替罗非班联合美托洛尔治疗急性心肌梗死的疗效及机制研究

摘要

目的：探讨替罗非班联合美托洛尔治疗急性心肌梗死的疗效及其作用机制。方法90例急性心肌梗死患者随机分为试验组45例和对照组45例。对照组给予美托洛尔口服治疗，试验组给予替罗非班静脉和美托洛尔口服治疗，治疗7 d后观察两组患者的临床疗效，彩色多普勒超声心动图测定血流动力学，心脏彩超检测心功能，ELISA检测血清基质金属蛋白酶9，免疫透射比浊法检测血清C反应蛋白，流式细胞仪检测患者循环血管内皮祖细胞。结果试验组的总有效率95．56％显著高于对照组的80．00％，两组比较差异有统计学意义（P＜0．05）。试验组的血流动力学参数左房平均压、平均二尖瓣压力差、肺动脉平均压改善程度优于对照组，心脏超声相关指标改善程度显著优于对照组，差异均有统计学意义（P＜0．05）。治疗后两组患者血清基质金属蛋白酶9水平和C反应蛋白降低，且试验组低于对照组，差异均有统计学意义（P＜0．01）。试验组患者的循环血管内皮祖细胞明显高于对照组，差异均有统计学意义（P＜0．05）。结论替罗非班联合美托洛尔治疗急性心肌梗死的临床疗效良好，可有效改善血流动力学参数和心脏超声相关指标，可能与降低患者基质金属蛋白酶9和C反应蛋白的表达水平，提高循环血管内皮祖细胞的数量有关。%Objective To explore the efficacy and mechanism of tirofiban combined with metoprolol in patients with acute myocardial infarction.Methods Ninety patients with acute myocardial infarction were randomized into experimental group (n=45 )and control group (n=45 ).The control group was treated by oral administration of metoprolol,and the experimental group by oral administration of metoprolol and intravenous admistration of tirofiban.After 7 days of treatment,the clinical curative effect,hemodynamic parameters,car-diac function indexes,the level of serum matrix metalloproteinases 9,C -reactive protein and endothelial progenitor cells were ob-served.Results The total effective rate in experimental group (95.56%)was higher than the control group (80.00%,P<0.05). The LAP MVP and mPAP of hemodynamic parameters and the echocardiogram related indexes in experimental group were better than those in control group (P<0.05).The serum levels of matrix metalloproteinases 9 and C-reactive protein in experimental group were lower than those in control group (P<0.01).The endothelial progenitor cells in experimental group were higher than those in control group (P<0.05).Conclusions Tirofiban combined with metoprolol in patients with acute myocardial infarction achieved good clini-cal curative effect,which can improve the hemodynamic parameters and related parameters of cardiac ultrasound.They may be related to the decrease in the expression of matrix metalloproteinases 9 and C-reactive protein and the increase of the endothelial progenitor cells.