Abstract:
Objective To observe the efficacy of trimetazidine in the treatment of patients with myocardial ischemia-reperfusion injury.
Methods A total of 90 patients with myocardial ischemia-reperfusion injury were randomly divided into control group and study group, with 45 cases in each group. The control group was treated with routine treatment, while the study group was treated with routine treatment and trimetazidine. Before and after treatment, the levels of myocardial oxygen radical injury indexes levelsglutathione peroxidase (GSH-Px), superoxide dismutase (SOD), malondialdehyde (MDA), total antioxidant capacity (T-AOC), inflammatory indexes levelsnuclear factor κB (NF-κB), Toll-like receptor 2 (TLR2), hypersensitive C-reactive protein (hs-CRP), myocardial injury indexes anti-apoptotic protein B-cell lymphoma factor-2 (Bcl-2), protease activated receptor-2 (PAR-2), cardiac troponin I (cTnI), creatine kinase MB isoenzyme (CK-MB), autophagy gene Beclin1, ischemia modified albumin (IMA), cardiac function indexes levelsleft ventricular ejection fraction (LVEF), maximum early diastolic flow velocity of mitral valve (EV), left ventricular end diastolic diameter (LVEDd) and clinical efficacy were compared between two groups.
Results After treatment, the levels of MDA, NF-κB, TLR2, hs-CRP, PAR-2, Beclin1, cTnI, IMA, CK-MB and LVEDd in the study group were significantly lower than those in the control group, while the levels of GSH-Px, SOD, T-AOC, Bcl-2, LVEF and EV were significantly higher than those in the control group (P < 0.05). The total effective rate of treatment in the study group was 97.78%, which was significantly higher than 86.67% of the control group (P < 0.05).
Conclusion Trimetazidine is safe and effective in the treatment of patients with myocardial ischemia-reperfusion injury, which can inhibit the level of oxygen radical, alleviate myocardial peroxidation injury, inhibit the levels of inflammation related factors, reduce the levels of PAR-2 and Beclin1, increase the Bcl-2 level, and improve cardiac function.