ENDOKARDYT (endocarditis; Greek endon inside + kardia heart + - itis) — an inflammation of an endocardium
(an internal cover of heart). The inflammation can preferential be localized in the endocardium covering a cavity of ventricles or auricles (parietal, pristenochny E.), covering papillary (papillary) muscles (trabecular E.)? forming chords (chordal E.), or, most often — on shutters of valves of heart (valvulitis) that usually leads to formation of valve defects (see the Heart diseases acquired). The term «endocarditis» entered Zh. Buyo in 1836 into a wedge, terminology.
In most cases E. is not an independent disease, and represents private manifestation of damage of heart at various noninfectious and infectious diseases, and also at injuries. A tendency to consider E. infectious, including virus and fungal, the origin under one general name «infectious endocarditis» does not correspond to a nosological orientation and reflects only its most general division on an etiology on infectious and noninfectious. In the international statistical classification of diseases (1975) endocarditises are included in headings of those diseases, at to-rykh they are observed (rheumatism, viral diseases, a meningococcal infection etc.), except for acute and subacute bacterial E., presented under one heading as an independent nosological form. Nek-ry clinical physicians consider acute bacterial E. within the general sepsis (see), but isolate as a separate nosological form subacute bacterial E. (see the Endocarditis bacterial subacute). The last, as well as in general any infectious E., it is accepted to subdivide on primary, i.e. developed in an intact endocardium, and secondary — arisen against the background of the available heart disease, napr, inborn, rheumatic.
Most often E. it is caused by active rheumatism (see), at Krom it is observed in 80 — 90% of cases and is a basis of formation of rheumatic heart diseases. Quite often E. arises also at other collagenic diseases (see), in particular at a system lupus erythematosus (see) — a so-called endocarditis of Libma-na — the Saxophone, at a pseudorheumatism (see). Infectious E. arises owing to implementation in an endocardium of usually nonspecific bacterial or fungal flora or a virus (e.g., Cox-ki virus); its development is often promoted by existence of the inborn or acquired heart diseases and change immunol. reactivity of a macroorganism. Also exceptional cases specific infectious E are described. at tuberculosis, syphilis. Various forms aseptic E. develop at an injury of an endocardium, influence of endogenous or exogenous toxicants, substrates of allergic reactions, at autoimmune damage of an endocardium. Among noninfectious E. consider also nek-ry defeats of an endocardium with adjournment on it of fibrin and trombotichesky masses owing to hemocoagulative disturbances at poorly expressed inflammatory reaction. Such E. arises at the diseases which are followed by a cachexia (not bacterial tromboticheskiya E., or so-called cachectic E.), sometimes at a myocardial infarction (see). Possibility E is noted. at a carcinoid syndrome owing to long impact on an endocardium of active humoral substances (serotonin, kinin) cosecreted by a tumor (see Carcinoid). In the outcome of it E. formation of the combined heart disease — insufficiency of the three-leaved valve and a stenosis of the mouth of a pulmonary trunk was observed. The etiology of nek-ry forms of defeat of an endocardium remains obscure. It belongs, in particular, to a so-called fetalis (inborn) endocarditis (see the Fibroelastosis of subendokardialniya) and fibroplastic parietal E. with an eosinophilia (an eosinophilic endocarditis of Leffler).
Pathogeny E. in the fundamental units matches a pathogeny of an inflammation (see) — infectious, aseptic (depending on an etiology), including allergic, including special types of an inflammation on an immune basis at rheumatism (see) and other collagenic diseases.
To change immunol. significance in a pathogeny practically of all forms E is attached to reactivity of an organism. An inflammation of an endocardium at collagenic diseases, an eosinophilic endocarditis of Leffler, infectious and allergic myocarditis and Abramov's myocarditis — Fidlera (see Myocarditis) belongs to allergic on the essence. The general in a pathogeny E. at these diseases the damage of fabric structures of an endocardium by cell-bound immune complexes or sensitized immunocompetent cells which is followed by emergence of an immune inflammation is. The last develops as giperergichesky reaction of the immediate or slowed-down type; change or a combination of types of reaction on process patol are possible. process. The role of immune disturbances and in a pathogeny infectious E is proved. (see the Endocarditis bacterial subacute).
