CARDIOSCLEROSIS (Greek kardia heart + sklerosis consolidation; synonym: myocardiosclerosis, myofibrosis, sclerosis of heart, fibrosis of heart) — the growth of connecting fabric in a cardiac muscle occurring usually after death of muscle fibers or parallel to it.
To., as a rule, process secondary, is an outcome various on the etiology and a pathogeny of processes in a myocardium. To. can be manifestation coronary heart disease (see). Primary To. meets extremely seldom. Morphologically distinguish postinfarction To., replaceable To., miokarditicheskiya To. and To. owing to cardiomyopathy (see) various etiology; To. develops also at a bazedovy disease.
A postinfarction cardiosclerosis
the Postinfarction cardiosclerosis (macrofocal To., a callosity of a myocardium, scattered focal To., the postinfarction hem) arises owing to disturbance of the coronary circulation bringing to to a myocardial infarction (see) as to display of coronary heart disease. Is much more rare postinfarction To. is a consequence of a necrosis of the site of a myocardium as a result of an embolism of coronal arteries trombotichesky masses at an endocarditis of the mitral valve or pristenochny blood clots in the left half of heart; defeats of branches of coronary arteries at rheumatism or arteritis of various nature (e.g., at generalized nonspecific arteritis, or Takayasu's disease, a nodose panarteritis), during the narrowing of their mouths as a result of a syphilitic mesaortitis, a stenosis of an aortal opening at syphilitic heart disease or at the isolated calcification of aortal valves. Apparently, is a consequence of an embolism also macrofocal To., observed selectively in the field of a top of heart at the cardiomegalies connected with a Chagas disease, and at an idiopathic hypertrophy of heart, the pristenochny blood clots which are followed, as a rule, by education in a left ventricle of heart.
Formation To. at a macrofocal myocardial infarction occurs by substitution of the died site of a muscle of heart young connecting fabric. The died muscle fibers are exposed to coagulation and the subsequent disintegration at first with participation of leukocytes, and then the macrophages absorbing decomposition products. At the same time there is a reproduction of fibroblasts, a new growth of capillaries, thin-walled sinusoidal vessels from the remained sites of a stroma, especially around vessels, accumulation of glikozaminoglikan and formation of young connecting fabric to formation of network of argyrophil and collagenic fibers. The amount of collagenic fibers in process of maturing of connecting fabric increases, they get the arranged arrangement in parallel each other, the quantity of glikozaminoglikan and cellular elements decreases, a part of vessels zapustevat and the dense connective tissue hem is formed (tsvetn. fig. 1) with a small amount of cellular elements and vessels, sometimes further with adjournment of salts of lime. Elastic fibers are presented in a hem is very poor in the form of the separate randomly located fibrils, in a large number in the form of the dense networks located between bunches of collagenic fibers. Sometimes the hem, especially on the periphery or around the remained intramural arteries, can include small groups of the remained myocardial cells, is frequent with various manifestations of dystrophic changes. In fields postinfarction To. after extensive heart attacks in the center sometimes sites of a nekrotizirovanny myocardium remain for a long time.
Healing of melkoochagovy myocardial infarctions proceeds similarly, differing in only sizes of the formed hem and speed of its formation.
Postinfarction To. according to the sizes of the postponed heart attack can take all thickness of a myocardium or its separate layers; after repeated heart attacks the extensive hems of different localization, extents isolated or which are closed with each other can be observed. The most frequent localization To. the top of heart, a lobby are, the back wall of a left ventricle, an interventricular partition, papillary muscles is slightly more rare. Postinfarction To. a right ventricle in some cases it is observed along with postinfarction To. a left ventricle, usually being continuation of changes in a left ventricle. The isolated defeat of a right ventricle is observed very seldom. Postinfarction To. auricles it is found, as a rule, along with cicatricial changes in a left ventricle, but usually is not their continuation; isolated postinfarction To. auricles meets seldom.
