Wiśniewski Adam, Sikora Joanna, Karczmarska-Wódzka Aleksandra, Sobczak Przemysław, Lemanowicz Adam, Zawada Elżbieta, Masiliūnas Rytis, Jatužis Dalius
Department of Neurology, Faculty of Medicine, Nicolaus Copernicus University in Toruń, Collegium Medicum in Bydgoszcz, 85-094 Bydgoszcz, Poland.
Biotechnology Research and Teaching Team, Department of Transplantology and General Surgery, Faculty of Medicine, Nicolaus Copernicus University in Toruń, Collegium Medicum in Bydgoszcz, 85-094 Bydgoszcz, Poland.
Diagnostics (Basel). 2021 Feb 27;11(3):405. doi: 10.3390/diagnostics11030405.
High on-treatment platelet reactivity or its equivalent-resistance to the antiplatelet agent-significantly reduces the efficacy of the therapy, contributing to a negative impact on stroke course. Previous studies demonstrated that aspirin resistance is associated with a larger size of acute ischemic infarct. Due to the increasing use of clopidogrel in the secondary prevention of stroke, we aimed to assess the impact of clopidogrel resistance on the size and extent of ischemic lesions, both acute and chronic.
This prospective, single-center and observational study involved 74 ischemic stroke subjects, treated with 75 mg of clopidogrel. We used impedance aggregometry to determine platelet reactivity 6-12 h after a dose of clopidogrel as a first assessment and 48 h later as the second measurement. A favorable dynamics of platelet reactivity over time was the decrease in the minimum value equal to the median in the entire study. The volume of acute ischemic infarct was estimated within 48 h after onset in diffusion-weighted imaging and fluid-attenuated inversion recovery sequences of magnetic resonance and the severity of chronic vascular lesions by Fazekas scale.
Subjects with mild severity of chronic vascular lesions (Fazekas 1) exhibited a significant decrease of platelet reactivity over time ( = 0.035). Dynamics of platelet reactivity over time differed between subjects with large, moderate, mild and insignificant size of acute ischemic lesion (Kruskall-Wallis H = 3.2576; = 0.048). In multivariate regression models, we reported unfavorable dynamics of platelet reactivity alone and combined with a high initial value of platelet reactivity as independent predictors of higher risk of a significant ischemic infarct volume (OR 7.16 95%CI 1.69-30.31, = 0.008 and 26.49 95%CI 1.88-372.4, = 0.015, respectively).
We emphasized that unfavorable dynamics of platelet reactivity over time during clopidogrel therapy in acute phase of stroke affect the volume of acute infarct and the severity of chronic vascular lesions.
治疗期间血小板高反应性或其等效物——对抗血小板药物的抵抗——会显著降低治疗效果，对卒中病程产生负面影响。既往研究表明，阿司匹林抵抗与急性缺血性梗死灶面积较大有关。由于氯吡格雷在卒中二级预防中的使用日益增加，我们旨在评估氯吡格雷抵抗对急性和慢性缺血性病变的大小及范围的影响。
这项前瞻性、单中心观察性研究纳入了74例接受75mg氯吡格雷治疗的缺血性卒中患者。我们使用阻抗聚集法在服用一剂氯吡格雷后6 - 12小时作为首次评估来测定血小板反应性，并在48小时后进行第二次测量。血小板反应性随时间的良好动态变化是最小值下降至整个研究中的中位数。在磁共振的扩散加权成像和液体衰减反转恢复序列中，在发病后48小时内估计急性缺血性梗死体积，并通过Fazekas量表评估慢性血管病变的严重程度。
慢性血管病变轻度（Fazekas 1级）的患者血小板反应性随时间显著下降（P = 0.035）。急性缺血性病变大小为大、中、小和无显著意义的患者之间，血小板反应性随时间的动态变化有所不同（Kruskall - Wallis H = 3.2576；P = 0.048）。在多变量回归模型中，我们报告血小板反应性单独的不良动态变化以及与血小板反应性高初始值相结合，是显著缺血性梗死体积较高风险的独立预测因素（分别为OR 7.16，95%CI 1.69 - 30.31，P = 0.008和OR 26.49，95%CI 1.88 - 372.4，P = 0.015）。
我们强调，卒中急性期氯吡格雷治疗期间血小板反应性随时间的不良动态变化会影响急性梗死体积和慢性血管病变的严重程度。