In a basis morfol. changes at E. processes of disorganization of connecting fabric, dystrophy of an endothelium, inflammation, thrombosis, the organization of blood clots and a sclerosis of a pristenochny endocardium and valves of heart lie. Defeat of any valve, but most often is possible, especially at rheumatism, mitral and aortal valves are surprised.
Valve E. it is characterized by a combination of alterativny, exudative, trombotichesky and proliferative processes. Alterativny changes consist in dystrophy, a necrobiosis and a necrosis, disorganization of connecting fabric of valves (mucoid and fibrinoid swelling, a fibrinoid necrosis), desquamation of an endothelium, various on extent of manifestation. The expressed al-terativno-necrotic changes can lead to formation of aneurisms and ulcers on the surface of valves, perforation of shutters and even to their final fracture. The exudative component of an inflammation is expressed at valve endocarditises rather poorly because valves are presented by avascular braditrofny connecting fabric. However are possible treatment of fabric a blood plasma, inflammatory infiltration by its cells.
The thrombogenesis on the surface of valves with polypostural (warty) imposings (thrombendocarditis) is connected with destruction of an endothelium and surface layers of fabric. Proliferative processes are shown by reproduction of endothelial cells, histiocytes (macrophages) and proliferation of fibroblasts, to-rye grow into trombotichesky imposings (the organization of blood clots). At the same time granulyatsionny fabric with neogenic vessels can form. Dominance of productive changes leads to bystry development of a sclerosis of valves with deformation of their shutters.
Degree of manifestation of the described changes and a ratio among themselves define them morfol. picture of an endocarditis. A. I. S I rub k,
V. V. Serov (1979) allocate the following anatomic forms E.: diffusion, acute warty, returnable and warty, acute ulcer, polipozno-ulcer, fibroplastic.
The diffusion endocarditis (a simple endocarditis, according to A. I. Abrikosov, or deep a valve of litas, according to V. T. Talalayev) meets almost only at rheumatism. Changes are characterized by mucoid and fibrinoid swelling of shutters of the valve and fibrous rings without defeat of an endothelium and adjournment of fibrin. Cellular reaction is shown in the form of accumulation of histiocytes (macrophages) and proliferation of fibroblasts; histiocytes in a pristenochny endocardium often take the form specific ashoff-tala-layevskikh of granulomas (see Rheumatism), in shutters of valves atypical granulemopodobny infiltrates meet more often. The described changes find generally in podendo-telialny and superficial elastic layers of an inner surface of valves ^желудочковой — in the valve of an aorta, atrial — at the mitral valve), but often process takes also deeper elas-ticheski-fibrous and fibrous layers of valves. Externally the endocardium of valves is changed a little: the uneven thickening of shutters, especially through short circuit of valves is noted, to-rye become translucent. More often changes come to light only microscopically. Outcomes diffusion E. are various. Are possible full reversibility of process (at mukotsdny swelling), the hyalinosis of connecting fabric of the valve developing as a result of fibrinoid changes and leading to a thickening of shutters without their deformation, the sclerosis of valves which is a consequence of active cellular proliferation and a kollagenogenez. The sclerosis defines transition of a diffusion endocarditis to fibroplastic and leads usually to deformation of valves and rheumatic heart disease.
