symptoms of this disease.

I degree - the flaps are thickened to 3-5 millimeters, while the closure of the valve is not violated, so there is no clinical manifestation in the patient, because of this, it is possible to identify the disease at this stage possible only during the survey of diseases of other systems or on preventive inspections.

Any special treatment of Mitral Valve Mixomatosis does not require, even physical exertion restrictions are not given, the main thing healthy image Life, try not to hurt various viral and streptococcal infections and periodically carry out preventive inspections (most often recommended 2 times a year).

Degenerative Mitral Valve Disease

II degree - the thickening of the sash reaches 5-8 millimeters, the closure of the valve is broken, there is a reverse blood casting. Also during the examination, single chord separations and deformation of the contour of the mitral valve are detected. At this stage, the doctor paints lifestyle, power and frequency of preventive inspections.

III degree - the thickening of the flaps exceeds 8 millimeters, the closure of the valve does not occur, complete chords are observed. At the same time, the patient's condition deteriorates sharply, symptoms of acute left ventricular deficiency arise, therefore, an emergency specialized treatment for the patient and this stage is very important early appeal to medical care.

Features and causes of pathology

Mitra Valve Mixomatous Degeneration

The exact cause of the mixture degeneration of the mitral valve is not known, often this pathology is associated with hereditary predisposition. People who are disturbed by the formation of cartilage fabric are subject to this disease, there are congenital defects and joint diseases.

Degeneration of Mitral Valve (Mitral Valve Mixing) in last years Scientists are associated with hormonal disorders of various origins. There is also a certain relationship between this pathology and various viral diseases that provide a damaging effect on the heart sash, as well as streptococcal infection, which causes direct damage not only the valve apparatus, but also the heart endocarda.

Cardiovascular disease

Mitra valve mixture refers to a common heart disease, which is diagnosed in people of various age categories. IN modern medicine A few names of such pathology are used and most often experts use terms such as valve prolaps and degeneration.

Prolapse is a swelling or flexing heart valve in the direction of the proximally located organ of the organ. In the event that we are talking about the prolapse of the mitral valve, then such a pathology is accompanied by swelling of the flaps towards the left atrium.

Polaps refers to the most common pathology, which can be detected in patients at all ages.

Mitral valve mixture may develop for various reasons and specialists allocate primary and secondary prolapse:

under the primary valve prolapse implies pathology, the development of which is not connected with any known pathology or defects of development
secondary prolapse progresses against the background of many diseases and changes in pathological nature

Specialists suggest that the development of both the primary and secondary prolapse can occur in adolescence.

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

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

Cardiology

UDC 619: 616.12

Mitrocatus Mitral Valve Degeneration of Yorkshire Terriers

VC. Illarionova ( [Email Protected])

Veterinary clinic "Biocontrol" (Moscow).

The article discusses the most common pathology of the heart in yorkshire terriers as dog representatives small breeds - Mixomatous degeneration of atrioventricular valves, or endocardium. The pathophysiological mechanism for the development of heart failure under this pathology is described, the main criteria for diagnostics are listed and approaches to the treatment of dogs with different stages of heart failure are determined.

Keywords: Mixomatous degeneration of valves, heart failure, endocardium, echo cardiography

Abbreviations: AORTA AORTA, V / B - intravenous, in / m - intramuscular, IAPF - inhibitors of angiotensin-converting factor, KDOi - a finite-diastolic volume index, DCP - finite systolic size, La - pulmonary artery, LH - pulmonary hypertension, LV - left ventricle, LP - left atrium, MK - Mitral valve, MR - Mitral regurgitation, MRP - intercostal intervals, MT - body weight, PZ - right ventricle, p / k - subcutaneous, PP-right atrium, PPT - Square body surfaces, TSK - three-rolled valve, FV - Emission fraction, Fu - Trigger fraction, ACVIM - American College of Veterinary Internal Medicine (American College of Veterinary Medicine internal Diseases)

The Yorkshire Terrier is one of the most popular dog breeds in the world. Here is just one quote from the magazine of the American Kennel Club, dedicated to this breed: "The Yorkshire Terrier is a truly phenomenal dog, a small miracle of zootechnia." Modern Yorkshire terriers really have a very attractive appearance: a small size, beautiful and comfortable wool, a round head, a shortened face and large eyes - a classic set of key incentives of the parent feeling. This is one of the young dog breeds, derived from the crossing of various terriers of England. In 1874, the breed was registered by the British Kennel Club and entered into the breeding book. Yorks of that time had a pretty long body and a larger size, usual for them was MT 6 .. .7 kg. MT of modern yorkshire terriers is from 1.5 to 3 kg. The rapid artificial decrease in MT and the shortening of the body was reflected not only on the exterior, but also on the interior - the inner structure of the dog. At the same time, characteristic pathologies were also secured together with the peculiarities of the breed.

