Diabetic cardiomyopathy is a type of cardiac dysfunction resulting from diabetes, independent of vascular or valvular pathology. It clinically manifests initially as asymptomatic diastolic dysfunction and then progresses to symptomatic
heart failure. Two major contributors to the development of
diabetic cardiomyopathy, which are unique to diabetes, are
hyperglycemia and diabetes-related alterations in myocardial metabolism.
Diabetes mellitus is characterized by reduced
glucose and
lactate metabolism and enhanced
fatty acid metabolism, which are the early consequences of the disease. Studies on the effect of intensive
glucose control on
heart failure events in patients with diabetes have been conducted with neutral results. However, no study on the effect of metabolic modulators on the prevention of
heart failure has been reported.
Trimetazidine, a 3-ketoacyl
coenzyme A thiolase (3-KAT) inhibitor, shifts cardiac energy metabolism from
free fatty acid oxidation to
glucose oxidation by inhibiting mitochondrial long-chain 3-KAT, and is used clinically as an effective antianginal agent. Studies have shown that
trimetazidine improves heart function in patients with idiopathic
cardiomyopathy and in diabetic patients with cardiac
ischemia or
heart failure. In addition to being effective,
trimetazidine has only mild side effects. Therefore, instead of routine administration of
trimetazidine for the treatment of
diabetic cardiomyopathy, we hypothesize that the early application of
trimetazidine may prevent or ameliorate
diabetic cardiomyopathy. In addition to life style modifications, ACEI, ARB, and beta-blockers, which have been recommended in the past,
trimetazidine should be administered to those patients with
impaired glucose tolerance or patients in the early course of diabetes. In this way, we may reduce the prevalence of
heart failure and improve the long-term survival of patients with diabetes through early normalization of the myocardial substrate metabolism.