The acute warty endocarditis, or thrombendocarditis, often happens at rheumatism, and also is observed at a system lupus erythematosus, intoxications, an injury of an endocardium, at nek-ry inf. diseases, napr, at scarlet fever, diphtheria, pneumonia, quinsy, belly and sypny typhus, tuberculosis, syphilis (at such E. the corresponding activator from blood and valves is sowed very seldom that testifies rather to the toksiko-allergic nature E.), sometimes and at sepsis, especially at initial forms, an easy current or timely and vigorous treatment by antibiotics. At rheumatism along with disorganization of connecting fabric, especially subendothelial layer, there is a destruction of an endothelial vystilka in this connection on the surface of valves turned to a blood flow, there are trombotichesky warty imposings in the form of grayish translucent small as grains of sand, are more rare than the warts which are located in one row through short circuit — at the basis of shutters or in a middle part of their surface. These imposings easily are removed a knife. Further they increase in volume, often form conglomerates in the form of clusters, a beads, nipples, polyps (a polypostural endocarditis). More deeply the lying imposings are fixed to an endocardium and separate hardly. If damages of valves were superficial, then as a result of reparative processes on them there are only small fibrous thickenings. More often, however, the progressing sclerosis leads to a considerable thickening, shortening and an union of shutters with disturbance of functions of valves (a stenosis or insufficiency), a cut
is quite often aggravated with a thickening, consolidation and accretion of tendinous chords of valves. Parietal warty E. it is usually observed in the presence of valve E., very seldom separately. Most often it develops in a left ventricle and in the left auricle and differs from valve in vascular reaction in the form of a hyperemia and neutrophylic infiltration. In its outcome there are whitish thickenings of an endocardium. At a system lupus erythematosus unlike rheumatic E. trombotichesky imposings are located not on the line of a smykaniye of shutters, and on both of them surfaces otstupya from free edge or at the basis of shutters. Imposings wider and flat, than at rheumatism. Microscopically in the centers of damage gematoksilinovy little bodies (the remains of nuclear material), characteristic of a lupus erythematosus, are found. Toxic (including cachectic, or marantic) E. usually have superficial character with preferential defeat of an endothelium and formation of warts.
Returnable and warty endocarditis, i.e. repeated rheumatic E. against the background of already sclerous the changed and deformed valves, arises at an exacerbation of rheumatism. The new centers of disorganization, a granulomatosis, damage of an endothelium and trombotichesky imposings on the surface of valves with the subsequent their organization come to light that leads to progressing of heart disease.
The acute malignant endocarditis, as a rule, is acute infectious E. Morfologicheski's expression it is characterized by dominance of alterativny (destructive and necrotic) processes with formation of ulcers, sometimes in combination with the expressed trombotichesky changes (acute polipozno-yazven-ny an endocarditis). At the beginning of process at the edges of shutters the lurid plaque is visible, during the stripping to-rogo minor defects of fabric — an ulcer and an uzura are found. Further ulcer defects extend in breadth and deep into, at their edges and day imposings of trombotichesky masses, in one cases insignificant, in others — in the form of plentiful polypostural growths appear. Process of destruction causes developing of eminating aneurisms of shutters, their perforation or gaps. Transition of ulcer process to tendinous chords leads to their gap, and on a pristenochny endocardium — in rare instances to development of ulcer aneurism of a wall of heart and even to its gap. At microscopic examination the extensive fields of a necrosis of shutters delimited by accumulation of the leukocytes migrating from vessels of the basis of valves are found. Extent of leukocytic infiltration is various — from total absence of neutrophils before diffusion infiltration. In necrotic and trombotichesky masses numerous colonies of microbes are visible. Reproduction of histiocytes and fibroblasts for an acute malignant endocarditis malokharakterno. If process does not pass into a subacute or long form, then its stop with a gradual rassasyvaniye and the organization of trombotichesky masses, scarring and wrinkling of shutters is possible.
The Polipozno-malignant endocarditis develops, as a rule, at a subacute (long) form of infectious E. V zones of defeat of an endocardium trombotichesky imposings, usually massive, being in different phases organizations come to light. Under them it is frequent, as well as at acute
E., the ulcer valvulitis (more often than the valve of an aorta) with various extent of defeat of shutters, including their perforation and aneurisms, the necrotic centers in trabeculas, sometimes in a parietal endocardium is found. Unlike acute E. around the centers of a necrosis cellular infiltrates are always visible. Since 70th, according to V. V. Serov with sotr. (1982), the frequency of detection of destruction of valves at this form E. decreases a little.
The fibroplastic (fibrous) endocarditis usually meets at rheumatism as an outcome diffusion acute or returnable borodavcha - that E., quite often from the very beginning the productive component of an inflammation which is characterized by dominance and the strengthened fibrosis of shutters. Microscopically along with proliferation of fibroblasts and a sclerosis it is possible to see the centers of disorganization, histiocytic and lymphoid infiltrates. Fibroplastic type E. it is characteristic also for E. at a carcinoid syndrome and for parietal eosinophilic fibroplastic E. Posledny is usually combined with eosinophilic myocarditis and eosinophilic infiltrates in different fabrics. In an acute stage the thickening of an endocardium with a mural thrombosis, in chronic — the progressing fibrosis is observed. Sometimes valves are involved in process.