The indisputable advantages of yorkshire terriers are friendly temper, courage, dedication, as well as the convenience of content. People are ready to purchase a companion, a comrade for games, in other words, joy, but often in addition to get a bouquet of diseases. For veterinary doctors, Yorkshire terriers became one of the inalienable parts of therapeutic practice. In veterinary cardiology, one of the most common diseases of this breed is chronic illness Atrioventricular valves, developing as a result of degenerative pathology - micketer degeneration of valves (another name of the disease - endocardiose valves).

Etiology, pathophysylogide, clinical signs

Mixomatous degeneration of valves - the result of changes affecting the entire valve device MK or, less likely, TSC. They suffer mainly dog \u200b\u200bof small breeds of old age. The disease is characterized by gradually thickening and deformation of valve sesters, starting from free edges and ending with the involvement of the entire surface of the sash and tendon threads (Fig. 1).

The deformation process of valve includes four stages, starting with single thickens along the edges and ending with drain changes in sash and tendon threads. The lesions arise as a result of the redistribution of the extracellular matrix, the accumulation of glycosoaminoglycans, thinning and fragmentation of collagen in the subendocardium layer of valve flaps. Similar changes are detected at a man's prolapse. Thus, the valve gradually loses its locking function, and the blood begins to partially throw into the atrium during the period of stomach systole. The amount of blood flow (regurgitation) depends on several factors, but the main is the size of the defect of the sash and the difference between systolic pressure in the ventricles and atrium. The atrium is chronically overloaded with blood volume and are gradually dilated to compensate the pressure growing in them. At the same time, the hemodynamic overload of the pulmonary veins and the LV, which in the diastole is obtained by the volume of blood increased by regurgitation, which leads to its eccentric hypertrophy. At the same time, the antitegrad blood release in AO (with deficiency of MK) or LA (with TCC insufficiency) decreases due to the preferred flow of blood flow into the atrium with lower pressure. To ensure normal blood circulation and pumping additional blood volume, the heart increases the shock volume according to the Frank Starling law, in which the increase in the ventricular CDO causes a greater stretching of myofibrils and initiates a stronger reduction. Thus, myocardiums in chronic insufficiency of atrioventricular valves are in a state of hypercup-tality for a long time. Over time, the compensatory reserves of the body decrease, the pressure in the LP (with mitral insufficiency) is growing, which causes chronic pulmonary blood flow overload with the development of LH

Fig. 1. Macrobreparat: Thickening and deformation of MK sash

Fig. 3. Phonocardiographic image Fig. 2. Macrobreparation: Trombus from the sash MK noise of insufficiency of atrioventricular in mesenterior vessels of valves

and pulmonary swelling. LH aggravates blood circulation disorder in the right hearts, which provokes congestive phenomena in the venous bed big Circle blood circulation with signs of fluid delay (ascites, hydrotorax, hydropericard). When the backup capabilities of the heart muscle are exhausted, its systolic function is reduced. This causes a fall heart Emission and the development of general weakness, lethargy and fainting. With pronounced structural changes in the valve apparatus and LP, such complications may rarely arise such complications as the rupture of tendon threads or LP, the formation of thrombus on deformed sashs with the development of blood circulation thromboembolism (Fig. 2).

The disease has a rather long asymptomatic period, which is provided by compensatory reserves of the body, in particular, the activation of rining-angiotensin-aldosterone and sympathetic-ad-radar systems.

The earliest symptom of pathology - cough, which has a comprehensive pathophysiological mechanism. One of the most significant causes of cough is the compression of the left major bronchum dilati-produced LP. At the same time, there is a mechanical irritation of coughing receptors and the development of a loud barking cough similar to the cleavage foreign bodies From the respiratory tract. Similar cough is developing at the collapse of trachea, which is also often frequent of yorkshire terriers. Under the progression of heart failure, stagnant phenomena in the lung vessels are developing, which stimulates Yuchstapulm-molded receptors involved in the formation of the cas left reflex. With the development of interstitial and alveolar edema, the cough may acquire a softer and humid character.

Tahipne and shortness of breath, wearing expiratory or mixed character, arise in the development of interstitial or alveolar edema of the lungs. Such pathological disorders of breathing do not pass and at rest.

Fainting, manifested by a sudden short-term loss of consciousness with a sudden drop of muscle tone, may arise as a result of heart rhythm disorders, manifest themselves with a decrease in cardiac output with a sudden physical or emotional

load or provoke cough attacks with the development of reflex bradycardia.

The most significant feature of the disease in physical animal study is the pansistolic noise of mitral or triple regurguses at the points of the MK auscultation (6th MPP at the level of coatrocondral joints on the left) or TSC (5th MRP at the level of coatonchondral joints on the right). Noise has a smooth configuration and merges with the first and second tones of the heart (Fig. 3). The volume of noise correlates with the degree of severity of valve deficiency. With volumetric overload of LV, the pathological third tone of the heart can appear. In the development of LH, the second tone increases due to the pulmonary component. Filling the pulse for a long time remains normal. With a decrease in the systolic function of myocardium, the pulse becomes empty by filling. With severe heart failure, tachycardia is manifested. With auscultation of the lungs, wheezing in patients with signs of pulmonary edema. However, it is necessary to carefully approach these changes, since wheezing may be symptoms of broncho-pulmonary pathology, which is often found at yorkshire terriers.