Heart at postinfarction To. it is increased, his cavities are expanded; on a section in a wall whitish fields of connecting fabric of various extent and a form are visible. Depending on the sizes of a heart attack they can have an appearance of layers or extend to all thickness of a myocardium — a so-called callosity of a myocardium (tsvetn. fig. 4). In the latter case the wall of a ventricle is thinned, a leathery look, sometimes owing to adjournment of salts of lime crackles at a section. As a result of thinning of a wall the so-called internal aneurism of heart which is not changing its outside contours is formed. Cicatricial fields are deprived of sokratitelny ability and under the influence of systolic pressure further can be exposed to stretching with formation of aneurisms («outside aneurism») which sizes can vary over a wide range. The cavity of aneurisms is often executed by the trombotichesky imposings able to be a source of embolisms. After subendocardial myocardial infarctions develops To., localized directly under an endocardium. At extensive defeats such cavity of a left ventricle on a big extent is as if surrounded with a case from cicatricial fabric, with a sclerosis of trabecular muscles, a zapustevaniye of intertrabecular spaces and an obliteration of mouths of the smallest veins of heart (a tebeziyeva of a vein). Small - focal myocardial infarctions lead to formation of hems, number, the sizes and which localization can vary over a wide range — so-called scattered focal To. (tsvetn. fig. 5). It can be formed also in the result of the injuries of a myocardium which are usually followed by a lysis of muscle cells and a collapse of a stroma with the subsequent hyalinosis at the minimum reproduction of stromal cellular elements.
At the stenosing atherosclerosis of coronal arteries of heart the replaceable cardiosclerosis (myofibrosis) arising without focal necrotic changes in a myocardium owing to the gradual, slowly developing dystrophy, an atrophy and death of the separate muscle fibers in connection with a hypoxia and disturbance of metabolism of a myocardium accompanied with diffusion coarsening of a stroma can be also observed. The great value at the same time is attached to the phenomenon of a lymphostasis.
At an idiopathic hypertensia a starting point of development To. the hyperplasia, consensual with a hypertrophy of a myocardium, and coarsening is argyrophil) a framework of a stroma (fig. 1); further there is a formation of collagenic fibers and development of a diffusion myofibrosis. Characteristic of this look To. also existence in a myocardium of microscopic scars is (tsvetn. fig. 2) owing to death of separate myocytes or small groups them.
Miokarditichesky cardiosclerosis — an outcome myocardites (see) infectious and allergic, bacterial or virus etiology, followed by exudative and proliferative processes in a stroma of a myocardium and destructive changes of myocytes. Treats these processes To. after the postponed rheumatism, diphtheria, scarlet fever, infection with Koksaki-virusom or an entsefalomiokarditichesky virus, occasionally a virus of poliomyelitis or smallpox vaccination; an extraordinary rarity is To. after tubercular or syphilitic intersticial myocarditis. Miokarditichesky K. can have character of the diffusion myofibrosis which is localized preferential in a left ventricle and is expressed in widespread coarsening of an argyrophil stroma of a myocardium and formation of collagenic fibers that gives to a stroma a type of a rough lattice, in cells a cut separate muscle fibers or groups them are concluded. Such To. call stromogenny. In case of death of small groups of myocytes there are small scars, or ochazhka To. At diffusion rheumatic intersticial myocarditis with mucoid disorganization of a stroma the diffusion intersticial myofibrosis is observed (tsvetn. fig. 3) and at the same time as an outcome of rheumatic granulomas about vessels arise the oval or star-shaped scars which are an important diagnostic character of rheumatism (fig. 2). To. (a diffusion myofibrosis) it is observed also after allergic myocardites of not clear etiology (Fidler's myocarditis, the allergic myocarditis described by Ya. L. Rapoport).
