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Changes in cardiac metabolism: a critical step from stable angina to ischaemic cardiomyopathy

W.C. Stanley*

Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio, U.S.A.

* Correspondence: William C. Stanley, PhD, Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106-4970, U.S.A..

Abstract

Cardiac work requires a high rate of adenosine triphosphate (ATP) breakdown. ATP is resynthesized in the mitochondria with energy from the combustion of fatty acids, glucose and lactate. Fatty acids are the main fuel for the heart, supplying 60–90% of the energy, with the balance (10–40%) from pyruvate oxidation (formed from glycolysis and lactate). Fatty acid oxidation inhibits pyruvate oxidation in the mitochondria. During myocardial ischaemia, oxygen consumption and ATP production is reduced, causing accelerated glycolysis and lactate production; the pH falls and cell function is impaired. Paradoxically, with a partial reduction in coronary flow, the myocardium continues to derive most of its energy from the oxidation of fatty acids despite a high rate of lactate production; this fatty acid oxidation during ischaemia inhibits pyruvate oxidation, and drives pyruvate conversion to lactate. Partial inhibition of fatty acid oxidation in ischaemic myocardium, such as with the long-chain 3-ketoacyl thiolase inhibitor trimetazidine, reduces lactate production and H+ accumulation during ischaemia, and results in clinical benefit in patients with angina pectoris.

Key Words: Angina pectoris • cardiac • coronary artery disease • fatty acids • glucose • heart • lactate • metabolism • mitochondria


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