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Introduction. The concept of diabetic cardiomyopathy was first proposed by S. Rubler et al. more than 100 years ago, but this diagnosis іs rarely used by clinicians because of the existence of such co-morbidities as ischemic heart disease and arterial hypertension in those patients. Different mechanisms have been implicated in the pathogenesis of diabetic cardiomyopathy, however its specific features are not revealed till now. The aim of the investigation was to reveal the ultrastructural features of cardiomyocyte remodeling, typical for diabetic cardiomyopathy in the cases of concomitant ischemic heart disease and arterial hypertension. Material and methods. Ultrastructure of express-necropsies and intraoperative myocardial biopsies of 25 patients suffering from diabetes mellitus, arterial hypertension and different forms of ishemic heart disease were examined. Results. The ultrastractural mechanisms of cardiomyocyte hibernation, specific for diabetic cardiomyopathy, in comparison with changes characteristic for ischemic heart disease and arterial hypertension, were revealed. Cardiomyocyte hibernation in the cases of diabetes mellitus emergences on the early stages of the illness, prior the appearance of arterial hypertension and ischemic heart disease which cause predominantly their hypertrophy and stunning. Conclusions. Diabetic cardiomyopathy is a consequence of dysmetabolic and microcirculatory disorders causing cardiomyocyte hibernation. Decompensation of diabetes mellitus and the presence of ischemic heart disease or arterial hypertension are the main triggers of diabetic cardiomyopathy development. Hibernated cardiomyocytes die due to apoptosis or secondary necrosis transforming diastolic dysfunction of the left ventricle, typical for diabetes mellitus, into systolic type.
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