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为什么阿司匹林能降低静脉血栓栓塞风险?乙酰水杨酸的古老与新型抗血栓作用。

Why does aspirin decrease the risk of venous thromboembolism? On old and novel antithrombotic effects of acetyl salicylic acid.

机构信息

Institute of Cardiology, Jagiellonian University, Krakow, Poland.

出版信息

J Thromb Haemost. 2014 Nov;12(11):1776-87. doi: 10.1111/jth.12728. Epub 2014 Oct 15.

DOI:10.1111/jth.12728
PMID:25213262
Abstract

It is well established that aspirin, an irreversible inhibitor of platelet cyclooxygenase activity, is effective in secondary prevention of arterial thromboembolic events. The pooled results of the recent randomized, multicenter WARFASA and ASPIRE aspirin trials showed a 32% reduction in the rate of recurrence of venous thromboembolism (VTE) in patients receiving aspirin following VTE. These clinical data support evidence that platelets contribute to the initiation and progression of venous thrombosis and aspirin inhibits thrombin formation and thrombin-mediated coagulant reactions. In addition to the known acetylation of serine 529 residue in platelet cyclooxygenase-1, the postulated mechanisms of aspirin-induced antithrombotic actions also involve the acetylation of other proteins in blood coagulation, including fibrinogen, resulting in more efficient fibrinolysis. This review summarizes current knowledge on the aspirin-induced antithrombotic effects that potentially explain clinical studies showing reduced rates of VTE events in aspirin-treated subjects.

摘要

已证实,阿司匹林是一种不可逆的血小板环氧化酶活性抑制剂,在动脉血栓栓塞事件的二级预防中有效。最近随机、多中心 WARFASA 和 ASPIRE 阿司匹林试验的汇总结果表明,在 VTE 后接受阿司匹林治疗的患者中,静脉血栓栓塞症 (VTE) 复发率降低了 32%。这些临床数据支持血小板有助于静脉血栓形成的启动和进展的证据,并且阿司匹林抑制凝血酶形成和凝血酶介导的凝血反应。除了已知的血小板环氧化酶-1 丝氨酸 529 残基的乙酰化作用外,阿司匹林诱导的抗血栓作用的推测机制还涉及血液凝固中其他蛋白质的乙酰化,包括纤维蛋白原,从而导致更有效的纤维蛋白溶解。这篇综述总结了目前关于阿司匹林诱导的抗血栓作用的知识,这些作用可能解释了临床研究表明阿司匹林治疗组 VTE 事件发生率降低的原因。

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