Trimetazidine

Coronary revascularization is not a suitable option for all patients with chronic stable angina (CSA) and, even when such a strategy is adopted, in conjunction with optimal medical therapy (OMT) as suggested by international guidelines, not all of them succeed to be symptom free. Importantly, this subset represents an increasing population, being widespread among diabetics and elderly. Irrespective of the mechanism responsible for myocardial ischemia, it has been shown that when ischemia develops it promotes substantial changes at the level of myocardial metabolism and reduces cardiac efficiency. Indeed, an increase in fatty acids (FFAs) oxidation and a decrease in glucose oxidation are both observed during myocardial ischemia, along with intracellular proton (H+) accumulation and enhanced oxygen consumption (O2). In this scenario, therapeutic interventions that promote glucose utilization may improve cardiac efficiency and angina symptoms. This metabolic shift can be achieved by inhibiting fatty acid oxidation, stimulating glucose oxidation, or both. Anti-angina drugs exist that induce a cardiac metabolic shift from FFA oxidation toward glucose consumption, which, in turn, results in increased ATP generation per unit of O2 consumption. Trimetazidine, a partial inhibitor of fatty acid oxidation, is a ‘metabolic'’ anti-angina drug that can improve symptoms in patients with chronic stable angina. This agent can be safely added to conventional therapy i.e., β-blockers (BBs), calcium channel blockers (CCBs), and nitrates. The safety and clinical benefits of trimetazidine have been known since the early 1980s. Unfortunately, however, a relatively small group of European centres have access to this therapy.