Wiśniewski Adam, Sikora Joanna, Sławińska Agata, Filipska Karolina, Karczmarska-Wódzka Aleksandra, Serafin Zbigniew, Kozera Grzegorz
Department of Neurology, Faculty of Medicine, Nicolaus Copernicus University in Toruń, Collegium Medicum in Bydgoszcz, 85-094 Bydgoszcz, Poland.
Experimental 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.
J Clin Med. 2020 Jan 17;9(1):251. doi: 10.3390/jcm9010251.
Excessive platelet activation and aggregation plays an important role in the pathogenesis of ischemic stroke. Correlation between platelet reactivity and ischemic lesions in the brain shows contradictory results and there are not enough data about the potential role of stroke etiology and its relationships with chronic lesions. The aim of this study is to assess the relationship between platelet reactivity and the extent of ischemic lesions with the particular role of etiopathogenesis.
The study involved 69 patients with ischemic stroke, including 20 patients with large-vessel disease and 49 patients with small-vessel disease. Evaluation of platelet reactivity was performed within 24 h after the onset of stroke using two aggregometric methods (impedance and optical), while ischemic volume measurement in the brain was performed using magnetic resonance imaging (in diffusion-weighted imaging (DWI) and fluid-attenuated inversion recovery (FLAIR) sequences) at day 2-5 after the onset of stroke.
In the large-vessel disease subgroup, a correlation was found between platelet reactivity and acute ischemic focus volume (correlation coefficient (R) = 0.6858 and = 0.0068 for DWI; R = 0.6064 and = 0.0215 for FLAIR). Aspirin-resistant subjects were significantly more likely to have a large ischemic focus (Odds Ratio (OR) = 45.00, 95% Confidence Interval (CI) = 1.49-135.36, = 0.0285 for DWI; OR = 28.00, 95% CI = 1.35-58.59, = 0.0312 for FLAIR) than aspirin-sensitive subjects with large-vessel disease.
In patients with ischemic stroke due to large-vessel disease, high on-treatment platelet reactivity affects the extent of acute and chronic ischemic lesions.
血小板过度激活和聚集在缺血性卒中的发病机制中起重要作用。血小板反应性与脑缺血性病变之间的相关性结果相互矛盾，关于卒中病因的潜在作用及其与慢性病变的关系的数据也不足。本研究的目的是评估血小板反应性与缺血性病变程度之间的关系以及病因发病机制的特殊作用。
该研究纳入了69例缺血性卒中患者，包括20例大血管疾病患者和49例小血管疾病患者。在卒中发作后24小时内使用两种凝集测定方法（阻抗法和光学法）评估血小板反应性，而在卒中发作后第2 - 5天使用磁共振成像（在扩散加权成像（DWI）和液体衰减反转恢复（FLAIR）序列中）测量脑缺血体积。
在大血管疾病亚组中，发现血小板反应性与急性缺血灶体积之间存在相关性（DWI的相关系数（R）= 0.6858，P = 0.0068；FLAIR的R = 0.6064，P = 0.0215）。与大血管疾病的阿司匹林敏感受试者相比，阿司匹林抵抗受试者更有可能有较大的缺血灶（DWI的优势比（OR）= 45.00，95%置信区间（CI）= 1.49 - 135.36，P = 0.0285；FLAIR的OR = 28.00，95% CI = 1.35 - 58.59，P = 0.0312）。
在大血管疾病所致缺血性卒中患者中，治疗时的高血小板反应性会影响急性和慢性缺血性病变的程度。