Wedge, manifestations E. at various diseases have similar symptoms of defeat of the valve device of heart and the general tendency to tromboembolic episodes, but differ in the features determined by a picture and a pathogeny of a basic disease. The subacute bacterial endocarditis and a rheumatic endocarditis are described in the articles Endocarditis bacterial subacute (see) and Rheumatism (see). Besides, allocate acute infectious
E., the endocarditis caused by fungi, a fibroplastic endocarditis of Lef-flera and not bacterial tromboticheskiya E.
The acute infectious endocarditis is shown by a picture of the general sepsis caused, as a rule, by virulent flora — golden staphylococcus, a piogenic streptococcus, gram-negative bacteria, etc., and entrance infection atriums often are found (the injured skin or mucous membranes, inf. the center in lungs, an urinogenital path, etc.). High fever (the wrong type or gektichesky), the fever, perspiration, symptoms of the general intoxication with defeat of c are typical. N of page. The embolism in various bodies with development of the suppurative metastatic focuses is often observed. Increase in a liver and spleen, signs of damage of kidneys up to a picture of apostematous nephrite are usually noted. The diagnosis is confirmed at identification of signs of defeat of valves of heart with their insufficiency. Unlike subacute bacterial E. at acute infectious E. often intact valves, hl are surprised. obr. three-leaved and a pulmonary trunk, aortas are more rare. In blood the high leukocytosis with shift to the left and anemia, considerable acceleration of ROE usually comes to light. Major importance in treatment acute infectious E. the antibacterial therapy which is carried out by the general rules of treatment of sepsis (see) taking into account the installed activator has. If not Eden's activatortifitsirovan, it is reasonable to begin therapy with purpose of high doses of sodium salt of benzylpenicillin (60 OOO OOO — 80 OOO OOO ED a day) or on l at synthetic penicillin (ampioks 12 — 15 g a day) in combination with gentamycin (3 — 5 mg on 1 kg of body weight a day). At E. a staphylococcal etiology apply antistafilo-coccal plasma (6 — 8 injections on 200 ml of 1 times a day or every other day), immunoglobulin human antistaphylococcal (at the rate of 10 ME on 1 kg of body weight a day). At development of bacterial shock apply glucocorticoids. Carry out disintoxication therapy, correction of disturbances of electrolytic composition of blood. If necessary perform operational treatment primary and metastatic suppurative focuses.
The endocarditises caused by fungi — sorts Candida, gistoplazmy (is more rare a blastomyces, koktsidoida and cryptococci), are observed by aspergilla sometimes at persons, is long receiving antibiotics and corticosteroids, at undergone a heart operation, at the addicts entering to themselves drug intravenously. At the same time not only aortal and mitral valves, but also three-leaved often are surprised, and the operated patients have a fitted a prosthesis valve. Wedge, picture fungal E. usually that corresponds at a subacute bacterial endocarditis (see the Endocarditis bacterial subacute). Along with fever, emergence or change of noise of heart, existence of a gepatosplenomegaliya, defeat of a nervous system thromboembolisms with obstruction of large vessels of extremities are often noted. Recognition of an etiology of this endocarditis presents great difficulties. Inefficiency of antibiotics, the progressing aggravation of symptoms in the absence of acceleration ROE, a uveitis or an entophthalmia can give the grounds for the assumption of existence E., caused by fungi. Allocation of fungi from blood presents great difficulties and it is possible seldom, even during the use of special methods. Treatment of endocarditises of a fungal etiology is carried out by Amphotericinum In and other fungistatika (see. Antifungal antibiotics, Antifungal means). Cases of successful operational treatment of patients are described, at to-rykh the artificial valve struck with a fungus of a sort Candida was removed.
