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Lifelong Treatment With Clopidogrel Should Be Given After DES Implantation

机译:在DES植入后,应给出用氯吡格雷的终身处理

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Coronary stent thrombosis (ST) is an uncommon and potentially catastrophic complication of percutaneous coronary intervention (PCI) (1). The importance of potent dual antiplatelet therapy (DAT) with aspirin and a thienopyidine (usually clopidogrel) for prevention of ST is well-established (2). Aspirin blocks the thromboxane pathway of platelet activation while clopidogrel, which bind to the P_2Y_(12) platelet membrane receptor, blocks the adenosine diphosphate pathway of platelet activation. Bare-metal stent (BMS) thrombosis occurs in <1% of the cases, usually within the first month after PCI. Dual antiplatelet therapy was initially recommended for 1 month following BMS implantation. The advent of drug-eluting stents (DES) has raised concerns regarding later occurrence of ST, beyond the traditional 1 -month timeframe, especially in complex lesion subsets that were excluded from randomized trials that compared BMS to DES. Initially DAT was recommended for 3-6 months following DES implantation, however this period was later extended out to 1 year (3). Premature cessation of clopidogrel therapy is the most important risk factor for DES thrombosis (4). Studies have suggested an 0.6% annual thrombosis risk with DES beyond the first year post PCI (5). Animal and human studies have demonstrated a persistent peri-stent inflammatory response and incomplete vessel wall healing, which appear to be the pathological substrate underlying this phenomenon (6, 7). These findings have prompted many physicians to prescribe DAT indefinitely in order to prevent ST.
机译:冠状动脉支架血栓形成(ST)是经皮冠状动脉介入(PCI)(1)的罕见和潜在的灾难性并发症。有效的双抗血小板治疗(DAT)与阿司匹林和噻吩(通常氯吡格雷)的重要性用于预防ST是良好的(2)。阿司匹林阻断血小板活化的血栓激活途径,而氯吡格雷结合P_2Y_(12)血小板膜受体,阻断血小板活化的腺苷二磷酸途径。赤金支架(BMS)血栓形成发生在<1%的情况下,通常在PCI后的第一个月内。 BMS植入后最初推荐使用双抗血小板治疗1个月。药物洗脱支架(DES)的出现提出了关于ST的后续发生的担忧,超出了传统的1-个时间范围,特别是在从随机试验中排除的复杂病变子集中,该归因于比较BMS至DES。最初日期建议在DES植入后3-6个月,但这一时期后来延伸到1年(3)。氯吡格雷治疗的过早停止是DES血栓形成(4)的最重要的危险因素。研究表明,在PCI(5)的第一年后,DES的年血栓形成风险为0.6%。动物和人类研究已经证明了持续的围球炎症反应和不完全的血管壁愈合,这似乎是这种现象的病理基质(6,7)。这些调查结果促使许多医生无限期地规定DEA,以防止ST。

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