For differential diagnosis, a radiographic study of the chest, which allows you to estimate the condition of the lungs, respiratory tract, vessels and hearts. In yorkshire terriers, the heart looks large relative to the sizes of the chest, so it is necessary to calculate the cardioverteter size: the sum of the heart length (from the heart base under the tracheal bifurcation to the top) and the width of the heart (in the widest part, coinciding with the level of the ventral border of Kaudal Hollow vein). The measure of the length of each segment is breast vertebrae, starting with T4. The value of this indicator in yorkshire terriers varies - 9.9 ± 0.6 vertebrae. Assessing the heart shape in the picture in the lateral projection, the phases of breathing and cardiac activity should be taken into account, since the relative size of the heart can be increased by combining exhalation and diastole (Fig. 4). The most vivid radiographic signs of Dilation of LP in the lateral projection - an increase and straightening of the caudodoresal boundary of the heart to form a direct angle pattern, disappearance

Fig. 4. Diagram of changes in the relative size of the heart on the radiograph in the side projection, depending on the respiratory phase

Fig. 5. Diagram of changes in the relative size of the heart on the radiograph in lateral projection, depending on the phase of the cardiac cycle

caudal "Heart Waist", Dorsal shift of the trachea and the left major bronchus (Fig. 5). With an increase in the right-hand heart departments, the area of \u200b\u200bcar-dosiosterny contact is expanded and the right side of the heart silhouette on radiographs in the lateral projection is expanding.

The degree of congestive phenomena in the lungs is assessed by the severity of venous stagnation: with a large extent, the diameter of the lobar vein of the cranial lobe of the lung exceeds the diameter of the artery of the same name.

In an interstitial edema of the lungs, the X-ray picture of the "smoothness" or "duty" of the vascular pattern of the lungs occurs, with exacerbation of the situation and the development of alveolar edema, dense diffuse shades are noted first in the root area, and then in the caudodores of the lungs (Fig. 6, 7) .

In case of echocardiographic examination, signs of increasing LP and Eccentric LV Hypertrophy are detected during the insufficiency of MK. In case of insufficiency, TCK detect an increase in the cavities of PP and PJ. The severity of changes depends on the stage of the process. Sashes of atrioventricular valves are thickened and deformed to varying degrees.

In clinical practice, the most accessible assessment of mitral regurgitation on percentage

square jet area regurgitation to LP Square according to the results of color doppler mapping (Fig. 8): I degree less than 20%; II - 20 ... 30; III - up to 70, IV degree - 70% or more. The advantages of the method should include ease of use and high reproducibility. The disadvantage is that this is a semi-quantitative study method that does not give ideas about the volume of regurgitation.

Assessment of the contractility of myocardial LV with MP is difficult. Volumetric overload and the presence of MRs lead myocardium into the hyperkinosis state. Obtaining normal and subnormal indicators of FU and FV according to the teemok method indicates a decrease in the contractile function. DRP LV is less susceptible to various factors. Use the calculation of KSOi:

KSOi \u003d KSR3 / PPT

KSOi\u003e 30 ml / m2 indicates the systolic dysfunction of myocardium. Maximum speed Regurgongitations< 5 м/с говорит о высоком давлении в ЛП или снижении сократимости миокарда.

LH is due to a persistent increase in pressure in LA with the development of right-hand deficiencies. To detect the LH, systolic and diastolic pressure in LA are estimated at regurgitation rate on TCK and La Valve. In the absence of regurgitation, the average pressure in the LA is estimated by determining the acceleration time in the LA and the ratio of the flow acceleration time to the total length of the expulsion from the PJ. Indirect method - determination of the LA / AO ratio. Expansion pulmonary artery leads to an increase in LA / AO more than 1.

Electrocardiographic changes reflect the hypertrophy of the right and / or left sections of the heart only with pronounced structural changes in the latter. A characteristic feature of hypertrophy of LPs in case of insufficiency of the MK is the expansion of the PC (more than 0.05 seconds). LV hypertrophy manifests itself in increasing the amplitude of the teeth to and expand the OK8 complex (more than 0.06 c) (Fig. 9). Rhythm disorders are often manifested by soup-equalized extrasystoles and rhythms, and ventricular extrasystoles are less likely (Fig. 10), ventricular rhythms and atrial flications. The pronounced changes of the heart with the development of symptoms of heart failure are accompanied by sinus tachycardia with the disappearance of sinus arrhythmia.

Fig. 6. Radiograph of chest in lateral projection.

