The role of postoperative trimetazidine therapy in on-pump coronary artery bypass surgery

Abstract

Introduction: Coronary artery bypass surgery remains the gold standard in the treatment of patients with ischemic heart disease. However, the increased oxidative stress caused by the release of free radicals during the ischemia-reperfusion time is a well-known pathophysiological process during and after coronary revascularization procedures. It may lead to reversible and irreversible myocardial injury. The focus of this prospective single-blinded randomized controlled trial is to investigate and analyze the effectiveness of the drug trimetazidine on reducing postoperative myocardial ischemia-reperfusion injury. Aim: We evaluated the effects of trimetazidine on reactive oxygen species that may arise from myocardial ischemia-reperfusion period or systemic inflammation after coronary artery bypass grafting (CABG) surgery. Materials and methods: The study included 90 patients divided into two groups who underwent elective coronary artery bypass surgery between March 2018 and October 2018. The patients in one of the groups received 35 mg trimetazidine twice daily as soon as they were extubated. The remainder of the pharmaceutical therapy was the same for all participants. Preoperative and postoperative levels of several blood-based biochemical markers including malondialdehyde (MDA), creatinine kinase-MB fraction (CK-MB) and high-sensitivity troponin T (hs-TnT) were measured. The data was classified and analyzed by the timing of sample collection. Results: The results indicate that postoperative trimetazidine medication reduces MDA production, resulting in reduced oxidative stress and improved cardiac cell protection via antioxidant status augmentation. The follow-up was 6 months after the surgery. The Minnesota Living with Heart Failure Questionnaire was used to assess the quality of life of patients, and the results were excellent. Conclusions: Postoperative trimetazidine therapy leads to improvement of the myocardial cell metabolism and thus reduction in post CABG ischemia-reperfusion injury.