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.

Patients with nonobstructive coronary artery disease (NOCAD) have high risk associated with acute myocardial infarction (AMI), and fragmented QRS (fQRS) has a predictive value of AMI after percutaneous coronary intervention (PCI). A cohort of 254 participants were recruited including 136 NOCAD and 118 AMI patients from Xi’an No. 1 Hospital. Comprehensive metabolomics was performed by UPLC-Q/TOF-MS with multivariate statistical analyses. Hazard ratios were measured to discriminate the prognostic in AMI after PCI between differential metabolites and fQRS. OPLS-DA separated metabolites from NOCAD and AMI in serum. A total of 23 differential metabolites were identified between NOCAD and AMI. In addition, four differential metabolites, namely, acetylglycine, threoninyl-glycine, glutarylglycine, and nonanoylcarnitine, were identified between fQRS and non-fQRS in AMI. The hazard ratios demonstrate that the metabolites were associated with the risk of cardiac death, recurrent angina, readmissions, and major adverse cardiovascular events, which may clarify the mechanism of fQRS as a predictor in the prognostic of AMI after PCI. This study identified novel differential metabolites to distinguish the difference from NOCAD to AMI and clarify the mechanism of fQRS in prognostic of AMI after PCI, which may provide novel insights into potential risks and prognostic of AMI.