Signs of chronic insufficiency MK: an increase in LP (arrow) and LV, Dorsal trachea shift

Fig. 7. Radiograph of chest in lateral projection. Signs of alveolar pulmonary edema: cloud shading in the field of lung roots and caudodores

Fig. 8. Echocardiogram (right parastinal access on the short axis at the root level of the Patient with chronic insufficiency of MK. Significant expansion of the cavity of LP

Treatment depending on the process stage

The disease is developing gradually, which allows you to set the stage of the process. According to ACVIM classification, the following stages distinguish: A, B1, B2, C1, C2, D1, D2.

Stage A: Take dogs of predisposed breeds, geriatric population. Treatment is not recommended.

Stage B1: These are animals with MR, but without Cardioma-Galia. Does not exist drugSlowing the degenerative process in the valves. Treatment is not recommended.

Stage B2: These are dogs with MR, cardiomegaly, but without clinical signs. Among the specialists there is no agreement on whether the drugs of the IAPF class should be prescribed, since today there are two veterinary studies SVEP (2002) and VetProof (2007) with contradictory results.

Stage C1: include animals with clinical signs of heart failure in need of hospitalization. It may be a manifestation of the disease (signs appear for the first time after the asymptomatic period) or its exacerbation after remission. The aggravation is due to the breakdown of a tendon thread or LP, arrhythmia, excessive physical activity, increased consumption of a salt or progression of the disease. ACVIM has achieved consensus in the following drugs: furo-semi (B / B, in / m, p / k) 1 ... 4 mg / kg of MT or infusion with a constant speed of 1 mg / kg MT / h (treatment efficacy is evaluated by frequency respiratory movements and shortness of breath); Pimobhendan per os 0,25.0.3 mg / kg MT after 12 hours (based on clinical experience). There is no agreement on the use of IAPP, Dobutamin, Mazi Nitroglycerin.

Stage C2: These are dogs with clinical manifestations that have the ability to treat at home. ACVIM has achieved consensus for the use of the following drugs: Furosemide from 1.2 mg / kg MT PER OS 12 hours to 4.6 mg / kg MT PER OS after 8 hours, pimobhendan 0.25.0.3 mg / kg MT after 12 hours, IAPF 0.5 mg / kg MT after 12 hours, enalapril 0.5 mg / kg MT after 12 hours), Spironolactone (most ACVIM members approved). There is no consent of specialists in the use of digoxin, beta-blockers, diltiazem, bronchodylators, amlodipine (0.1 mg / kg MT after 12 h), hydrochlorosticiazide, (2.4 mg / kg MT after 12 h), thoracemide (0.2 mg / kg MT after 12.24 h).

Stage D1: Take dogs with symptoms of stagnant heart failure and / or reduced cardiac outlook in need of hospitalization. ACVIM has reached a consensus for the use of the following drugs: Furosemide B / in Bolusno\u003e 2 mg / kg MT or with a constant speed of 1 mg / kg of MT / h (used with caution when the content of creative-nine in serum is more than 2.3 mg / dl); Pimobandan 0.2 ... 0.3 mg / kg MT after 12 hours. Amlodipine is added to therapy (0.05.01 mg / kg MT PER OS, after 12 hours) with high arterial pressure. Try not to reduce systolic pressure less

Fig. 10. Electrocardiogram (II leading) patient with chronic insufficiency of MK.

Signs of hypertrophy of LP and LV

Fig. 11. Electrocardiogram (I lead) patient with chronic MK insufficiency.

Single stomatricular extrasyistol

85 mm RT. Art. And the average pressure is less than 60 mm. If necessary, add pimobandan or up-butamine. There is no consent among specialists in relation to the use of IAPF, Mazi nitroglycerin, high doses of pimobendan (0.3 mg / kg MT after 8 h), Dobutamine (2.15 MGK / kg MT / min).

Stage D2: These are patients refractming to standard therapy, with the possibility of treating at home. ACVIM reached a consensus for the use of the following drugs: Furosemide from 1.2 mg / kg MT PER OS 12 hours to 4.6 mg / kg MT PER OS after 8 hours. Partially agreed by the use of thoreside. Recommended hypothiazide 1.2 mg after 12.24.48 h; Spiro-nolacton 2 mg / kg MT after 12 hours, IAPF, Pimobhendan. There is no agreement on the following drugs: Digoxin, SP-Ronolacton, Sildenafil (from 0.5.1 mg / kg MT after 12 hours to 2.3 mg / kg after 12 h), bronchodulators (AMI-Noophullin 10 mg / kg MT after 8 hours, Theophylline With slow release of 20 mg / kg MT after 24 hours).

In this way, chronic insufficiency Atrioventricular valves as a result of a mixed degeneration - this is a chronic process in which a complex approach in diagnosis with the definition of the process stage. The development of therapeutic measures is based on the obtained diagnostic data. Tactics of treatment depends on the stage of the pathological process and monitoring the state of the animal in the course of therapy of the disease.

