Inhibition of fatty acid oxidation to treat heart failure in patients

Heart failure is a major cause of morbidity and mortality in the world. Cardiac energy metabolism, specifically fatty acid and glucose metabolism, is altered in heart failure and has been considered a contributing factor in the impaired heart function observed in patients with heart failure. Emerging evidence demonstrates that correcting these changes in energy metabolism by modulating mitochondrial oxidative metabolism may be effective treatment for heart failure. Promising strategies include the downregulation of fatty acid oxidation and increased coupling of glycolysis to glucose oxidation. Fatty acid ß-oxidation enzymes carnitine palmitoyl transferase I and pyruvate dehydrogenase kinase are examples of metabolic targets for the treatment of heart failure. This article reviews the existing evidence for inhibition of fatty acid oxidation to treat heart failure. Further studies are needed to confirm the potential benefit of modulating these metabolic targets as an approach to treating heart failure in clinical settings.