The cardiosclerosis as a result of cardiomyopathies in the majority of not clear etiology, develops at Frederik's disease, group of muscular dystrophies, a disease of accumulation of a glycogen, a gargoilizm, a family idiopathic heart trouble, a cardiomyopathy of not clear etiology of not hereditary character (a single idiopathic hypertrophy of a myocardium, a congestive and hypertrophic subaortic stenosis, an idiopathic endomyofibrosis and a cardiomegaly of residents of South Africa), and also at the cardiomyopathies connected with a lack of thiamin and hron, poisoning with cobalt. In these cases To. has character of the diffusion myofibrosis sometimes called by a replaceable myofibrosis: fibrous fabric replaces the muscle fibers (fig. 3) dystrophic changed, atrophying and perishing.
By data K. M. Danilova, close koronarogenny and neurohumoral mechanisms are the cornerstone replaceable To. at age involution.
Quite seldom To. it is observed at a bazedovy disease owing to thyrocardiac damage of a myocardium and at a myxedema as an outcome of metachromatic hypostasis of a stroma of a myocardium.
Primary cardiosclerosis as manifestation of a basic disease is observed extremely seldom. Carry to this look To. at some collagenic diseases, at an inborn fibroelastosis owing to a malformation of not clear etiology or the postponed pre-natal endocarditis. However in cases so-called primary To. it is difficult to exclude influence on a stroma of any pathogenic factors.
In experimental conditions To. it is possible to receive in the outcome of metabolic necroses of a myocardium, in particular at an electrolytic and steroid cardiopathy, at animals at contents them on the diet poor in potassium, etc.
the Clinical characteristic of a cardiosclerosis
In a wedge, to practice distinguish atherosclerotic (diffusion or macrofocal postinfarction) and a miokarditichesky cardiosclerosis. A. L. Myasnikov (1965) distinguished three options atherosclerotic To.: ischemic, developing slowly with diffusion damage of a cardiac muscle; postnecrotic (postinfarction) on site former necrosis; transitional, or mixed, at Krom against the background of slow diffusion development of connecting fabric the large fibrous centers after repeated myocardial infarctions are periodically formed.
A wedge, symptomatology atherosclerotic To. the long time can remain scanty. There are no complaints at early stages of its development, and the research of cardiovascular system by physical methods usually reveals insignificant quantity patol, symptoms. At emergence of symptoms of heart failure and arrhythmia change of anatomical structure of heart, sokratitelny function of a myocardium, a rhythm and conductivity is registered.
As a result of development of connecting fabric funkts, requirements to the remained intact fibers of a myocardium considerably increase, there is a compensatory hypertrophy, and then and dilatation of heart. More often the left ventricle of heart increases. At a hypertrophy of heart the diffuse apical beat is noted. Cicatricial processes can cause in the basis of valves in some cases development of an aortal or mitral stenosis or insufficiency of valves of various degree. Disturbance of the movement of shutters of the mitral valve can come owing to cicatricial processes in papillary muscles and tendinous threads.
Auskultativny picture at atherosclerotic To. it is characterized by easing of cordial tones, especially the I tone on a top of heart; systolic noise (see. Cordial noise ) it is listened on an aorta and can have various timbre, up to the aortal valve, very rough at a sclerosis. The systolic apex murmur owing to relative insufficiency of the mitral valve is listened quite often. At development of aneurism in heart the paradoxical pulsation comes to light and sharp systolic noise is listened. The ABP can be raised. On the roentgenogram in perednezadny situation increase in a left ventricle, a top clearly acts to-rogo it is rounded off. At a rentgenokimografiya sites with a reduced amplitude of teeth — postinfarction hems or aneurism of ventricles can come to light. The echocardiography reveals paradoxic movement of an interventricular partition in a systole at localization of aneurism in a partition in the direction from a back wall, but not to it as is normal. During a diastole the partition remains motionless. In cases of aneurism or cicatricial changes of a back wall of a left ventricle sometimes it is possible to write down paradoxic movement in a systole or asistolichesky segments, and also a hyperkinesia of a partition (fig. 4). Apply ultrasonic scanning to identification of localization and volume of affected areas of a myocardium. The volume of information considerably increases at use of sectoral scanning. Registration in the mode of real time scale, the two-dimensional image of structures of heart facilitate identification of cicatricial changes in area of a top (fig. 5) and a front wall, usually recognizable hardly.
