LAUSR

Objectives Trimetazidine is an anti-ischemic medication licensed for the treatment of angina pectoris. However, the molecular mechanisms underlying its action remain incompletely elucidated. In this study, therefore, we examined the potential beneficial effects of trimetazidine on myocardial injury and endothelial dysfunction in patients with unstable angina in the perioperative period of percutaneous coronary intervention (PCI). Methods A total of 97 patients with unstable angina were randomly divided into trimetazidine (n = 48) and control (n = 49) groups. All subjects received standard medical therapy. The trimetazidine group additionally received 20 mg trimetazidine three times daily 24 hours before and after PCI. Serum levels of creatine kinase-muscle/brain (CK-MB), cardiac troponin I (cTnI), heart-type fatty acid-binding protein (h-FABP), von Willebrand factor (vWF), and nitric oxide (NO) were measured before and the morning following PCI. Results In the control group, levels of CK-MB, cTnI, and vWF were significantly elevated (P < 0.05) and NO level was decreased after PCI (P < 0.05). By contrast, no significant changes in the levels of these proteins were observed in the trimetazidine group after PCI (P > 0.05). Moreover, h-FABP levels were not significantly altered after PCI whether in the control or in the trimetazidine group (P > 0.05). Finally, a time-dependent increase in the levels of h-FABP from 0 to 6 hours after PCI, followed by a progressive decline, was observed (P < 0.05). Conclusions PCI induces endothelial dysfunction and myocardial damage in patients with unstable angina. Trimetazidine therapy in the perioperative period can reduce this damage.