Bibliography

1. ATKINS, C.E. Pharmacologic Management of Myxomatous Mitral Valve Disease in Dogs / C.E. ATKINS, J. Haggstrom // Journal of Veterinary Cardiology, - 2012 - V. 14. - N. 1. - P. 165-184.

2. AUPPERLE, H. Pathology, Protein Expression and Signaling in Myxomatous Mitral Valve Degeneration: Comparison of Dogs and Humans / H. Aupperle, S. Dis-Atian // Journal of Veterinary Cardiology. - 2012-V. 14. - N. 1. - P. 59-71.

3. Borgarelli, M. Historical Review, Epidemiology and Natural History of Degenerative Mitral Valve Disease / M. Borgarelli, J.W. Buchanan // Journal of Veterinary Cardiology. 2012 - V. 14. - N. 1. - P. 93-101.

4. Borgarelli, M. Survival Characteristics and Prognostic Variables of Dogs with Pre-Clinical Chronic Degenerative Mitral Valve Disease Attributable to Myxomatous Degeneration / M. Borgarelli, S. Crosara, K. Lamba, P. Savarino, G. La Rosa, A. Tarducci, J. Haggstrom / J Vet Intern Med. - 2012 Jan-Feb. - V. 26. - N. 1. - P. 69-75.

5. ChetBoul, V. Echocardiographic Assessment of Canine Degenerative Mitral Valve Disease / V. ChetBoul, R. Tissier // Journal of Veterinary Cardiology. - 2012 - V. 14. - N. 1. - P. 127-148.

6. Connell, P.S. Differentiating The Aging Of The Mitral Valve from Human and Canine Myxomatous Degeneration / P.S. Connell, R.I. Han, K.J. Grande-allen // Journal of Veterinary Cardiology. - 2012 - V. 14. - N. 1. - P. 31-45.

7. Dillon, A.R. Left Ventricular Remodeling in Preclinical Experimental Mitral Regurgitation of Dogs / A.R Dillon., L.J. Dell'Italia, M. Tillson, C. Killingsworth, T. Denney, J. Hathcock, L. Botzman // Journal of Veterinary Cardiology. - 2012 - V. 14. - N. 1. - P. 73-92.

8. Fox, P.R. Pathology of Myxomatous Mitral Valve Disease In The Dog / P.R. Fox // Journal of Veterinary Cardiology. - 2012-V. 14. - N. 1. - P. 103-126.

9. Jepsen-Grant, K. Vertebral Heart Scores in Eight Dog Breeds / K. Jepsen-Grant, R.E. Pollard, L.R. Johnson // VET RADIOL ULTRASOUND.-2013 JAN-FEB. - V. 54. - N. 1. - P. 3-8.

10. Kellihan, H.B. Pulmonary Hypertension in Canine Degenerative Mitral Valve Disease / H.B. Kellihan, R.L. Stepien // Journal of Veterinary Cardiology. - 2012 - V. 14. - N. 1. - P. 149-164.

11. Orton, E.c. Mitral Valve Degeneration: Still More Questions Than Answers / E.C. Orton // Journal of Veterinary Cardiology. - 2012 - V. 14. - N. 1. - P. 3.

12. Orton, E.c. Signaling Pathways in Mitral Valve Degeneration / E.C. Orton

C.M.R. Lacerda, H.B. Maclea // Journal of Veterinary Cardiology. - 2012 - V. 14. - N. 1. - P. 7-17.

13. PARKER, H.G. Myxomatous Mitral Valve Disease in Dogs: Does Size Matter? / H.g. Parker, P. Kilroy-Glynn // Journal of Veterinary Cardiology. - 2012 - V. 14. - N. 1. - P. 19-29.

14. Richards, J.M. The Mechanobiology of Mitral Valve Function, Degeneration, and Repair / J.M. Richards, E.J. Farrar, B.G. Kornreich, N.S. Mo "ISE, J.T. Butcher // Journal of Veterinary Cardiology. - 2012 - V. 14. - N. 1. - P. 47-58.

15. Singh, M.K. Bronchomalacia in Dogs with Myxomatous Mitral Valve Degeneration / M.K. Singh, L.R. Johnson, m.d. Kittleson, R.E. Pollard // J Vet Intern Med. - 2012 Mar-Apr. - V. 26. N. 2. - P. 312-319.

Summary v.k. Illarionova.

Veterinary Clinic "Biocontrol" (Moscow).

Myxomatous Mitral Valve Disese in Yorkshire Terriers. The Article Considers ONE OF THE MOST COMMON HEART DISEASE IN YORKSHIRE TERRIERS - MYXOMATOUS MITRAL VALVE DISEASE, OR ENDOCARDIOSIS. The Pathophysiology of Heart Failure, The Main Criteria Of Diagnostics Of this Disease and Approaches to the Treatment Of Dogs with Different Stages of Heart Failure Is Described.

effective distribution as-market - an exclusive supplier of Allerumer preparation 1%

(AEP / ESHT 1%, DIMEDROL), 50 ml, injection, for veterinary use.

aU group of companies drug prescribe small home

animals and young animals for the prevention and relief of allergic reactions for serum diseases, anaphylaxis, anaphylactic shock, italy and atopic dermatitis, allergic conjunctivitis, rhinitis, polyarthritis, joint and muscle rheumatism, as a soothing means in combination with sleeping pills, with respiratory diseases Systems, urinary tract, for premium before overasty anesthesia.