The fibroplastic parietal endocarditis with an eosinophilia (W. Loeffler's endocarditis) is characterized by defeat of a parietal endocardium with the expressed fibrosis and its thickening that breaks distensibility of cameras of heart and leads to development of heart failure. The disease is followed by a high eosinophilia in blood, and also development of widespread eosinophilic vasculites in skin, muscles, internals. The disease is for the first time described in 1936 by W. Loeffler and belongs to rare. Its etiology is unknown. It is suggested that W. Loeffler's endocarditis and endomyocardial fibrosis described in 1948 by Davis (D. Davis) eurysynusic in nek-ry districts of South Africa, represent a uniform form of pathology. In a pathogeny of a disease disturbances immunol are of great importance, apparently. reactions what points frequent detection at patients of decrease in a caption of a complement, LE cells, change of level of immunoglobulins to. The wedge, a picture differs in the expressed polymorphism. The high eosinophilia in blood happens quite often first display of a disease, are possible the expressed fever (at an acute current), thromboembolisms of vessels of different areas. Signs of damage of heart, in particular emergence of cordial noise owing to defeat of tendinous chords or formation of insufficiency of mitral, are more rare three-leaved, the valve, come to light in the first weeks of a disease, but can appear also only in several months. In the subsequent the disease is characterized by the accruing heart failure, refractory to cardiac glycosides, a high eosinophilia. At the same time the damage of skin, muscles, kidneys, a liver, lungs caused by development in them eosinophilic vasculites can be observed (so-called eosinophilic collagenoses). The diagnosis comes easy when against the background of a hypereosinophilia signs of damage of heart with development of heart failure come to light. At the acute course of a disease the differential diagnosis is carried out with a nodular periarteritis which quite often (especially in case of damage of lungs) proceeds with a hypereosinophilia (see the Periarteritis nodular). Diagnosis of the last is helped by detection of paresis of motor peripheral nerves, signs of damage of kidneys, large arteries, to arterial hypertension. At a hypereosinophilia often there is a need of an exception of parasitic diseases — cmrongiloidoza (see), an opisthorchosis (see), a fascioliasis (see). Treatment of an endocarditis of W. Loeffler consists in prolonged use of glucocorticoid hormones, and in nek-ry cases and tsitostatik. During the developing of heart failure use of cardiac glycosides and diuretics is shown. At the expressed fibrosis of an endocardium in late stages of a disease cardiac glycosides are ineffective and often cause disturbances of a rhythm. In an end-stage also glucocorticoids are inefficient; treatment is limited generally to purpose of the mode with a minimum of physical activity.
Not bacterial trombotichesky endocarditis (not bacterial thrombosis of an endocardium) described also under the names «terminal endocarditis», «marantic endokar * dit», «cachectic endocarditis», «degenerative and warty endocarditis» is caused by widespread intravascular coagulation and adjournment of fibrin on valves of heart in the form of the warts of various form consisting of thrombocytes, fibrin and free of bacteria. The size of warts fluctuates from
2 — 7 mm to several centimeters. Inflammatory reaction in fabric of the valve is almost absent in this connection nek-ry pathologists consider the name «endocarditis» insufficiently op» ravdanny. Trombotichesky E. arises more often at patients with the serious illness which is followed by a cachexia: at malignant tumors (is more often in late stadiyakht already at development of metastasises) hron. leukoses, cirrhosis * hron. nephrites. Sometimes such E. arises also at acute diseases, napr, at pneumonia, a rupture of an aortic aneurysm, peritonitis. More often valves of an aorta and mitral are surprised. Trombotichesky E. can be suspected at emergence of the systolic apex murmur or an aorta observed almost at a half of patients. Fervescence (to subfebril-ache), acceleration of ROE is noted seldom. The separation of trombotichesky masses from the surface of the valve and an embolism in an artery of a big circle of blood circulation is in some cases observed. Disturbance of passability of an artery can be caused also by primary thrombosis in connection with hypercoagulation. Treatment and prevention come down to use of antiag-regant or anticoagulants.
Forecast E. depends on extent of defeat of an endocardium, especially valve device, and also timeliness of treatment.
Prevention matches prevention of those diseases, at to-rykh the inflammation of an endocardium is observed. Prevention of a bacterial endocarditis — see the Endocarditis bacterial subacute.
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