Trimetazidine effects on oxidative damage

Abstract

Trimetazidine is an anti anginal medication and ensures the proper functioning of transmembrane ionic channels by maintaining intracellular ATP production in ischemic conditions. Trimetazidine prevents the accumulation of calcium in cardiomyocytes, adjusts cellular acidosis, and decreases production of free oxygen radicals. Trimetazidine blocks long chain 3-ketoacyl coenzyme A thiolase activity, thereby shifting ATP production more towards glucose oxidation instead of fatty acid β-oxidation during myocardial ischemia. By inhibiting fatty acid β-oxidation, fewer free radicals are formed in the cardiomyocytes with more efficient oxygen consumption and ATP production, resulting in recovery of myocardial contractile function and inhibition of malignant arrhythmias. Moreover, cardiac enzymatic activities such as phosphorylase and ATPase increased significantly in ischemic areas with trimetazidine pretreatment before myocardial ischemia. Protective effects of trimetazidine by increasing ventricular fibrillation threshold during coronary artery occlusion were consistent in animal studies. © 2013 by ISSN.