Effects of trimetazidine in patients with acute myocardial infarction: data from the Korean Acute Myocardial Infarction Registry

Excess myocardial fatty acid oxidation can cause a range of deleterious myocardial effects. Trimetazidine (TMZ) is a clinically effective antianginal agent that selectively inhibits long-chain 3-ketoacyl CoA thiolase, reducing fatty acid oxidation and stimulating glucose oxidation. The role of TMZ in acute myocardial infarction (AMI), however, remains unclear. Our retrospective analysis explores the effect on clinical outcomes of adding TMZ to standard treatment in patients with AMI. All 13,733 AMI patients registered in the Korean Acute Myocardial Infarction Registry from 2005 to 2008 were retrospectively enrolled. Patients were divided into two groups: those treated with TMZ during their in-hospital management period and those who were not. Primary endpoints were all-cause death combined in-hospital and 12-month death and major adverse cardiac events (MACE), which included all-cause death, recurrent myocardial infarction (MI), repeated percutaneous coronary intervention (PCI) for target lesion revascularization (TLR), and coronary artery bypass graft. Propensity-matched patients were analyzed using an adjusted Cox proportional hazards model. Baseline clinical and angiographic characteristics in the TMZ and no-TMZ groups were generally similar, with the exceptions of pre-PCI thrombolysis in myocardial infarction flow grade, stent type, and stent length. Over 12 months, the relative risk of all-cause death fell by 59 % (event rate 2.3 vs. 6.4 %; hazard ratio 0.41, 95 % CI 0.18-0.97, P = 0.042) and the relative risk of MACE fell by 76 % (event rate 2.3 vs. 9.5 %; hazard ratio 0.24, 95 % CI 0.10-0.56, P = 0.001) in the TMZ group compared with those in the no-TMZ group. Trimetazidine appeared to improve clinical outcomes in AMI patients by significantly reducing all-cause mortality and MACE over 12 months.