Despite the recent introduction of new therapeutic approaches to treat heart failure, mortality from heart failure remains high, and patients still frequently experience progression of contractile dysfunction and ongoing left ventricular enlargement. Therefore, new treatments are needed for heart failure that work independently of mechanisms already targeted. Emerging evidence suggests that the failure of the myocardium in heart failure is affected by alterations in the energy substrate metabolism. In particular, there is now evidence that in the failing heart, shifting metabolism away from a preference for fatty acids toward more carbohydrate oxidation can improve contractile function and slow the progression of pump failure.
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