The use of insulin by diabetics has largely removed the threat of death from 
ketotic coma but cardiovascular dysfunction remains a major cause of death in 
patients with diabetes. Recent research has indicated a generalized membrane 
defect, which may cause abnormalities of calcium metabolism in nerves, cardiac 
and smooth muscle as well as endothelial cells and thus may lead respectively to 
the development of neuropathy, primary cardiomyopathy, microangiopathy and 
atherosclerosis in the diabetic population. Each of these pathogenic processes, 
which are associated with insulin deficiency, alone or in combination with 
others, may result in cardiac dysfunction in chronic diabetes. Activation of the 
sympathetic nervous system and abnormalities in catecholamine metabolism have 
been identified in diabetes; their involvement in the genesis of cardiac pump 
failure as well as large and small vessel disease is likely. The membrane 
defects as indicated by changes in both plasma membrane and glycocalyx in 
diabetic cardiomyopathy appear to be complex and may involve alterations in the 
metabolism of lipids and pyrimidine nucleotides. It seems that intracellular 
calcium overload is intimately involved in the development of diabetic 
cardiomyopathy; however, a concentrated research effort is required to 
understand the primary biochemical lesion in the pathogenesis of cardiac 
dysfunction in diabetes. In the meantime, a heightened awareness on the part of 
clinicians concerning the susceptibility of diabetic patients to cardiovascular 
problems may help in reducing mortality and morbidity in the diabetic 
population.