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目的观察既往经皮冠状动脉介入治疗(PCI)的急性心肌梗死(AMI)患者急诊PCI时罪犯病变的特点,推断这类患者AMI的发病机制。方法回顾性分析从2004年4月到2006年4月在阜外心血管病医院行急诊PCI治疗的61例既往PCI的AMI患者的临床资料。结果61例患者(62.1±10.0岁,男性88.5%)罪犯病变位置为左前降支(LAD)47.5%、右冠状动脉(RCA)39.5%、左回旋支(LCX)13.0%。在既往PCI1年后,除了阿司匹林的应用率无明显变化(93.8%比100%,P=0.113)外,全部患者均停用了氯吡格雷,应用β受体阻滞剂、血管紧张素转换酶抑制剂和他汀类调脂药的比率明显降低(与PCI后1年内比较,分别为46.9%比75.0%,P=0.001;34.4%比70.8%,P=0.001;28.1%比77.1%,P=0.000)。61例患者的罪犯病变特点:支架内急性和亚急性血栓形成12例(19.7%),晚期和晚晚期血栓形成6例(9.8%),非支架内血栓43例(70.5%),没有支架内再狭窄因素引起。AMI距既往PCI的时间:1个月以下者13例(21.3%),除了1例因术后3天在另一支冠状动脉发生斑块破裂外,其余均因支架内急性/亚急性血栓形成;1个月~1年者16例(26.2%),其中4例为晚期血栓形成,12例为非支架内血栓;1年以上者32例(52.5%),除了2例为支架内晚晚期血栓形成,其余30例均为非支架内血栓因素。结论既往PCI患者AMI的发病机制主要是斑块破裂。冠心病二级预防对减少PCI术后AMI的发生起重要作用。
Objective To investigate the characteristics of culprit lesions in patients with acute myocardial infarction (AMI) who underwent percutaneous coronary intervention (PCI) and to infer the pathogenesis of AMI in these patients. Methods The clinical data of 61 patients with AMI who had received PCI during the emergency PCI at Fu Wai Hospital from April 2004 to April 2006 were retrospectively analyzed. Results 61 (62.1 ± 10.0 years, 88.5% of men) had a lesion location of 47.5% of the left anterior descending artery (LAD), 39.5% of the right coronary artery (RCA) and 13.0% of the left circumflex coronary artery (LCX). Clopidogrel was discontinued in all patients except for aspirin (93.8% vs. 100%, P = 0.113) after 1 year of previous PCI, with beta-blockers, angiotensin converting enzyme The ratio of inhibitors to statin lipid-lowering drugs was significantly lower (46.9% vs. 75.0%, P = 0.001; 34.4% vs. 70.8%, P = 0.001; P = 0.000). Sixty-one patients (19.7%) had acute and subacute thrombosis, 6 (9.8%) had advanced and late thrombosis, 43 (70.5%) had non-stent thrombosis, and no stent-graft Restenosis causes. AMI time from previous PCI: 13 cases (21.3%) under 1 month, except for 1 case of plaque rupture in the other coronary artery 3 days after surgery, the rest were due to acute / subacute thrombosis within the stent ; 16 cases (26.2%) from 1 month to 1 year, of which 4 cases were advanced thrombosis and 12 cases were non-stent thrombosis. One year or more were 32 cases (52.5%), except two cases were late stent- Thrombosis, and the remaining 30 cases were non-stent thrombosis factors. Conclusion The pathogenesis of AMI in patients with previous PCI is mainly plaque rupture. Secondary prevention of coronary heart disease plays an important role in reducing the occurrence of AMI after PCI.