Continued Infarction Growth and Penumbral Consumption After Reperfusion in Vaccine-Naive Patients With COVID-19: A Case-Control Study.

Neurologic sequelae of SARS-CoV-2 include potentially malignant cerebrovascular events arising from complex hemodynamic, hematologic, and inflammatory processes occurring in concert. This study concerns the hypothesis that despite angiographic reperfusion COVID-19 promotes continued consumption of at-risk tissue volumes after acute ischemic stroke (AIS), yielding critical insights into prognostication and monitoring paradigms in vaccine-naive patients experiencing AIS. This retrospective study compared 100 consecutive COVID-19 patients with AIS presenting between March 2020 and April 2021 with a contemporaneous cohort of 282 AIS patients without COVID-19. Reperfusion classes were dichotomized into positive (extended thrombolysis in cerebral ischemia [eTICI] score = 2c-3) and negative (eTICI score < 2c) groups. All patients underwent endovascular therapy after initial CT perfusion imaging (CTP) to document infarction core and total hypoperfusion volumes. Ten COVID-positive (mean age ± SD, 67 ± 12 years; seven men, three women) and 144 COVID-negative patients (mean age, 71 ± 16 years; 76 men, 68 women) undergoing endovascular reperfusion, with antecedent CTP and follow-up imaging, comprised the final dataset. Initial infarction core and total hypoperfusion volumes (mean ± SD) were 1.5 ± 18 mL and 85 ± 100 mL in COVID-negative patients and 30.5 ± 34 mL and 117 ± 80.5 mL in COVID-positive patients, respectively. Final infarction volumes were significantly larger in patients with COVID-19, with median volumes of 77.8 mL versus 18.2 mL among control patients ( = .01), as were normalized measures of infarction growth relative to baseline infarction volume ( = .05). In adjusted logistic parametric regression models, COVID positivity emerged as a significant predictor for continued infarct growth (OR, 5.10 [95% CI, 1.00-25.95]; = .05). These findings support the potentially aggressive clinical course of cerebrovascular events in patients with COVID-19, suggesting greater infarction growth and ongoing consumption of at-risk tissues, even after angiographic reperfusion. SARS-CoV-2 infection may promote continued infarction progression despite angiographic reperfusion in vaccine-naive patients with large-vessel occlusion AIS. The findings carry potential implications for prognostication, treatment selection, and surveillance for infarction growth among revascularized patients in future waves of infection by novel viral strains.