[Diabetic cardiomyopathy. Pathophysiology and clinical implications].

The accumulating body of data indicate that the occurrence of diabetic cardiomyopathy is an independent phenomenon from macroangiographic changes in coronary arteries and hypertension. Results from animal studies, human histological results and clinical observations provided support for this phenomenon. Although the clinical symptoms have been identified, however, the pathogenesis of diabetic cardiomyopathy is uncertain. The definition of diabetic cardiomyopathy describes both specific defects in the myocytes from diabetics and associated changes in the heart which have developed during the course of diabetes. The following defects in myocytes have been identified and are postulated to contribute to diabetic cardiomyopathy: The changes in carbohydrates metabolism, in fatty-acid metabolism, calcium and potassium transport, microvascular narrowing and micro aneurysms, hypertrophy, defects in collagen structure, myocardial fibrosis and perivascular fibrosis, abnormalities in conducting system, the decrease in the function of autonomic nerves. The clinical presentation of diabetic cardiomyopathy lead to the description of two phases of the disease. First, asymptomatic diabetic subjects with subclinical abnormalities of the left-ventricular diastolic function, measured by Doppler echocardiography. In the second phase--clinically evident diabetic cardiomyopathy is described by congestive cardiac failure without evident arteriosclerotic changes in coronary arteries and hypertension. Diabetic cardiomyopathy can be diagnosed early after the onset of diabetes mellitus and is independent phenomenon from late diabetic complications. The main cause of mortality in diabetic subjects is largely due to macroangiopathic changes in the coronary arteries (evaluated by coronarography), not the heart failure.