DIABETIC CARDIOMYOPATHY: A REVIEW

Supriya Roy, Tarique Mahmood* and Arshiya Shamim

ABSTRACT

Diabetes is recognized as a prevalent risk factor for cardiovascular morbidity and mortality. The core metabolic defects that mark diabetes, including impaired glucose tolerance, insulin resistance and proinflammatory state leading to endothelial dysfunction forms the pathogenesis of diabetic cardiomyopathy. Hyperglycemia triggers series of maladaptive stimuli that result in myocardial fibrosis and collagen deposition. Hyperglycemia induced mitochondrial reactive oxygen species (ROS) is also a significant contributor. Moreover, increases in sympathetic tone with diabetes are associated with changes in cardiac and vascular functions. ANS is responsible for modulating the activity of the sinus node (heart rate), ventricular (end systolic and diastolic volume) and blood vessels (systemic vascular resistance) and the dysfunction of the ANS may contribute to the development of arterial stiffness, left ventricular hypertrophy and ventricular diastolic dysfunction and cardiac autonomic neuropathy; such changes forms the symptoms for cardiomyopathy. Echocardiography is the preferred diagnostic approach for diabetic cardiomyopathy. Magnetic resonance imaging and spectroscopy along with contrast agents are now leading approaches in the diagnosis of myocardial fibrosis, cardiac and metabolic changes. Also, serum biomarkers offer clear picture of diabetes induced structural and functional changes in cardiac even at very early stages of the disease. Currently, there is no specific treatment for diabetic cardiomyopathy. The pillars in the treatment of diabetic cardiomyopathy include lifestyle changes, intense glycemic control through diet, oral hypoglycemics and insulin, modification of risk factors for cardiovascular disease, and management of heart failure symptoms. Although glycemic control is the main therapeutic approach, newer treatment targets are currently being explored.

Keywords: Diabetic cardiomyopathy (DCM), diabetes, cardiovascular disease, myocardial fibrosis, left ventricular hypertrophy.