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Review
. 2017 May-Jun;69(3):393-401.
doi: 10.1016/j.ihj.2017.04.001. Epub 2017 Apr 29.

Modulation of myocardial energetics: An important category of agents in the multimodal treatment of coronary artery disease and heart failure

Affiliations
Review

Modulation of myocardial energetics: An important category of agents in the multimodal treatment of coronary artery disease and heart failure

Jamshed J Dalal et al. Indian Heart J. 2017 May-Jun.

Abstract

The combined and relative contribution of glucose and fatty acid oxidation generates myocardial energy, which regulates the cardiac function and efficiency. Any dysregulation in this metabolic homeostasis can adversely affect the function of heart and contribute to cardiac conditions such as angina and heart failure. Metabolic agents ameliorate this internal metabolic anomaly, by shifting the energy production pathway from free fatty acids to glucose, resulting in a better performance of the heart. Metabolic therapy is relatively a new modality, which functions through optimization of cardiac substrate metabolism. Among the metabolic therapies, trimetazidine and ranolazine are the agents presently available in India. In the present review, we would like to present the metabolic perspective of pathophysiology of coronary artery disease and heart failure, and metabolic therapy by using trimetazidine and ranolazine.

Keywords: Heart failure; Ischemia; Metabolic therapy; Stable angina; Trimetazidine.

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Figures

Fig. 1
Fig. 1
Probable reasons of metabolic alterations in CAD and HF. ATP: adenosine triphosphate; PCr: phosphocreatine.
Fig. 2
Fig. 2
Metabolic alterations in CAD and HF. ADP: adenosine diphosphate; ATP: adenosine triphosphate; CPT: carnitine palmitoyl transferase; PDH: pyruvate dehydrogenase; TCA: tricarboxylic acid cycle.
Fig. 3
Fig. 3
Phosphocreatine shuttle system. ADP: adenosine diphosphate; ATP: adenosine triphosphate; CK: creatinine kinase; Cr: free creatinine; PCr: phosphocreatinine.

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