Myocardial fatty acid metabolism and drug therapy in rats with heart failure.

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Dilated cardiomyopathy is a set of heterogeneous diseases of left ventricular dysfunction of unknown etiology, which has a variety of clinical courses and pathological findings. Long-chain fatty acids are one of the major cardiac energy substrates, so, understanding long-chain fatty acid metabolism may help in elucidating the mechanisms of various heart diseases. Angiotensin(AT)-II receptor blockers (ARB) and angiotensin-converting enzyme inhibitors (ACEI) have been shown to reduce morbidity and mortality in patients with heart failure, but their inhibitory actions on AT-I-induced increases in blood pressure in heart failure are not clear. AT-I blocking and cardioprotective properties of the ARB candesartan and ACEI quinapril were studied in a rat model of dilated cardiomyopathy. Metaiodobenzylguanidine(MIBG) is a reliable marker for the detection of cardiac adrenergic neuronal damage in heart failure. The cardioprotective properties of carvedilol, a vasodilating β-adrenoceptor blocking agent, were studied in a rat model of dilated cardiomyopathy. Myocardial long-chain fatty acids metabolism was decreased in rats with heart failure. Although low-dose candesartan can block increases in blood pressure with circulating AT-I same to the extent as high-dose quinapril, it does not confer sufficient protection against injury from the rennin-angiotensin system in heart failure. Carvedilol has beneficial effects and protects cardiac adrenergic neurons in dilated cardiomyopathy.