Diabetic cardiomyopathy (CMP) is defined as cardiac failure when possible etiologies such as alcohol, hypertension, and coronary and structural heart disease have been excluded in diabetic patients. In a previous study using type II diabetes mellitus (DM) rats model, diabetic CMP was characterized functionally by the presence of left ventricular diastolic dysfunction, and histologically by interstitial fibrosis and collagen accumulation. Diabetic CMP has been reported in 30-75% of diabetic patients, and is an important cause of heart failure. The worldwide prevalence of diabetes has been estimated to increase from 2.8% in 2000 to 4.4% in 2030, this could lead to an increase of diabetic CMP. Although coronary artery diseases are the main cause of heart failure and deteriorating function, the high incidence of diabetic CMP indicates that diabetes itself is an important factor in myocardial damage. In the diabetic heart, the functional alterations are preceded by a variety of structural, molecular and cellular changes, many of which are present in asymptomatic diabetic individuals and experimental models of diabetes. Moreover, the undermining of myocardial and vascular integrity appears to begin during the pre-diabetic stage. In a recent study, changes in cardiac heparin sulfate proteoglycan expression and the diastolic dysfunction, an early sign of diabetic CMP occurred as parallel events. Although several pathophysiological mechanisms have been proposed to explain the diabetic CMP, it remains poorly understood. In diabetic CMP, diastolic dysfunction is well on the way even before symptoms appear in the patient. Although various animal models have been used to investigate diabetes-related changes in the myocardium including interstitial fibrosis, cardiomyocyte loss, impaired energy utilization, small vessel disease and neuropathy, the pathophysiology of diabetic cardiomyopathy remains to be fully elucidated. Clinical implications from the current understanding of the diabetic CMP may be more preemptive control of overexpression of the angiotensin II signaling on one hand and long-term control of blood pressure and blood glucose level on the other hand. In addition, it should be underscored that myocardial damage via impaired coronary blood flow still remains as the major etiology of the heart failure in diabetes patients.