摘要目的：研究曲美他嗪对急性心肌梗死（AMI）患者经皮冠状动脉介入治疗（PCI）后冠脉血流及炎性因子表达的影响。方法选取2014年9月至2015年9月80例 AMI 患者作为研究对象，采用随机数表法分为两组，每组40例。对照组行 PCI 配合常规治疗，观察组在对照组基础上加用曲美他嗪。比较两组治疗效果及对患者冠脉血流和炎性因子表达水平的影响。结果观察组治疗后左室射血分数为（50.29±4.27）%，显著高于治疗前和对照组治疗后，差异有统计学意义（P <0.05）。观察组术后超敏 C-反应蛋白、白细胞介素-2及干扰素-γ分别为（4.31±1.26）mg/ L、（27.20±2.34）pg/ ml 及（237.31±28.89）pg/ ml，均显著低于对照组，差异有统计学意义（P <0.05）。观察组治疗后冠脉再通率为95%，显著高于对照组（80%），差异有统计学意义（P <0.05）。结论曲美他嗪对 AMI 患者 PCI 术后心肌损害具有较好的抑制作用，能显著改善心功能，这与曲美他嗪改善冠脉血流和抑制炎性因子表达密切相关。

abstractsObjective To study the effect of trimetazidine on coronary flow and expression of inflammatory factors in acute myocardial infarction( AMI)patients treated with percutaneous coronary intervention(PCI). Methods From September 2014 to September 2015,a total of 80 AMI patients were taken as the clinical research objects,and these patients were divided into observation group (40 cases)and control group(40 cases). Each group was treated with PCI and conventional treatment. On this basis,the observation group received additional trimetazidine in order to compare their effects of treatment,coronary flow and expression of inflammatory factors. Results After treatment,the left ven-tricular ejection fraction(LVEF)in the observation group was(50. 29 ± 4. 27)% ,which was significantly higher than that before treatment and the control group,and their differences were significant( P <0. 05);the high sensitive C reactive protein(hs-CRP),interleukin-2(IL-2)and interferon-γ(INF-γ) in the observation group were respectively(4. 31 ± 1. 26)mg / L,(27. 20 ± 2. 34)pg / ml and(237. 31 ± 28. 89)pg / ml,which were significantly lower than those in the control group,and the differences were significant(P < 0. 05);the reperfusion rate in the observation group was 95% ,which was significantly higher than that in the control group ( 80% ),and the difference was significant( P < 0. 05 ). Conclusions Trimetazidine has satisfactory inhibition effect on myocardial damage in AMI patients trea-ted with PCI,which can significantly improve the cardiac function and coronary flow,and inhibit the expression of inflammatory factors.