新型冠状病毒2型感染预示急性缺血性卒中患者梗死体积更大。
SARS-CoV-2 infection predicts larger infarct volume in patients with acute ischemic stroke.
作者信息
De Michele Manuela, Lorenzano Svetlana, Piscopo Paola, Rivabene Roberto, Crestini Alessio, Chistolini Antonio, Stefanini Lucia, Pulcinelli Fabio M, Berto Irene, Campagna Roberta, Amisano Paolo, Iacobucci Marta, Cirelli Carlo, Falcou Anne, Nicolini Ettore, Schiavo Oscar G, Toni Danilo
机构信息
Emergency Department, Stroke Unit, Sapienza University of Rome, Rome, Italy.
Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy.
出版信息
Front Cardiovasc Med. 2023 Jan 10;9:1097229. doi: 10.3389/fcvm.2022.1097229. eCollection 2022.
BACKGROUND AND PURPOSE
Acute ischemic stroke (AIS) is a fearful complication of Coronavirus Disease-2019 (COVID-19). Aims of this study were to compare clinical/radiological characteristics, endothelial and coagulation dysfunction between acute ischemic stroke (AIS) patients with and without COVID-19 and to investigate if and how the SARS-CoV-2 spike protein (SP) was implicated in triggering platelet activation.
METHODS
We enrolled AIS patients with COVID-19 within 12 h from onset and compared them with an age- and sex-matched cohort of AIS controls without COVID-19. Neuroimaging studies were performed within 24 h. Blood samples were collected in a subset of 10 patients.
RESULTS
Of 39 AIS patients, 22 had COVID-19 and 17 did not. Admission levels of Factor VIII and von Willebrand factor antigen were significantly higher in COVID-19 patients and positively correlated with the infarct volume. In multivariate linear regression analyses, COVID-19 was an independent predictor of infarct volume (B 20.318, Beta 0.576, 95%CI 6.077-34.559; = 0.011). SP was found in serum of 2 of the 10 examined COVID-19 patients. Platelets from healthy donors showed a similar degree of procoagulant activation induced by COVID-19 and non-COVID-19 patients' sera. The anti-SP and anti-FcγRIIA blocking antibodies had no effect in modulating platelet activity in both groups.
CONCLUSIONS
SARS-CoV-2 infection seems to play a major role in endothelium activation and infarct volume extension during AIS.
背景与目的
急性缺血性卒中（AIS）是2019冠状病毒病（COVID-19）的一种可怕并发症。本研究的目的是比较合并或未合并COVID-19的急性缺血性卒中（AIS）患者的临床/影像学特征、内皮及凝血功能障碍，并研究严重急性呼吸综合征冠状病毒2（SARS-CoV-2）刺突蛋白（SP）是否以及如何参与触发血小板活化。
方法
我们纳入了发病12小时内的合并COVID-19的AIS患者，并将其与年龄和性别匹配的未合并COVID-19的AIS对照组进行比较。在24小时内进行神经影像学检查。在10例患者的亚组中采集血样。
结果
39例AIS患者中，22例合并COVID-19，17例未合并。COVID-19患者的凝血因子VIII和血管性血友病因子抗原的入院水平显著更高，且与梗死体积呈正相关。在多变量线性回归分析中，COVID-19是梗死体积的独立预测因子（B 20.318，β 0.576，95%CI 6.077-34.559；P = 0.011）。在10例接受检查的COVID-19患者中的2例血清中发现了SP。健康供体的血小板对COVID-19患者和非COVID-19患者的血清表现出相似程度的促凝活化。抗SP和抗FcγRIIA阻断抗体在两组中均对调节血小板活性无作用。
结论
SARS-CoV-2感染似乎在AIS期间的内皮激活和梗死体积扩大中起主要作用。
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