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目的探讨冠心病患者行冠状动脉内支架置入术前后血小板活化指标的变化,了解冠心病不同临床类型支架置入数与血小板活化指标之间的关系。方法利用流式细胞术和单克隆抗体测定48例稳定型心绞痛、45例不稳定型心绞痛患者与37例急性心肌梗死患者外周血中血小板膜糖蛋白CD62p、CD63和凝血酶敏感蛋白的阳性表达率,并与45例冠状动脉造影正常者作对照分析。结果稳定型心绞痛患者、不稳定型心绞痛患者和急性心肌梗死患者支架置入后CD62p、CD63和凝血酶敏感蛋白的阳性表达率均显著高于支架置入前(P<0.01);不稳定型心绞痛组和急性心肌梗死组治疗前亦高于对照组(P<0.01),而稳定型心绞痛组治疗前与对照组比较差异无显著性(P>0.05)。稳定型心绞痛组和不稳定型心绞痛组CD62p、CD63和凝血酶敏感蛋白的阳性表达率与支架置入个数有关,置入支架越多阳性表达率越高。结论不稳定型心绞痛患者及急性心肌梗死患者存在血小板高活化状态、动脉粥样硬化斑块破裂以及急性血栓形成。支架置入术对冠状动脉内皮的损伤加强了血小板的活化,增加了血栓形成的风险。
Objective To investigate the changes of platelet activation before and after coronary stenting in patients with coronary heart disease (CHD) to find out the relationship between the number of platelets inserted in different clinical types of coronary heart disease and the indices of platelet activation. Methods The positive rate of CD62p, CD63 and thrombin-sensitive protein in 48 patients with stable angina pectoris, 45 patients with unstable angina pectoris and 37 patients with acute myocardial infarction were determined by flow cytometry and monoclonal antibody , And compared with 45 cases of normal coronary angiography for control analysis. Results The positive rates of CD62p, CD63 and thrombin sensitive protein in patients with stable angina, unstable angina pectoris and acute myocardial infarction were significantly higher than those before stent implantation (P <0.01). Unstable angina pectoris Group and acute myocardial infarction group before treatment was also higher than the control group (P <0.01), while stable angina group before treatment compared with the control group no significant difference (P> 0.05). The positive expression rates of CD62p, CD63 and thrombin-sensitive protein in stable angina group and unstable angina group were related to the number of stent implantation, and the higher the positive expression rate was, the higher the stent placement was. Conclusion Patients with unstable angina and acute myocardial infarction have platelet activation, ruptured atherosclerotic plaque and acute thrombosis. Stent implantation injury to the coronary artery endothelium enhances platelet activation and increases the risk of thrombosis.