Rheumatic endocarditis

Lately there has been more favorable course of rheumatic fever in children (3. I. Edelman, 1962; O. D. Sokolov-Ponomareva, 1965; A. C. Dolgopolova, 1977, and others), rarely began to experience severe heart failure as pancarditis. There are some peculiarities in the course of rheumatic endocarditis.
Currently there is a trend towards less frequent formation of rheumatic heart diseases, representing the outcome of endocarditis. Even according to A. B. Volovik, related to 1965, during the last 5 years rheumatic heart disease after primary endocarditis are formed 4.5 times less than in previous years.
Primary endocarditis rarely develops in the 1st attack of rheumatism, which contributes to a lower frequency of education after her heart diseases (11% according to A. B. Volovik, 1965; in 14%according to A. C. Dolgopolova, 1969; 14.4%-by L. M. Anikanova, 1970). Recurrent rheumatic endocarditis, where there are more significant defeat of the endocardium, also recently rarely leads to the formation of heart disease : according to O. D. Sokolova-Ponomareva (1969), this form of endocarditis heart disease is formed in 50% of children, whereas in the 50-ies it was formed in 65-80% (A. N. Volovik, 1965, and others).
The inflammatory process in rheumatoid arthritis most often localized in the field of valves (valve endocarditis). The defeat of the other departments of the endocardium is less common. The valves are most often suffers mitral (almost 100%). The defeat of the aortic valve is observed much less often, but recently the aortic valve endocarditis began to meet more often. According to 3. A. Tatochenko, Etc. Churakova (1970), frequency of lesions aortic valve among patients with rheumatic endocarditis in the period of 1959-1965 was 4.5%, while in the period from 1965 to 1968 increased to 9.4%. According to our data, the frequency of lesions endocardial aortic valve patients with rheumatism and treated in the cardiological Department of the hospital. K. A. in St Petersburg in 1971 - 1973, was 12%.
Currently has adopted the following classification of rheumatic endocarditis:
I. Clinical characteristics of the process:
1. Endocarditis primary (if possible it is desirable to specify the localization process).
2. Endocarditis return (without blemish valves, Vice valves).
II. During the process: acute, sub-acute; slow, prolonged; continuously relapsing; latent.
As for pathological changes of the endocardium rheumatism, they occur as warty endocarditis and valvulitis.
Warty endocarditis is manifested by the formation of surface valves small, irregular warts red-grey, with a diameter from 0,5 to 2 mm Warts usually tight valve, often have the form of a solid scallop, located in the place of the greatest trauma valve along the line of its closure. Used to think that rheumatism in the surface layers of the valve occurs necrosis of the endothelium, the damaged places deposited masses of fibrin and platelets, which form the warts. Then it was found that in rheumatic endocarditis there defeat of collagen tissue valve in the form muhidnova swelling and fibrinoidnogo necrosis. Modified swollen tissue valve rises in the form of fibers above its surface, and these fibers is the deposition of fibrin and platelets. Thus, in the pathological process involved not only the endocardium, but all of the valve.
In those cases when along with the loss of surface endocardium rheumatism involved in a pathological process and the basis of connective tissue valve, rheumatic the defeat of the latter is termed "valvula" (I. I. Talalaev, 1930; M. A. Skvortsov, 1946; A. I. Strukov, 1968; B. the Ionas, 1960). In connective tissue valve develops typical for rheumatism process consisting of the following stages: initial disorganization of the connective tissue in the form muhidnova swelling, which is reversible - if it, according to A. I. Strukov I A. G. Beglaryan (1963), you may complete recovery; phase fibrinoid representing more pronounced degree of disorganization of the connective tissue (if rheumatic process does not progress further, the outcome of fibrinoid is sclerosis); phase proliferation, when a rheumatic granuloma and phase scarring. In the result of scarring valves are deformed and cannot close the valve hole; developing their failure, shutters can tie between themselves, which makes stricture formation of the hole. Rheumatic endocarditis bacteria in infected valves are normally not found (G. F. LPG, 1958; C. S. Nesterov, 1974).
On autopsy findings M. A. Skvortsova (1946), in childhood diffuse rheumatic valvular is the main form of rheumatic endocarditis and occurs almost 100%.
Rheumatic endocarditis generally, the process involved the limited territory, there is often a defeat of one or two valves, chords, and so on, that enables in a clinical diagnosis detailing the location of endocarditis (for example, autokarta mitral valve, hordit and so on).
Endocarditis rheumatism is not isolated, but is almost always combined with myocardial damage and less pericardium.
The combination of endocarditis with other heart disease makes it difficult diagnosis. Particularly complex diagnostics with sluggish, latent period of rheumatic endocarditis.
Morphological inflammatory changes in rheumatic endocarditis develop over a long period of time (1-2 years).

  • Clinic of rheumatic endocarditis