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Effects of Trimetazidine Pretreatment on Endothelial Dysfunction and Myocardial Injury in Unstable Angina Patients Undergoing Percutaneous Coronary Intervention

Cardiol Res Pract. 2019 Sep 2;2019:4230948.
Effects of Trimetazidine Pretreatment on Endothelial Dysfunction and Myocardial Injury in Unstable Angina Patients Undergoing Percutaneous Coronary Intervention.
Shao S1, Shi Z2, Tse G3,4, Wang X1, Ni Y1, Liu H1, Liu T1, Li G1.
Author information
1 Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Tianjin Institute of Cardiology, Department of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin 300211, China.
2 Xi’An Number One Hospital, Xi’an 710002, China.
3 Department of Medicine and Therapeutics, Chinese University of Hong Kong, Hong Kong SAR, China.
4 Li Ka Shing Institute of Health Sciences, Faculty of Medicine, Chinese University of Hong Kong, Hong Kong SAR, China.
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).
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.
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).
PCI induces endothelial dysfunction and myocardial damage in patients with unstable angina. Trimetazidine therapy in the perioperative period can reduce this damage.
Copyright © 2019 Shuai Shao et al.
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