Department of Neurology, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA.
Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA.
Transl Stroke Res. 2020 Jun;11(3):322-325. doi: 10.1007/s12975-020-00818-9. Epub 2020 May 7.
The COVID-19 pandemic is associated with neurological symptoms and complications including stroke. There is hypercoagulability associated with COVID-19 that is likely a "sepsis-induced coagulopathy" and may predispose to stroke. The SARS-CoV-2 virus binds to angiotensin-converting enzyme 2 (ACE2) present on brain endothelial and smooth muscle cells. ACE2 is a key part of the renin angiotensin system (RAS) and a counterbalance to angiotensin-converting enzyme 1 (ACE1) and angiotensin II. Angiotensin II is proinflammatory, is vasoconstrictive, and promotes organ damage. Depletion of ACE2 by SARS-CoV-2 may tip the balance in favor of the "harmful" ACE1/angiotensin II axis and promote tissue injury including stroke. There is a rationale to continue to treat with tissue plasminogen activator for COVID-19-related stroke and low molecular weight heparinoids may reduce thrombosis and mortality in sepsis-induced coagulopathy.
新型冠状病毒病（COVID-19）与包括中风在内的神经系统症状和并发症有关。COVID-19 存在高凝状态，可能是一种“脓毒症诱导的凝血障碍”，并可能导致中风。SARS-CoV-2 病毒与脑内皮细胞和平滑肌细胞上的血管紧张素转换酶 2（ACE2）结合。ACE2 是肾素血管紧张素系统（RAS）的关键部分，是血管紧张素转换酶 1（ACE1）和血管紧张素 II 的平衡物。血管紧张素 II 具有促炎作用，可收缩血管并促进器官损伤。SARS-CoV-2 对 ACE2 的耗竭可能使平衡倾向于“有害的” ACE1/血管紧张素 II 轴，并促进组织损伤，包括中风。对于 COVID-19 相关性中风，继续使用组织型纤溶酶原激活物治疗是合理的，低分子量肝素类药物可能会降低脓毒症诱导的凝血障碍中的血栓形成和死亡率。
