Relation of Aspirin Failure to Clinical Outcome and to Platelet Response to Aspirin in Patients With Acute Myocardial Infarction
Relation of Aspirin Failure to Clinical Outcome and to Platelet Response to Aspirin in Patients With Acute Myocardial Infarction
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DOI：
10.1016/j.amjcard.2010.09.025
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发表时间：
2011-02-01
影响因子：
2.8
通讯作者：
Matetzky, Shlomi
中科院分区：
文献类型：
--
作者：
Beigel, Roy;Hod, Hanoch;Matetzky, Shlomi
阿司匹林失效，定义为急性冠状动脉综合征的发生，尽管使用阿司匹林，与较高的心血管风险和较差的预后有关。这种现象是患者特征的表现，还是阿司匹林对血小板抑制不足的表现，尚无研究。我们评估了174例连续的急性心肌梗死患者。其中118例（68%）为阿司匹林初治，56例（32%）为阿司匹林失效。在所有患者服用阿司匹林72小时后分析血小板功能。用透射聚集体法和流动条件研究了血小板的反应性。测定6个月主要不良冠状动脉事件（死亡、复发急性冠状动脉综合征和/或中风）的发生率。阿司匹林失效的患者年龄较大（p = 0.002），高血压较多（p < 0.001），高脂血症较多（p < 0.001），既往心血管事件和/或手术的可能性较大（p < 0.001）。阿斯匹林衰竭组6个月累积主要不良冠脉事件发生率较高（14.3% vs 2.5% p < 0.01）。与未服用阿司匹林的患者相比，阿司匹林失效患者在阿司匹林治疗后花生四烯酸诱导的血小板聚集较低（32 +/- 24 vs 45 +/- 30, p = 0.003）。然而，在调整基线特征差异后，这并不显著（p = 0.82）。同样，在流动条件下，二磷酸腺苷诱导的血小板聚集和血小板沉积也没有显著差异。总之，我们的研究结果表明阿司匹林失效仅仅是高危患者的一个标志，而不是血小板对阿司匹林治疗反应不足的表现。(C) 2011爱思唯尔公司版权所有。（美国医学杂志2011；107:339-342）
Aspirin failure, defined as occurrence of an acute coronary syndrome despite aspirin use, has been associated with a higher cardiovascular risk profile and worse prognosis. Whether this phenomenon is a manifestation of patient characteristics or failure of adequate platelet inhibition by aspirin has never been studied. We evaluated 174 consecutive patients with acute myocardial infarction. Of them, 118 (68%) were aspirin naive and 56 (32%) were regarded as having aspirin failure. Platelet function was analyzed after >= 72 hours of aspirin therapy in all patients. Platelet reactivity was studied by light-transmitted aggregometry and under flow conditions. Six-month incidence of major adverse coronary events (death, recurrent acute coronary syndrome, and/or stroke) was determined. Those with aspirin failure were older (p = 0.002), more hypertensive (p < 0.001), more hyperlipidemic (p < 0.001), and more likely to have had a previous cardiovascular event and/or procedure (p < 0.001). Cumulative 6-month major adverse coronary events were higher in the aspirin-failure group (14.3% vs 2.5% p < 0.01). Patients with aspirin failure had lower arachidonic acid induced platelet aggregation (32 +/- 24 vs 45 +/- 30, p = 0.003) after aspirin therapy compared to their aspirin-naive counterparts. However, this was not significant after adjusting for differences in baseline characteristics (p = 0.82). Similarly, there were no significant differences in adenosine diphosphate induced platelet aggregation and platelet deposition under flow conditions. In conclusion, our results suggest that aspirin failure is merely a marker of higher-risk patient profiles and not a manifestation of inadequate platelet response to aspirin therapy. (C) 2011 Elsevier Inc. All rights reserved. (Am J Cardiol 2011;107:339-342)