ABSTRACT
The pathogenesis of diabetic cardiomyopathy is uncertain; however, small vessel disease and/or a direct myocardial effect of diabetes have been postulated. T. J. Regan et al. demonstrated increased interstitial glycoprotein and collagen in the hearts of diabetic dogs, a finding which correlated with a diminished left ventricular compliance. Biochemical studies showing unchanged collagen formation in the hearts of streptozotocin-induced diabetic rats are also available in the literature. Various investigators have reported ultrastructural alterations in hearts from a wide variety of experimental models of diabetes18–25 and the observations have established the occurrence of cardiomyopathy in conditions of poorly controlled diabetes. Diabetes mellitus in man has been shown to be associated with an increased incidence of congestive cardiomyopathy independent of coronary artery disease and atherosclerosis. On the basis of extensive studies carried out by many investigators, it is possible to propose a membrane hypothesis to explain the mechanisms responsible for the development of cardiomyopathy in uncontrolled chronic diabetes.
