Preprint Review Version 2 This version is not peer-reviewed

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

Version 1 : Received: 22 May 2020 / Approved: 24 May 2020 / Online: 24 May 2020 (16:17:00 CEST)
Version 2 : Received: 14 July 2020 / Approved: 15 July 2020 / Online: 15 July 2020 (03:36:29 CEST)

How to cite: Katneni, U.K.; Alexaki, A.; Hunt, R.C.; Schiller, T.; DiCuccio, M.; Buehler, P.W.; Ibla, J.C.; Kimchi-Sarfaty, C. Coagulopathy and Thrombosis as a Result of Severe COVID-19 Infection: A Microvascular Focus. Preprints 2020, 2020050385 (doi: 10.20944/preprints202005.0385.v2). Katneni, U.K.; Alexaki, A.; Hunt, R.C.; Schiller, T.; DiCuccio, M.; Buehler, P.W.; Ibla, J.C.; Kimchi-Sarfaty, C. Coagulopathy and Thrombosis as a Result of Severe COVID-19 Infection: A Microvascular Focus. Preprints 2020, 2020050385 (doi: 10.20944/preprints202005.0385.v2).

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, ADAMTS13 play important role in the maintenance of microvascular hemostasis. In inflammatory conditions, imbalanced VWF-ADAMTS13 characterized by elevated VWF levels and inhibited and/or reduced activity of ADAMTS13 has been reported. Also, an imbalance between ADAMTS13 activity and VWF antigen is associated with organ dysfunction and death in patients with systemic inflammation. A thorough understanding of VWF-ADAMTS13 interactions during early and advanced phases of COVID-19 could help better define the pathophysiology, guide thromboprophylaxis and treatment and improve clinical prognosis.

Subject Areas

COVID-19; Thrombosis; Inflammation; ADAMTS13; Von Willebrand Factor

Comments (1)

Comment 1
Received: 15 July 2020
Commenter: Chava Kimchi-Sarfaty
Commenter's Conflict of Interests: Author
Comment: The manuscript was thoroughly revised to address the comments and suggestions of the reviewers and to account for the most recent publications on this topic.
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