Abstract
Although neurohumoral antagonism has successfully reduced HF morbidity and mortality, the residual risk remains unacceptably high. The concept of myocardial energetic deficiency in the pathogenesis of HF, and the consequent rationale for treating this energy deficiency clinically by metabolic modulation using long-chain 3-ketoacyl coenzyme A thiolase inhibitior (e.g., trimetazidine), late sodium current inhibitor (e.g., ranolazine), carnitine palmitoyl transferase inhibitior (e.g., perhexiline) and carnitine palmitoyl transferase I and/or II inhibitors (e.g., etomoxir) would be recognized.
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