Cardiovascular manifestation of diabetes has remarkable therapeutic and prognostic implications. Diabetic cardiomyopathy is a distinct heart muscle disease in patients with well-controlled diabetes mellitus that cannot be ascribed to coronary artery disease, hypertension or any other known cardiac disease. It is characterized by left ventricular diastolic dysfunction that can be detected in 52-60% of well-controlled type II diabetic subjects using contemporary Doppler techniques. Pathophysiologically, hyperglycaemia causes myocardial necrosis and fibrosis, as well as the increase of myocardial free radicals and oxidants, which decrease nitric oxide levels, worsen the endothelial function and induce myocardial inflammation. Insulin resistance with hyperinsulinaemia and decreased insulin sensitivity are responsible for left ventricular hypertrophy. Clinical manifestations of diabetic cardiomyopathy are dispnoea, arrhythmias, atypical chest pain or dizziness. The treatment of diabetic cardiomopathy should be initiated as early as diastolic dysfunction is identified. Various therapeutic options include improving diabetic control with both diet and drugs (metformin and thiazolidinediones), use of ACE inhibitors, beta blockers and calcium channel blockers. Daily physical activity and reduction in body mass index may improve glucose homeostasis by reducing the glucose/insulin ratio, and the increase of both insulin sensitivity and glucose oxidation by the skeletal and cardiac muscles. Metformin and thiazolidinendiones are used to treat insulin resistance, but have different mechanisms of action. Metformin reduces free fatty amino acids effluvium from fat cells, thereby suppressing hepatic glucose production and indirectly improving peripheral insulin sensitivity and the endothelial function. In contrast, thiazolidinediones improve peripheral insulin sensitivity by reducing circulating free fatty amino acids, but also increasing production of adiponectin, which improves insulin sensitivity. Beta-adrenoceptor blocking agents are effective in preventing or reversing myocardial dilatation and remodelling, while ACE inhibitors facilitate blood flow through microcirculation in coronary vascular bed, fat and skeletal muscle, as well as improve insulin action at the cellular level.