Protective effects of trimetazidine on ischaemic myocardial dysfunction

Experimental and clinical studies have shown that trimetazidine has a numbe r of potentially useful cytoprotective features. The drug has been reported to limit intracellular acidosis, sodium and calcium accumulation, to prese rve contractile function and to limit cytolysis and membrane damage caused by oxygen free radicals. All these effects contribute towards reducing the deleterious effects of ischaemic insult. improved cellular function during ischaemia could explain the beneficial effects of trimetazidine on resting and dobutamine-induced myocardial ischaemic dysfunction. Preserving mitocho ndrial function and energy metabolism from chronic oxygen deprivation may r educe ischaemic left ventricular dysfunction. Experimental studies also sug gest that trimetazidine acts by affecting myocardial substrate utilization because the drug inhibits oxidative phosphorylation and utilization of fatt y acid substrates and shifts metabolism from fatty acid to glucose oxidatio n. As these effects occur in the absence of detectable changes in systemic and coronary haemodynamics, the in vivo effects of trimetazidine on ischaemic myocardium are likely to depend on direct cytoprotection.