Phone +7 / 495 / 916-91-64, www.as-market.ru

Elkolin- ■.

t "< фо«с М ОО 314 ПК

Yalazіshiyia

(Ahervetum 1%) Sterile Alya Injection

"001 g Yaro *.: * -

_ ^ "*" Lrazyo XXUNUEWOWCC *? *

at Temlergus * "

From a large number of reasons for transformation, the following main factors can be distinguished in the norm of elastic flaps in the mixture:
- hereditary deterministic mixture transformation of sash;

Congenital microanoms of architecture of sash, chore and an atrioventricular ring, resulting in a valve mixture transformation;

Mixomatosis as a purchased process.

In some cases, the mixture changes of the valve may be due to genetic reasons. With autosomal dominant inheritance of the syndrome genes on chromosomes 16p12.1 (OMIM 157700), P11.2 (OMIM 607829) and 13. Another locus is detected on x chromosome and causes a rare PMC form, which is denoted by the "X-clutched mixture valve dystrophy" .

To histological manifestations of hereditary deterministic mixomatosis, some authors relate to the following provisions.

It is a fact that the thickness of the spongiosis zone in mitral flaps (the main structure producing mucopolysaccharides) is regulated by the genotype. The thickening of the spongiosis zone (over 60% of the total sash thickness) predisposes to the PMK syndrome. The presence of Blanc-B-loci surface antigen of lymphocytes (HLA antigens) is associated with an increase in the likelihood of mixture degeneration of mitral valve flaps 50 times.

The features of the architecture of the skin capillaries (according to the data of capillaryroscopy and laser-doppler flumetria) in patients with the primary prolapse of the mitral valve are similar to those hereditary diseases connective tissue (marfana disease). This allowed the authors to believe that there is a phenotypic continuum between the primary prolapse of the mitral valve and the Martan's disease, and the PMK syndrome itself is, in fact, is a stood (incomplete) form of hereditary disease of the connective tissue. The family character of PMK was confirmed in 20% of cases, and he, as a rule, was observed in the mothers of the samples. In 1/3 of the family cases, the signs characteristic of the inferiority of the connective tissue can be trained in relatives of the sample. varicose extension veins, funnelized thoracic deformation, scoliosis, hernia.

It is known that fibrillin is one of the structural components of elastin-associated microfibrils, which are found in the mitral valve. With the help of a polymerase chain reaction C. Yosefy and A. Ben Barak (2007) revealed polymorphism of fibrillin - 1 gene in EXON 15 TT and EXON 27 GG. This polymorphism was reliably associated with PMK.

In the pathogenesis of the mixture degeneration of the mitral valve, a polymorphism of the T4065C gene may be responsible for the production of the plasminogen-plasminogen activator.

In the immunohistochemical analysis of the sashs of mixture valves, removed during the operation, the impaired distribution of fibriline, elastine, collagen I and III compared to normal valves was detected.

In experimental studies, an increase in the activity of NADPH-Diaphorase in the mixture sash is established.

Association has been established between the polymorphism of the gene angiotensink-converting enzyme and a mitral valve prolapse, especially the M235T gene.

Mixomatosis may also occur due to congenital microanoms of the architecture of sash, chore and an atrioventricular ring, which over time due to repeated microtransmissions against the background of hemodynamic effects become more pronounced, accompanied by excessive products in the stroma of collagen valve mainly type III.

It is distinguished by the hypothesis of the primary defect for the development of the connective tissue apparatus of the mitral valve, the latter is combined with an increase in the number of diembogenesis stygme.

Confirmation of the hypothesis of congenital microallions of the mitral valve is a high frequency of detection of the disturbed distribution of tendon chord to mitral sash, anomalous chord in the left ventricle.

These anomalies met in the control group of healthy children without a mitral valve prolust syndrome. However, such microanomalia, as the dilaration of the right atrioventricular hole, the pulmonary artery barrel, the sinuses of the waltzalver and the incorrect distribution of the chord of the front mitral sash, were observed during the primary PMC significantly more often than in control.

Most of the listed microanomalies are related to the connective tissue structures of the heart. Some small anomalies, for example, disturbed chord distribution may be directly related to PMK syndrome, being a causal factor. Other anomalies, such as the dration of the main vessels, coronary sinus and others, reflect the inferiority of the connective tissue structures.

Of particular importance are abnormally fastening tendon chords of the linked apparatus. A number of authors consider their cause of a mitral valve prolapse.

