Myocardial energy metabolism in dilated cardiomyopathy

Dilated cardiomyopathy can be broadly defined as heart failure with an enlarged left ventricular chamber, but with no evidence of ischemic heart disease or myocardial infarction. Recent studies from patients and animal models show that dilated cardiomyopathy results in a decrease in myocardial content of adenosine-50-triphosphate (ATP) and phosphocreatine and a decrease in the capacity for mitochondrial oxidative metabolism and aerobic ATP production. There is a switch in the source of fuel, with a decrease in the rate of myocardial fatty acid oxidation and greater glucose oxidation. Pharmacologically preventing the decrease in fatty acid oxidation with a peroxisome proliferatoractivated receptor-a agonist does not appear to be beneficial. On the other hand, treatment with partial inhibitors of myocardial fatty acid oxidation has favorable effects on cardiac energy metabolism, contractile function, and structure. Heart Metab. 2011;49:5–8.