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对先前接受过阿司匹林治疗的急性缺血性中风患者血小板功能的评估。

Assessment of platelet function in acute ischemic stroke patients previously treated with aspirin.

作者信息

Lago Aida, Parkhutik Vera, Tembl Jose Ignacio, Vallés Juana, Santos Maria Teresa, Moscardó Antonio

机构信息

Department of Neurology, Hospital Universitari La Fe, Valencia, Spain.

Department of Neurology, Hospital Universitari La Fe, Valencia, Spain.

出版信息

J Stroke Cerebrovasc Dis. 2014 Nov-Dec;23(10):2794-2799. doi: 10.1016/j.jstrokecerebrovasdis.2014.07.007. Epub 2014 Oct 16.

Abstract

BACKGROUND

Platelet inhibition measured by platelet function tests could be critical to understand the reasons for early recurrence and to guide therapeutic recommendations. We assess the platelet function during the acute phase of ischemic stroke in patients pretreated with aspirin who continue their treatment with aspirin only, are started on clopidogrel only, or add clopidogrel to aspirin.

METHODS

Sixty-four patients were taking aspirin before the stroke. Depending on the administered antiplatelet, 3 groups were defined: ASA: patients who continued on aspirin orally or intravenous acetylsalicylate of lysine, n = 30; CLO: patients who discontinued aspirin and were started on clopidogrel, n = 16; and ASA + CLO: patients who were prescribed both aspirin and clopidogrel, n = 10. Collagen-induced thromboxane A2 (TXA2) synthesis, ADP (adenosine diphosphate)-induced aggregation, and occlusion time (PF-100) were measured.

RESULTS

CLO group only had a marked elevation of TXA2 (17.44 ± 15.62 ng/mL, P = .000) and a shortening of the platelet function analyzer (PFA)-100 closure time (157.13 ± 88 seconds, P = .047) compared with the other 2 groups (ASA: TXA2, .62 ± 1.59 ng/mL; ASA + CLO: TXA2 1.79 ± 4.59 ng/mL). They achieved a small (13%) but significant reduction of ADP-induced aggregation (87.00 ± 23.06 mm, P = .008) compared with the ASA group (102.82 ± 22.38 seconds).

CONCLUSIONS

Stopping aspirin intake within the first 72 hours of the acute stroke drastically increases TXA2 synthesis. During the same time window, the freshly prescribed clopidogrel manages to reduce the ADP-induced aggregation only slightly (13%). This study offers analytic proof that the common practice of replacing aspirin with clopidogrel does not leave stroke patients fully protected during the first days after an ischemic stroke. Possible solutions could be to preserve aspirin during a few days or to use loading doses of clopidogrel at hospital admission.

摘要

背景

通过血小板功能测试来测定血小板抑制作用,对于理解早期复发原因以及指导治疗建议可能至关重要。我们评估了在缺血性卒中急性期,仅继续服用阿司匹林、仅开始服用氯吡格雷或在阿司匹林基础上加用氯吡格雷的患者的血小板功能。

方法

64例患者在卒中前服用阿司匹林。根据所给予的抗血小板药物,分为3组:阿司匹林组(ASA):继续口服阿司匹林或静脉注射赖氨匹林的患者,n = 30;氯吡格雷组(CLO):停用阿司匹林并开始服用氯吡格雷的患者,n = 16;阿司匹林+氯吡格雷组(ASA + CLO):同时服用阿司匹林和氯吡格雷的患者,n = 10。测量胶原诱导的血栓素A2(TXA2)合成、二磷酸腺苷(ADP)诱导的聚集以及闭塞时间(PF - 100)。

结果

与其他2组相比,氯吡格雷组仅TXA2显著升高(17.44±15.62 ng/mL,P = 0.000),血小板功能分析仪(PFA)-100关闭时间缩短(157.13±88秒,P = 0.047)(ASA组:TXA2,0.62±1.59 ng/mL;ASA + CLO组:TXA2 1.79±4.59 ng/mL)。与阿司匹林组(102.82±22.38秒)相比,他们的ADP诱导聚集有小幅(13%)但显著的降低(87.00±23.06毫米,P = 0.008)。

结论

在急性卒中的头72小时内停止服用阿司匹林会大幅增加TXA2合成。在同一时间窗内,新开具的氯吡格雷仅略微降低(13%)ADP诱导的聚集。本研究提供了分析证据,表明在缺血性卒中后的头几天,用氯吡格雷替代阿司匹林的常见做法并不能使卒中患者得到充分保护。可能的解决办法是在几天内保留阿司匹林或在入院时使用氯吡格雷负荷剂量。

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