Department of Neurology, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
Department of Neurology, Faculty of Medicine, On Dokuz Mayis University, Samsun, Turkey.
J Stroke Cerebrovasc Dis. 2015 Apr;24(4):745-50. doi: 10.1016/j.jstrokecerebrovasdis.2014.10.015. Epub 2014 Oct 31.
A significant proportion of ischemic strokes occur while using aspirin and therefore can be considered as clinical aspirin resistance. Apart from this clinical description, aspirin resistance can be defined by laboratory tests of in vitro platelet reactivity. The correlation between clinical and laboratory-defined resistance, however, is far from perfect, and the heterogenous nature of stroke pathophysiology might play a role in this discrepancy.
The level of in vitro platelet inhibition by aspirin was prospectively evaluated using the VerifyNow Aspirin Assay (Accumetrics, San Diego, CA) in patients presenting with ischemic stroke while using aspirin (n = 78). Demographic and clinical features, including stroke etiology, were compared among patients with and without sufficient level of platelet inhibition and an additional set of patients suffering from stroke while not using aspirin (n = 257). Similar analyses were performed in a separate validation cohort.
Laboratory evidence of insufficient platelet inhibition was detected in 16 of 78 patients (21%) with clinical aspirin resistance. On the other hand, 30 patients (38%) had stroke etiologies well known to be inadequately responsive to aspirin therapy. Overall, laboratory-defined resistance by itself could be considered to be accountable for the ischemic event in only 15% of these patients. The corresponding figure was 9% in validation cohort. Patients with sufficient level of platelet inhibition were more likely to harbor an anticoagulant responsive etiology compared with aspirin naive patients (odds ratio, 2.0; P = .033).
Our findings highlight that laboratory aspirin resistance because of insufficient platelet inhibition is relatively uncommon, whereas pathophysiologic resistance, signifying the presence of etiologies that cannot be efficiently treated with aspirin treatment, is a major contributor of clinical resistance in ischemic stroke.
相当一部分缺血性中风发生在使用阿司匹林期间，因此可以被认为是临床阿司匹林抵抗。除了这种临床描述外，阿司匹林抵抗还可以通过体外血小板反应性的实验室检测来定义。然而，临床和实验室定义的抵抗之间的相关性远非完美，中风病理生理学的异质性可能在这种差异中发挥作用。
前瞻性地使用 VerifyNow 阿司匹林测定法（Accumetrics，圣地亚哥，CA）评估 78 例正在使用阿司匹林的缺血性中风患者的体外血小板抑制水平。比较了血小板抑制水平充分的患者与未充分抑制的患者以及不使用阿司匹林的中风患者（n = 257）之间的人口统计学和临床特征，包括中风病因。在另一个验证队列中进行了类似的分析。
在 78 例临床阿司匹林抵抗患者中有 16 例（21%）检测到血小板抑制不足的实验室证据。另一方面，30 例患者（38%）的中风病因已知对阿司匹林治疗反应不足。总的来说，实验室定义的抵抗本身只能解释这些患者中 15%的缺血事件。在验证队列中，这一数字为 9%。与阿司匹林未治疗的患者相比，血小板抑制水平充分的患者更有可能存在抗凝反应性病因（比值比，2.0；P = 0.033）。
我们的发现强调，由于血小板抑制不足导致的实验室阿司匹林抵抗相对少见，而病理生理抵抗，即存在不能有效用阿司匹林治疗的病因，是缺血性中风临床抵抗的主要原因。