Congenital microanomalies of the heart, according to our data, reliably occurred in children with primary PMK, whose mothers were working on chemical production during pregnancy (hydrogen sulfur, servo-carbon). The prolapse of the Mitral Valve is much more common in children born and living in environmentally unfavorable zones (Aral region, Ust-Kamenogorsk). In the era of ecological disadvantage, this fact is of great importance in the understanding and origin of the diembogenesis of the heart and its connecting elements.

Some congenital anomalies They lead to the prolapse of mitral flaps, accompanied by mitral regurgitation. For example, the heavy prolapse of the mitral valve, with naked noise and mitral regurgitation, is observed in the absence of commissioned tendon threads of the mitral valve. This anomaly is detected with two-dimensional dopplerhocardiography and is found at 0.25%, according to autopsy. Congenital mitral insufficiency with large prolapse is observed in annular ectasia.

A number of authors consider mixture as a purchased process. It is known that the mixing line is presented in minor quantities in the sash of intact valves. Local or diffuse propagation is detected at various valve lesions, for example: with rheumatic heart disease, congenital mitral insufficiency, infectious endocardite. In connection with this, the mixing transformation is associated with a non-specific reaction of the connective tissue valve structures on any pathological process.

Proponents of the hypothesis of "embryonic mixomatosis" view mixtosis as a result of unfinished differentiation of valve tissues, when the influence of factors that stimulate its development weakens on an early embryonic stage. However, this hypothesis is not confirmed by the data of epidemiological studies of the frequency of prolapse in the process of ontogenetic development. According to this theory, PMK must meet more often in children of early age, which is not confirmed by population research.

Along with the "mixture" reasons for the occurrence of primary PMK, there is a "myocardial" hypothesis based on the fact that in patients with sfolders are detected in angiographic studies of changes in left-handhold contracts and relaxation of the following types:
1) "hourglass";
2) lower bazal hypocinezia;
3) inadequate shortening of the long axis of the left ventricle;
4) anomalous reduction in the left ventricle according to the type of "Noga Ballerina";
5) hyperkinetic reduction;
6) premature relaxation of the front wall of the left ventricle.

Such variants of asiergic contracts and relaxation can lead to the dysfunction of the mitral valve, its sagging in the left atrium during systole. However, the disturbance of the calculation and relaxation of myocardial myocardium is not found in all patients, is mainly documented with congenital anomalies of coronary arteries in children and ischemic Disease Hearts in adults.

Many authors are of particular importance in the etiopathogenesis of the mitral valve prolapse attach a violation of trace elements. Magnesium deficiency is considered as the main etiopathogenetic factor leading to the valve propagation.

Some authors consider the occurrence of the prolapse of the mitral valve in connection with the violation of the valve innervation arising from various vegetative and psycho-emotional violations. There is a close relationship between the mitral valve prolapse and panic disorders, nervous anorexia. However, the etiopathogenesis of shifting sash in connection with the disturbed valve innervation is more complex. Thus, with a nervous anorexia, along with innervation anomalies, a disorder of metabolism and trace elements is determined, mainly hyoponatremia, hypocalemia, hypochloremia, hypophosphatemia, hypoglycemia and hyperazotemia.

In recent years, there have been a large number of publications about the high frequency of PMK in patients with coronary arterial anomalies, for example, the overall extinguishing of coronary arteries from the right sine waltzalva. According to autopsy, congenital abnormalities of coronary arteries are detected in 0.61% of cases and 30% are accompanied by a mitral valve prolapse. The PMK syndrome is most often detected with an abnormal disorder of the right coronary artery from the left or inappropriate aortic sinus. Probably, minor anomalies of the coronary arteries cause local dyskinesia of left-detection segments, mainly in the field of papillary muscles, which leads to their dysfunction and valve propagation. Thus, the left ventricular ischemia determines the predominantly prolapse of the rear mitral sash, its central and rearbed shares.

The occurrence of the secondary prolapse of the mitral valve is observed in many states and diseases. PMK is observed in patients with hereditary pathology of the connective tissue (Martan Syndrome, Elessa-Danlos, Elastic Pseudochantomy, etc.), valve-ventricular disproportion, neuroendocrine anomalies (hyperthyroidism).

In the hereditary pathology of the connective tissue, a genetically deterministic defect of the synthesis of collagen and elastic structures, deposition in the stroma of glycosaminoglycan valve valve.

Many authors bind the emergence of PMK with the valve-ventricular disproportion, when the mitral valve is too large for ventricle or ventricle - too small for the valve. This reason determines the emergence of PMK at most congenital defects Hearts accompanied by the "underload" of the left heap departments: Ebestein anomalies, atrioventricular communication and a defect of the interproveserving partition, anomalous drainage of the pulmonary veins, etc.

Thus, the mitral valve prolapse is a polyethological disease, in the genesis of which are of both genetic and environmental factors. Each of the above hypotheses of the prolapse of the mitral valve finds confirmation in the clinical picture, which causes the phenotypic polymorphism of the syndrome.

