Circulating Levels of Tissue Plasminogen Activator and Plasminogen Activator Inhibitor-1 Are Independent Predictors of Coronavirus Disease 2019 Severity: A Prospective, Observational Study
Brandon Michael Henry, Isaac Cheruiyot, Justin L. Benoit, Giuseppe Lippi, Zoltán Prohászka, Emmanuel J. Favaloro, Stefanie W. Benoit
Abstract
A substantial pool of evidence suggests that the pathophysiology of the severe form of coronavirus disease 2019 (COVID-19) is mediated, in part, by a hypercoagulable state termed COVID-19-associated coagulopathy (CAC),[1] [2] [3] and characterized by micro- and macrovascular thrombosis.[4] [5] Approximately 27% of critically ill intensive care unit (ICU)-admitted COVID-19 patients develop venous thromboembolism during admission,[6] while 4.4% experience arterial thrombotic complications.[7] Autopsy studies on COVID-19 patients have demonstrated extensive presence of microthrombi within pulmonary capillaries, associated with diffuse alveolar damage and neoangiogenesis.[8] [9] Other organs may also be affected by this form of thrombotic microangiopathy, resulting in multiple organ dysfunction syndrome and eventually death.[10] Laboratory profiles seen in patients with severe COVID-19 (elevated D-dimers and fibrin degradation products [FDPs], and prolonged prothrombin time) are also consistent with a hypercoagulable state.