[Cardiac syndrome in opisthorchiasis].
According to the intensity and duration of invasion, superinvasion opisthorchiasis in laboratory animals and human beings involves all cardiac layers; the myocardium is mostly damaged. In its early phase, vascular inflammation of the microcirculatory bed, dystrophy, necrosis of striated muscle fibers progressing to diffuse cardiosclerosis result from abnormal immunological processes; due to reflex exposures (Botkin's syndrome), there may be persistent cardialgias that may progress to the clinical manifestations of chronic ischemic heart disease. Unpredictable dissipative clusters of metabolic Opistorchis may predispose to different forms of myocarditis progressing to focal and diffuse cardiosclerosis. In these cases, the death of patients with superinvasion opisthorchiasis results from acute or chronic heart failure. Dehelmintization in these patients fails to eliminate myocardial changes (cardiosclerosis) that further determine the clinical presentation of cardiac pathology.
Krylov
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D000818:Animals; D009202:Cardiomyopathies / Q000209:etiology* / Q000469:parasitology / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology; D006224:Cricetinae; D004195:Disease Models, Animal; D018450:Disease Progression; D006801:Humans; D018485:Muscle Fibers, Skeletal / Q000473:pathology; D018482:Muscle, Skeletal / Q000473:pathology; D009205:Myocarditis / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D009336:Necrosis; D009889:Opisthorchiasis / Q000150:complications*; D009891:Opisthorchis; D012598:Sclerosis / Q000473:pathology; D013577:Syndrome