The results of a comprehensive examination of children with primary PMCs make it possible that in the occurrence of shifting of the sash in these children, several factors are at the same time, the main of which are the inferiority of the connective tissue valve structures, minor anomalies of the valve apparatus and pivothegetative dysfunction that promotes hemodynamic disregulation.

Myxomatous degeneration of the Mitral Valve is not such a serious pathology, as it may seem at first glance. It has several alternative names that a person can hear from the cardiologist after passing a survey: endocardium, valve prolapse.

To be able to learn more about such a vice as a mixture degeneration of mitral valve sash, what it is and how to deal with it, consider further. We are talking about thickening and stretching valve flaps, contributing to a loose closure. As a result - the formation of inverse blood flow directed towards ventricles.

Several degrees of pathology are distinguished, depending on which forecasts for a person are changing, a decision will be made about the appointment of effective treatment:

1 degree - there is a thickening of the valve flaps up to 3-5 mm. Such changes do not violate their closure, therefore the symptoms of pathology in humans are usually absent. Doctors do not beat the alarm in the diagnosis of such a stage of the disease, it is recommended to revise the lifestyle, conduct preventive inspections twice a year;
2 Degree - sash stretched, more thickened, their indicators reach 5-8 mm. In addition, the deformation of the contour of the mitral hole is observed. The tensile and single chord breaks are diagnosed. Fixtures are broken;
3 degree - thickening of mitral flaps noticeably very well, the thickness of them exceeds 8 mm. There is a deformation of the mitral ring, stretching and chord breaks. Locking sash is completely absent.

Conclusion: 1 Stage of pathology is considered safe, there are no disorders in the work of the heart, there is no regurgitation (reverse blood flow). On 2 and 3 stages, blood in a certain volume returns back, because the closure of the flaps is broken or completely absent. Such a state of affairs should not be ignored, because the high risk of developing serious complications.

Important! In order for the left ventricle to cope with blood volumes that increased due to the inverse blood flow, it will begin to increase in size. As a result - hypertrophy of LV. But, this is just one of the negative consequences of the vice considered by us.

It is known that the mixing degeneration of mitral valve flaps with age is only progressing. The risk of additional complications appears: MK deficiency, bacterial endocarditis, stroke, sudden death. Forecasts are not crowded, therefore it is worth taking care of the possibility of timely identifying this pathology that allows effective measures to take effective measures to treat and prevent complications as soon as possible.

Signs of MD

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

reducing performance, general weakness, fast fatigue even with minimal loads;
shortness of breath appearing with a minimum physical or emotional load, a sense of air shortage;
heart pains that are most often manifested in the form of tingling. Occur periodically, have a brief character;
dizziness, accompanied by arrhythmia, often leading a person to a pre-diffulous state;
cough, it should be considered as an additional symptom that may not appear. At first it is dry, then accompanied by the release of sputum, which may contain streaks of blood.

When visiting the doctor, signs of violation of the cardiac system will first be seen when listening to the heart. The doctor will hear noises that accompany the reverse outflow of blood to the ventricle. This will be able to become a reason for a more detailed examination, which includes the collection of anamnesis, laboratory tests, electrocardiography, echocardiography.

If the electrocardiography shows only the presence of a violation, its stage, then the ultrasound of the heart will be able to give more complete informs, because it will determine the size of the sash, the features of their deformation, simply speaking, all pathological changes in this case.

How to treat MD

At the initial stage of the development of the disease, treatment will be absent, because it will not be acute need. The patient will recommend only a systematic visit to the cardiologist in order to determine the intensity of the progression of the state, the control of pathology.

If the mixing degeneration of the mitral valve flaps is aggravated, the person will prescribe a number of medicines that will help to fight symptoms, slow down the ailment. These are drugs that disseminate excess fluid from the body, thus, removing an excess load from the heart; Medicines restoring heart rate, eliminating arrhythmia, other medicines that will be relevant in this case.

MD prophylaxis

When it comes to serious disease or pathology representing a high danger to human health and his life always becomes relevant to the issue of prevention. In order to choose these measures, you need to learn about the reasons provoking one or another ailment. In the case of MD, the exact reasons for its appearance is not yet known. Doctors suggest that it develops due to genetic location, but this statement has not been proven.

Accordingly, it is difficult to speak about the measures of prevention in this case. The only thing that will help preserve the health of the heart and extend its work for many years is a healthy lifestyle, from this state of the health of the body of each of us depends by 80%, including the work of its main motor - heart. Therefore, it is better to refuse harmful habits, start to eat well and relax right, do physical culture, but not too diligent.

In contact with

The main causes of the mix of the valve. Myxomatous Degeneration of Mitral Valve Mixomatosis Heart

Similar documents

3 pathogenesis of the development of the disease

Features and causes of pathology

Signs of MD

How to treat MD

MD prophylaxis

Report typos

The text that will be sent to our editors:

Your comment (optional):