Coagulopathy and Thrombosis as a Result of Severe COVID-19 Infection: A Microvascular Focus
Author
Katneni, Upendra KAlexaki, Aikaterini
Hunt, Ryan C
Schiller, Tal
DiCuccio, Michael
Buehler, Paul W
Ibla, Juan C
Kimchi-Sarfaty, Chava
Date
2020-08-24Journal
Thrombosis and HaemostasisPublisher
ThiemeType
Article
Metadata
Show full item recordAbstract
Coronavirus disease of 2019 (COVID-19) is the clinical manifestation of the respiratory infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). While primarily recognized as a respiratory disease, it is clear that COVID-19 is systemic illness impacting multiple organ systems. One defining clinical feature of COVID-19 has been the high incidence of thrombotic events. The underlying processes and risk factors for the occurrence of thrombotic events in COVID-19 remain inadequately understood. While severe bacterial, viral, or fungal infections are well recognized to activate the coagulation system, COVID-19-associated coagulopathy is likely to have unique mechanistic features. Inflammatory-driven processes are likely primary drivers of coagulopathy in COVID-19, but the exact mechanisms linking inflammation to dysregulated hemostasis and thrombosis are yet to be delineated. Cumulative findings of microvascular thrombosis has raised question if the endothelium and microvasculature should be a point of investigative focus. von Willebrand factor (VWF) and its protease, a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS-13), play important role in the maintenance of microvascular hemostasis. In inflammatory conditions, imbalanced VWF-ADAMTS-13 characterized by elevated VWF levels and inhibited and/or reduced activity of ADAMTS-13 has been reported. Also, an imbalance between ADAMTS-13 activity and VWF antigen is associated with organ dysfunction and death in patients with systemic inflammation. A thorough understanding of VWF-ADAMTS-13 interactions during early and advanced phases of COVID-19 could help better define the pathophysiology, guide thromboprophylaxis and treatment, and improve clinical prognosis.Rights/Terms
Thieme. All rights reserved.Identifier to cite or link to this item
http://hdl.handle.net/10713/13711ae974a485f413a2113503eed53cd6c53
10.1055/s-0040-1715841
Scopus Count
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