Diabetic cardiomyopathy is a distinct pathophysiological entity characterized by cellular changes leading to diastolic and eventually systolic dysfunction, necessitating comprehensive management of glycemia, hypertension, and ischemia.
The increased incidence of congestive heart failure and the increased mortality and morbidity in the diabetic patient following myocardial infarction or coronary artery bypass graft can be explained by the presence of diabetic cardiomyopathy. Noninvasive studies in young diabetic patients show no cardiac abnormality, but in older diabetic patients mild cardiac diastolic dysfunction is detectable. This mild cardiomyopathy can become clinically detectable in the presence of hypertension and can be severe in the presence of myocardial ischemia. Microvascular disease is unlikely to cause diabetic cardiomyopathy. Cellular changes, including defects in calcium transport and fatty acid metabolism, may lead to myocellular hypertrophy and myocardial fibrosis, initially causing diastolic dysfunction that may advance to systolic dysfunction. Glycemic control, energetic detection and treatment of hypertension with appropriate antihypertensive agents, and early detection and treatment of ischemic heart disease are essential in preventing and treating diabetic cardiomyopathy.
David S.H. Bell (Mon,) studied this question.