From the Department of Neurology (J.M.K., R.B.L., M.G., S.V.P., R.I.K., S.N., S.A.).
Feinstein Institute for Medical Research at Northwell Health (J.J.W.), Manhasset, New York.
AJNR Am J Neuroradiol. 2021 Jan;42(2):257-261. doi: 10.3174/ajnr.A6920. Epub 2020 Oct 29.
Coronavirus disease 2019 (COVID-19) appears to be an independent risk factor for stroke. We hypothesize that patients who develop stroke while hospitalized for severe COVID-19 will have higher inflammatory markers and distinct stroke imaging patterns compared with patients positive for COVID-19 with out-of-hospital stroke onset and milder or no COVID-19 symptoms.
This is a retrospective case series of patients positive for COVID-19 on polymerase chain reaction testing with imaging-confirmed stroke treated within a large health care network in New York City and Long Island between March 14 and April 26, 2020. Clinical and laboratory data collected retrospectively included complete blood counts and creatinine, alanine aminotransferase, lactate dehydrogenase, C-reactive protein, ferritin, and D-dimer levels. All CT and MR imaging studies were independently reviewed by 2 neuroradiologists who recorded stroke subtype and patterns of infarction and intracranial hemorrhage.
Compared with patients with COVID-19 with outside-of-hospital stroke onset and milder or no COVID-19 symptoms ( = 45, 52.3%), patients with stroke already hospitalized for severe COVID-19 ( = 41, 47.7%) had significantly more frequent infarctions (95.1% versus 73.3%, = .006), with multivascular distributions (56.4% versus 33.3%, = .022) and associated hemorrhage (31.7% versus 4.4%, = .001). Patients with stroke admitted with more severe COVID-19 had significantly higher C-reactive protein and ferritin levels, elevated D-dimer levels, and more frequent lymphopenia and renal and hepatic injury (all, < .003).
Patients with stroke hospitalized with severe COVID-19 are characterized by higher inflammatory, coagulopathy, and tissue-damage biomarkers, supporting proposed pathogenic mechanisms of hyperinflammation activating a prothrombotic state. Cautious balancing of thrombosis and the risk of hemorrhagic transformation is warranted when considering anticoagulation.
新型冠状病毒病 2019（COVID-19）似乎是中风的一个独立危险因素。我们假设，与因 COVID-19 而住院但症状较轻或无症状的院外卒中患者相比，因重度 COVID-19 住院并发卒中的患者具有更高的炎症标志物和不同的卒中影像学模式。
这是一项回顾性病例系列研究，研究对象为 2020 年 3 月 14 日至 4 月 26 日期间在纽约市和长岛的一家大型医疗保健网络内，经聚合酶链反应检测确诊 COVID-19 阳性且影像学证实为卒中的患者。回顾性收集的临床和实验室数据包括全血细胞计数和肌酐、丙氨酸氨基转移酶、乳酸脱氢酶、C 反应蛋白、铁蛋白和 D-二聚体水平。所有 CT 和 MR 成像研究均由 2 位神经放射科医生独立审查，记录卒中亚型和梗死及颅内出血模式。
与因 COVID-19 而院外卒中且症状较轻或无症状的患者（ = 45，52.3%）相比，因重度 COVID-19 而住院并发卒中的患者（ = 41，47.7%）梗死更频繁（95.1%比 73.3%，= .006），多血管分布（56.4%比 33.3%，= .022）和相关出血（31.7%比 4.4%，= .001）更常见。因 COVID-19 而住院的卒中患者的 C 反应蛋白和铁蛋白水平显著升高，D-二聚体水平升高，淋巴细胞减少和肝肾功能损伤更常见（均 < .003）。
因重度 COVID-19 而住院并发卒中的患者的炎症、凝血障碍和组织损伤生物标志物水平较高，支持过度炎症激活促血栓形成状态的潜在发病机制。在考虑抗凝时，需要谨慎平衡血栓形成和出血转化的风险。
