María E Ramos-Araque1,2, James E Siegler3, Marc Ribo4,5, Manuel Requena4,5, Cristina López2, Mercedes de Lera2, Juan F Arenillas2, Isabel Hernández Pérez2, Beatriz Gómez-Vicente2, Blanca Talavera2, Pere Cardona Portela6, Ana Nuñez Guillen6, Xabier Urra7, Laura Llull7, Arturo Renú7, Thanh N Nguyen8, Dinesh Jillella9, Fadi Nahab9, Raul Nogueira10, Diogo Haussen10, Ryna Then11, Jesse M Thon11, Luis Rodríguez Esparragoza12, Maria Hernández-Pérez12, Alejandro Bustamante12, Ossama Yassin Mansour13, Mohammed Megahed14, Tamer Hassan15, David S Liebeskind16, Ameer Hassan17,18, Saif Bushnaq19, Mohamed Osman19, Alejandro Rodriguez Vazquez7. 1. Institute of Biomedical Research of Salamanca, Department of Neurology, Hospital Universitario de Salamanca, Salamanca, Spain. 2. Department of Neurology, Hospital Clínico Universitario de Valladolid, Valladolid, Spain. 3. Cooper Neurologic Institute, Cooper University Hospital, Camden, NJ, USA. siegler-james@cooperhealth.edu. 4. Stroke Unit, Department of Neurology, Vall d'Hebron Research Institute, Barcelona, Spain. 5. Departament of Medicina, Universitat Autónoma de Barcelona, Barcelona, Spain. 6. Department of Neurology, Hospital Universitari, Bellvitge, Barcelona, Spain. 7. Department of Neurology, Hospital Clínic, Barcelona, Spain. 8. Department of Neurology, Department of Radiology, Department of Neurosurgery, Boston Medical Center, Boston University School of Medicine, Boston, MA, USA. 9. Department of Neurology, Emory University School of Medicine, Atlanta, USA. 10. Department of Neurology, Grady Memorial Hospital, Atlanta, GA, USA. 11. Cooper Neurologic Institute, Cooper University Hospital, Camden, NJ, USA. 12. Stroke Unit, Neuroscience Department, Hospital Universitari Germans Trias i Pujol, Badalona, Barcelona, Spain. 13. Neurology Department, Stroke and neurointervention unit, Alexandria University, Alexandria, Egypt. 14. Critical care Department, Alexandria University, Alexandria, Egypt. 15. Neurosurgery Department, Stroke and Neurointervention unit, Alexandria University, Alexandria, Egypt. 16. Department of Neurology, Ronald Reagan UCLA Medical Center, Los Angeles, USA. 17. Department of Clinical Neuroscience Research, Valley Baptist Medical Center, Harlingen, TX, USA. 18. Department of Neurology, University of Texas Rio Grande Valley, Harlingen, TX, USA. 19. Neuroscience Institute, Bon Secours Mercy Health St. Vincent Hospital, Toledo, OH, USA.
Abstract
BACKGROUND AND PURPOSE: Coronavirus disease 2019 (COVID-19) is associated with a small but clinically significant risk of stroke, the cause of which is frequently cryptogenic. In a large multinational cohort of consecutive COVID-19 patients with stroke, we evaluated clinical predictors of cryptogenic stroke, short-term functional outcomes and in-hospital mortality among patients according to stroke etiology. METHODS: We explored clinical characteristics and short-term outcomes of consecutively evaluated patients 18 years of age or older with acute ischemic stroke (AIS) and laboratory-confirmed COVID-19 from 31 hospitals in 4 countries (3/1/20-6/16/20). RESULTS: Of the 14.483 laboratory-confirmed patients with COVID-19, 156 (1.1%) were diagnosed with AIS. Sixty-one (39.4%) were female, 84 (67.2%) white, and 88 (61.5%) were between 60 and 79 years of age. The most frequently reported etiology of AIS was cryptogenic (55/129, 42.6%), which was associated with significantly higher white blood cell count, c-reactive protein, and D-dimer levels than non-cryptogenic AIS patients (p</=0.05 for all comparisons). In a multivariable backward stepwise regression model estimating the odds of in-hospital mortality, cryptogenic stroke mechanism was associated with a fivefold greater odds in-hospital mortality than strokes due to any other mechanism (adjusted OR 5.16, 95%CI 1.41-18.87, p = 0.01). In that model, older age (aOR 2.05 per decade, 95%CI 1.35-3.11, p < 0.01) and higher baseline NIHSS (aOR 1.12, 95%CI 1.02-1.21, p = 0.01) were also independently predictive of mortality. CONCLUSIONS: Our findings suggest that cryptogenic stroke among COVID-19 patients carries a significant risk of early mortality.
BACKGROUND AND PURPOSE:Coronavirus disease 2019 (COVID-19) is associated with a small but clinically significant risk of stroke, the cause of which is frequently cryptogenic. In a large multinational cohort of consecutive COVID-19patients with stroke, we evaluated clinical predictors of cryptogenic stroke, short-term functional outcomes and in-hospital mortality among patients according to stroke etiology. METHODS: We explored clinical characteristics and short-term outcomes of consecutively evaluated patients 18 years of age or older with acute ischemic stroke (AIS) and laboratory-confirmed COVID-19 from 31 hospitals in 4 countries (3/1/20-6/16/20). RESULTS: Of the 14.483 laboratory-confirmed patients with COVID-19, 156 (1.1%) were diagnosed with AIS. Sixty-one (39.4%) were female, 84 (67.2%) white, and 88 (61.5%) were between 60 and 79 years of age. The most frequently reported etiology of AIS was cryptogenic (55/129, 42.6%), which was associated with significantly higher white blood cell count, c-reactive protein, and D-dimer levels than non-cryptogenic AIS patients (p</=0.05 for all comparisons). In a multivariable backward stepwise regression model estimating the odds of in-hospital mortality, cryptogenic stroke mechanism was associated with a fivefold greater odds in-hospital mortality than strokes due to any other mechanism (adjusted OR 5.16, 95%CI 1.41-18.87, p = 0.01). In that model, older age (aOR 2.05 per decade, 95%CI 1.35-3.11, p < 0.01) and higher baseline NIHSS (aOR 1.12, 95%CI 1.02-1.21, p = 0.01) were also independently predictive of mortality. CONCLUSIONS: Our findings suggest that cryptogenic stroke among COVID-19patients carries a significant risk of early mortality.
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