ABSTRACT
[Figure: see text].
Subject(s)
COVID-19/metabolism , Inflammation/metabolism , Ischemic Stroke/metabolism , Thrombophilia/metabolism , Aged , Aged, 80 and over , Blood Sedimentation , C-Reactive Protein/metabolism , COVID-19/complications , Cluster Analysis , Female , Ferritins/metabolism , Fibrin Fibrinogen Degradation Products/metabolism , Fibrinogen/metabolism , Hospital Mortality , Humans , Interleukin-6/metabolism , Ischemic Stroke/complications , L-Lactate Dehydrogenase/metabolism , Leukocyte Count , Logistic Models , Machine Learning , Male , Middle Aged , Myocardial Infarction/complications , Myocardial Infarction/metabolism , Partial Thromboplastin Time , Pulmonary Embolism/complications , Pulmonary Embolism/metabolism , Retrospective Studies , SARS-CoV-2 , Severity of Illness Index , Venous Thrombosis/complications , Venous Thrombosis/metabolismABSTRACT
COVID-19 associated coagulopathy and mortality related to thrombotic complications have been suggested as biological mediators in racial disparities related to COVID-19. We studied the adjusted prevalence of acute ischemic stroke, pulmonary embolism, myocardial infarction, and deep venous thrombosis stratified by race in hospitalized patients in one New York City borough during the local COVID-19 surge. The multi-racial cohort included 4299 patients hospitalized with COVID-19, 9% of whom were white, 40% black, 41% Hispanic and 10% Asian or other. We found a 6.1% prevalence of composite thrombotic events. There were no significant race-specific differences in thrombotic events when adjusting for basic demographics, socioeconomic factors, medical comorbidities or biomarkers using a stepwise regression model. We therefore found no evidence that the racial disparities related to COVID-19, and specifically thrombotic complications, are caused by biological differences in race.