Severe acute respiratory syndrome coronavirus (SARS-CoV-2) is responsible for an unprecedented worldwide pandemic that has severely impacted the United States. As the pandemic continues, a growing body of evidence suggests that infected patients may develop significant coagulopathy with resultant thromboembolic complications including deep vein thrombosis, pulmonary embolism, myocardial infarction, and ischemic stroke. However, this data is limited and comes from recent small case series and observational studies on stroke types, mechanisms, and outcomes.1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 Furthermore, evidence on the role of therapeutic anticoagulation in SARS-CoV-2 infected patients with elevated inflammatory markers, such as D-dimer, is also limited. We report the case of a middle-aged patient who presented with a large vessel ischemic stroke likely resulting from an underlying inflammatory response in the setting of known novel coronavirus infection (COVID-19). Histopathologic analysis of the patient's ischemic brain tissue revealed hypoxic neurons, significant edema from the underlying ischemic insult, fibrin thrombi in small vessels, and fibroid necrosis of the vascular wall without any signs of vasculature inflammation. Brain biopsy was negative for the presence of SARS-CoV-2 RNA (RT-PCR assay). Along with a growing body of literature, our case suggests that cerebrovascular thromboembolic events in COVID-19 infection may be related to acquired hypercoagulability and coagulation cascade activation due to the release of inflammatory markers and cytokines, rather than virus-induced vasculitis. Further studies to investigate the mechanism of cerebrovascular thromboembolic events and their prevention is warranted.

严重的急性呼吸系统综合症冠状病毒（SARS-CoV-2）造成了前所未有的全球性流行病，严重影响了美国。随着大流行的继续，越来越多的证据表明，感染的患者可能会发展为严重的凝血病，并引起血栓栓塞性并发症，包括深静脉血栓形成，肺栓塞，心肌梗塞和缺血性中风。但是，该数据有限，来自最近的小病例系列研究以及对中风类型，机制和结果的观察性研究.1,2,3,4,5,6,7,8,9,10,11,12,13 ，[14]此外，关于治疗性抗凝在具有升高的炎性标记物（例如D-二聚体）的SARS-CoV-2感染患者中的作用的证据也很有限。我们报道了一个中年患者的病例，该患者表现出大血管缺血性中风，可能是由已知新型冠状病毒感染（COVID-19）的潜在炎症反应引起的。对患者缺血性脑组织的组织病理学分析显示，缺氧性神经元，来自潜在的缺血性损伤的明显水肿，小血管中的纤维蛋白血栓以及血管壁的肌瘤坏死，而没有任何脉管系统炎症的迹象。对于SARS-CoV-2 RNA的存在，脑活检为阴性（RT-PCR分析）。随着越来越多的文献报道，我们的案例表明，在COVID-19感染中脑血管血栓栓塞事件可能与炎症因子和细胞因子的释放引起的获得性高凝和凝血级联激活有关，而不是病毒引起的血管炎。有必要进行进一步研究以研究脑血管血栓栓塞事件的机制及其预防措施。