The circulatory unefficiency develops as a result of decrease in sokratitelny function of heart. Important and its early manifestation is asthma (see), tachycardia (see), in the beginning appearing at or after loading, and then and at rest. The liver increases, hypostases of legs, an edema of cavities come to light later (see. Swelled ). Against the background of hron, circulatory unefficiencies at atherosclerotic To. the acute heart failure can develop.
Disturbances of a rhythm and conductivity — a ciliary arrhythmia, premature ventricular contraction, blockade of different degree and various sites of the carrying-out system — frequent and essential symptoms atherosclerotic
K. Klien, manifestations miokarditichesky To. vary depending on etiol, forms of myocarditis, it morfol. features and with the known difficulty are differentiated with hron. and long myocardites (see). For miokarditichesky To. infectious diseases in the anamnesis, existence hron are characteristic, the centers of an infection, the young age of patients, on an ECG of change of diffusion character or preferential right ventricle is more often. Disturbances of a rhythm and conductivity meet more often than symptoms of heart failure. Differential diagnostic characters atherosclerotic and miokarditichesky To. are presented in the table.
Treatment of patients atherosclerotic To. includes the actions normalizing lipidic exchange, coagulant system of blood, elimination of a circulatory unefficiency, disturbances of a rhythm and conductivity. Treatment miokarditichesky To. consists in elimination of infectious process in a myocardium if it is not complete; careful sanitation hron, the centers of an inflammation is made. In the absence of inflammatory process treatment miokarditichesky To. does not differ from treatment at atherosclerotic To.
the Forecast is defined by extensiveness of damages of a myocardium, and also existence and a type of disturbances of a rhythm of reduction of heart and conductivity. At melkoochagovy To. and absence of arrhythmias the forecast is quite favorable: at extensive cicatricial fields and diffusion To. with development of heart failure, tolerant to treatment — the forecast bad. Existence of ventricular premature ventricular contraction, ventricular tachycardia and disturbances of atrioventricular conductivity is fraught with danger of sudden death.
Table. Some differential diagnostic characters of an atherosclerotic and miokarditichesky cardiosclerosis
Bibliography: Vikhert A. M. Atherosclerosis of coronal arteries and a coronary disease of heart, Rubbed. arkh., t. 45, No. 12, page 107, 1973; Sudden death at acute coronary insufficiency, under the editorship of. I. K. Shkhvatsabaya and M. E. Rayskina, page 19, M., 1968; Galakhov I. E. Heart attack and cardiosclerosis of a right ventricle of heart, Arkh. patol., t. 34, No. 6, page 39, 1972; Gasilin V. S. Chronic forms of coronary heart disease, page 61, M., 1976, bibliogr.; Danilova K. M. Cardiosclerosis and aging, Arkh. patol., t. 36, No. 5, page 12, 1974; The Myocardial infarction, under the editorship of E. I. Chazov, page 5, M., 1971; Butchers A. L. Ateroskleroz, M., 1960, bibliogr.; Smolyannikov A. V. and H and d-dachina T. A. Morfogenez of a cardiosclerosis at chronic coronary insufficiency, Arkh. patol., t. 32, No. 2, page 14, 1970; Hodzhayeva D. Yu. Change of auricles at a myocardial infarction and a postinfarction cardiosclerosis of a left ventricle of heart, Cardiology, t. 14, No. 10, page 94, 1974; Shkhvatsaby I. K. Coronary heart disease, M., 1975; Arteriosclerosis, v. 1 — 2, Washington, 1971; Cardiomyopathies, ed. by E. Bajusz a. o., Lancaster, 1973; Hudson R. E. B. Cardiovascular pathology, L., 1965; Pathology of the heart and blood vessels, ed. by S. E. Gould, p. 601, 723, Springfield, 1968, bibliogr.
A. M. Vikhert; H. M. Mukharlyamov, R. A. Charchoglyan (cards.).