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. 2021 Jan;42(2):257-261.
doi: 10.3174/ajnr.A6920. Epub 2020 Oct 29.

COVID-19 Severity and Stroke: Correlation of Imaging and Laboratory Markers

Affiliations

COVID-19 Severity and Stroke: Correlation of Imaging and Laboratory Markers

J M Katz et al. AJNR Am J Neuroradiol. 2021 Jan.

Abstract

Background and purpose: 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.

Materials and methods: 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.

Results: Compared with patients with COVID-19 with outside-of-hospital stroke onset and milder or no COVID-19 symptoms (n = 45, 52.3%), patients with stroke already hospitalized for severe COVID-19 (n = 41, 47.7%) had significantly more frequent infarctions (95.1% versus 73.3%, P = .006), with multivascular distributions (56.4% versus 33.3%, P = .022) and associated hemorrhage (31.7% versus 4.4%, P = .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, P < .003).

Conclusions: 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.

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Figures

FIG 1.
FIG 1.
Cerebral hemorrhage in patients with COVID-19. A, Noncontrast CT of the head shows a large left basal ganglia intraparenchymal hemorrhage, with diffuse subarachnoid and left frontal subdural (blue arrow) hemorrhages in a woman with asymptomatic COVID-19. B, Noncontrast CT of the head showing extensive bilateral multifocal cerebral infarctions with hemorrhagic conversion in a comatose man with multiorgan failure. C, Brain MR imaging FLAIR and D, MR venogram show hemorrhagic venous infarction in the left temporal lobe (C) secondary to thrombosis of left transverse and sigmoid sinuses and internal jugular vein (D) in a young woman presenting with seizures.
FIG 2.
FIG 2.
Multivascular territory infarctions in COVID-19. MR imaging of the brain diffusion-weighted imaging demonstrates watershed-pattern infarctions in a 52-year-old man with mild COVID-19 symptoms, who awoke at home with left hemiparesis (A) and an 86-year-old woman admitted for hypoglycemia, dehydration, and COVID-19 pneumonia (B) and found to have new-onset atrial fibrillation; 8 days into her hospitalization, she developed lethargy, left hemiparesis, expressive aphasia, and dysphagia.

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