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    Coagulopathy and Thrombosis as a Result of Severe COVID-19 Infection: A Microvascular Focus

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    Author
    Katneni, Upendra K
    Alexaki, Aikaterini
    Hunt, Ryan C
    Schiller, Tal
    DiCuccio, Michael
    Buehler, Paul W
    Ibla, Juan C
    Kimchi-Sarfaty, Chava
    Date
    2020-08-24
    Journal
    Thrombosis and Haemostasis
    Publisher
    Thieme
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.1055/s-0040-1715841
    Abstract
    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.
    Keyword
    COVID-19
    thrombosis
    inflammation
    ADAMTS-13
    von Willebrand factor
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/13711
    ae974a485f413a2113503eed53cd6c53
    10.1055/s-0040-1715841
    Scopus Count
    Collections
    UMB Coronavirus Publications
    UMB Open Access Articles

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