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Despite advances in treatment, chronic heart failure is still associated with significant morbidity and a poor prognosis. The scope for further advances based on additional neurohumoral blockade is small. Effective adjunctive therapies acting via a different cellular mechanism would, therefore, be attractive. Energetic impairment seems to contribute to the pathogenesis of heart failure. The findings from several studies have shown that the so-called metabolic agents could have potential as adjunctive therapies in heart failure. These agents cause a shift in the substrate used by the heart away from free fatty acids, the oxidation of which normally provides around 70% of the energy needed, towards glucose. The oxygen cost of energy generation is lessened when glucose is used as the substrate. In this review we aim to draw attention to the metabolic alteration in heart failure and we present evidence supporting the use of metabolic therapy in heart failure.

Original publication




Journal article


Nat Clin Pract Cardiovasc Med

Publication Date





490 - 498


Acetanilides, Adrenergic beta-Antagonists, Animals, Cardiac Output, Low, Cardiovascular Agents, Energy Metabolism, Epoxy Compounds, Fatty Acids, Nonesterified, Glycine, Heart, Humans, Myocardium, Oxygen, Perhexiline, Piperazines, Ranolazine, Trimetazidine