Degeneration of cardiac muscle followed by cell transformation, regeneration and fibrogenesis in rheumatic fever.
In acute rheumatic fever, various types of myocardial degeneration and subsequent transformation of the damaged muscle fibers into a variety of cells, classified and unclassified, are described from microscopic examination of autopsy specimens. This study suggests that in the origin of Aschoff bodies, the diagnostic feature of rheumatic fever, there are three different pathways (Types A, B and C) for cytogenesis of Aschoff cells from altered muscle fibers. Type A cytogenesis takes place through the stage of Anitschkow myocytes of cardiac muscle origin (McDONALD 1963), and the Type B pathway, through the stage of dedifferentiated cells arising in lysing cardiac muscle fibers. These dedifferentiated cells with capacity for regeneration of regular cardiac muscle fibers (McDONALD 1975), show abortive or atypical development of muscle cells through the Aschoff cell stage. The Type C cytogenesis of Aschoff cells takes place through direct transformation of cardiac muscle fibers which show central hyalinization of myoplasm and changes in nuclei from normal to single or multinucleated large vesicular forms. The fibrinoid material of Aschoff bodies is shown to be the product of muscle origin. The mechanism of formation of fibrous scars in the myocardium and fibrous thickening of subendocardium are explained on the basis of fibrous transformation of cardiac muscle. Altered muscle fibers have been shown to give rise to cells which simulate inflammatory cells and others which cannot be classified.
D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D005260:Female; D006321:Heart / Q000502:physiology; D006801:Humans; D008297:Male; D009206:Myocardium / Q000166:cytology / Q000473:pathology*; D012038:Regeneration; D012214:Rheumatic Heart Disease / Q000473:pathology*; D012215:Rheumatic Nodule / Q000473:pathology*