颅内外和颅内动脉粥样硬化相关的复发性缺血性脑卒中的高剂量阿司匹林血小板反应性差异

Kyung Chul Noh, Hye-Yeon Choi, Ho Geol Woo, Jun Young Chang, Sung Hyuk Heo, Dae-Il Chang, Bum Joon Kim
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引用次数: 2

摘要

背景和目的:尽管使用抗血小板药物,缺血性脑卒中仍会复发。颅内动脉粥样硬化(ICAS)和颅外动脉粥样硬化(ECAS)的复发涉及多种机制。高阿司匹林血小板反应性(HAPR)可能在ICAS和ECAS引起的复发性卒中中有所不同。方法:连续纳入服用阿司匹林后大动脉粥样硬化所致复发性缺血性脑卒中患者。根据罪魁祸首狭窄的位置将缺血性卒中分为ICAS或ECAS所致卒中。阿司匹林反应单位(ARU)值大于550 IU被定义为HAPR。比较两组HAPR及其相关因素,并考虑卒中发生机制。结果:190例卒中复发患者(ICAS 111例,ECAS 79例)中,HAPR 36例(18.3%)。ECAS组的ARU值高于ICAS组(492±83比465±78,平均±标准差;p=0.028), HAPR患者的比例也是如此(27.8%比12.6%,p=0.008)。男性和因ECAS引起的中风(参考=因ICAS引起的中风:优势比=5.760;95%置信区间=2.154-15.403;结论:与ICAS相比,ECAS所致卒中复发与HAPR和抗血小板抑制不足的相关性更强。ICAS或ECAS导致的复发性缺血性卒中的动脉对动脉栓塞与HAPR相关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

High-on-Aspirin Platelet Reactivity Differs Between Recurrent Ischemic Stroke Associated With Extracranial and Intracranial Atherosclerosis.

High-on-Aspirin Platelet Reactivity Differs Between Recurrent Ischemic Stroke Associated With Extracranial and Intracranial Atherosclerosis.

High-on-Aspirin Platelet Reactivity Differs Between Recurrent Ischemic Stroke Associated With Extracranial and Intracranial Atherosclerosis.

High-on-Aspirin Platelet Reactivity Differs Between Recurrent Ischemic Stroke Associated With Extracranial and Intracranial Atherosclerosis.

Background and purpose: Ischemic stroke recurs despite the use of antiplatelet agents. Various mechanisms are involved in recurrence due to intracranial atherosclerosis (ICAS) and extracranial atherosclerosis (ECAS). High-on-aspirin platelet reactivity (HAPR) may differ between recurrent stroke due to ICAS and ECAS.

Methods: Patients with recurrent ischemic stroke as a result of large-artery atherosclerosis despite taking aspirin were enrolled consecutively. Ischemic stroke was classified as stroke due to ICAS or ECAS according to the location of the culprit stenosis. An aspirin reaction units (ARU) value of >550 IU was defined as HAPR. HAPR and its associated factors were compared between the two groups and also considering the mechanism of stroke.

Results: Among the 190 patients with recurrent stroke (111 with ICAS and 79 with ECAS), 36 (18.3%) showed HAPR. The ARU value was higher in the ECAS than the ICAS group (492±83 vs. 465±78, mean±standard deviation; p=0.028), as was the proportion of patients with HAPR (27.8% vs. 12.6%, p=0.008). Being male and having stroke due to ECAS (reference=stroke due to ICAS: odds ratio=5.760; 95% confidence interval=2.154-15.403; p<0.001) was independently associated with HAPR. The ARU value differed according to the stroke mechanism, and was highest in those with artery-to-artery embolism. Artery-to-artery embolism was independently associated with HAPR in both the ICAS and ECAS groups.

Conclusions: Recurrent stroke due to ECAS was more strongly associated with HAPR and insufficient antiplatelet inhibition than was that due to ICAS. Artery-to-artery embolism was associated with HAPR in recurrent ischemic stroke as a result of ICAS or ECAS.

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