Recent studies have demonstrated that alterations in cardiac metabolism occur in ischemic heart disease and heart failure. This suggests that there is an increased utilization of non-carbohydrate substrates for energy production with a resultant reduction in the efficiency of myocardial oxygen consumption. A direct approach to modifying cardiac energy metabolism could involve altering substrate utilization. Trimetazidine, which acts by selectively inhibiting mitochondrial 3-ketoacyl-coenzyme A thiolase, (an enzyme involved in b-oxidation) is an antianginal drug that shifts the preference for energy substrate away from fatty acid metabolism and towards glucose metabolism. It has a reduces ischemia-reperfusion damage and left ventricular function by reducing cell damage, tissue inflammation and left ventricle remodeling. Recent research has demonstrated that the anti-inflammatory action of trimetazidine reduces long-term mortality in patient with ischemic cardiomyopathy.