Saji Naoki, Tone Shigenobu, Murotani Kenta, Yagita Yoshiki, Kimura Kazumi, Sakurai Takashi
Department of Stroke Medicine, Kawasaki Medical School, Japan; Center for Comprehensive Care and Research on Memory Disorders, National Center for Geriatrics and Gerontology, Japan.
Department of Biochemistry, Kawasaki Medical School, Japan; Laboratory of Molecular Developmental Biology, Graduate School of Science and Engineering, Tokyo Denki University, Japan.
J Stroke Cerebrovasc Dis. 2018 Jun;27(6):1639-1645. doi: 10.1016/j.jstrokecerebrovasdis.2018.01.020. Epub 2018 Feb 14.
The mechanism of progressive neurological deficit in patients with recent small subcortical infarcts has not yet been clarified. Inflammatory biomarkers and the use of cilostazol may be associated with this phenomenon.
Between May 2013 and April 2014, we evaluated consecutive first-ever patients with stroke due to recent small subcortical infarcts within 48 hours of onset. We divided patients into 2 groups according to the use of antiplatelet agents (cilostazol with or without aspirin versus aspirin alone). Plasma biomarkers such as matrix metalloproteinase-9, interleukin-6, high sensitive C-reactive protein, and amyloid β precursor protein (APP770, indicating endothelial dysfunction) were measured twice: (1) within 24 hours; and (2) 1 week after their admission. Multivariable logistic regression analyses were performed to identify the variables independently associated with progressive neurological deficit and poor functional outcome.
We analyzed 41 patients (male: 63.4%, mean age: 70.8 years). Most of the patients (90%) who were treated with cilostazol were concomitantly treated with aspirin. Matrix metalloproteinase-9 and high sensitive C-reactive protein were higher in patients with progressive neurological deficit compared with those without. APP770 were more likely to be decreased in cilostazol group compared with aspirin group. Multivariable analyses show that traditional risk factors such as age and National Institutes of Health Stroke Scale scores were independently associated with both progressive neurological deficit and poor functional outcome.
Inflammatory biomarkers may be associated with progressive neurological deficit. Early initiation of cilostazol may decrease the levels of plasma biomarkers.
近期发生小皮质下梗死的患者出现进行性神经功能缺损的机制尚未阐明。炎症生物标志物及西洛他唑的使用可能与这一现象有关。
在2013年5月至2014年4月期间，我们对发病48小时内首次发生近期小皮质下梗死所致卒中的连续患者进行了评估。根据抗血小板药物的使用情况（西洛他唑联合或不联合阿司匹林与单用阿司匹林）将患者分为两组。血浆生物标志物如基质金属蛋白酶-9、白细胞介素-6、高敏C反应蛋白和淀粉样β前体蛋白（APP770，提示内皮功能障碍）测量两次：（1）入院24小时内；（2）入院1周后。进行多变量逻辑回归分析以确定与进行性神经功能缺损和不良功能转归独立相关的变量。
我们分析了41例患者（男性：63.4%，平均年龄：70.8岁）。大多数接受西洛他唑治疗的患者（90%）同时接受了阿司匹林治疗。与无进行性神经功能缺损的患者相比，有进行性神经功能缺损的患者基质金属蛋白酶-9和高敏C反应蛋白水平更高。与阿司匹林组相比，西洛他唑组APP770更可能降低。多变量分析显示，年龄和美国国立卫生研究院卒中量表评分等传统危险因素与进行性神经功能缺损和不良功能转归均独立相关。
炎症生物标志物可能与进行性神经功能缺损有关。早期开始使用西洛他唑可能会降低血浆生物标志物水平。
