Microvascular Thrombosis as a Critical Factor in Severe COVID-19

Author:

Wadowski Patricia P.12ORCID,Panzer Benjamin3,Józkowicz Alicja2,Kopp Christoph W.1,Gremmel Thomas45ORCID,Panzer Simon6,Koppensteiner Renate1

Affiliation:

1. Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, 1090 Vienna, Austria

2. Department of Medical Biotechnology, Faculty of Biophysics, Biochemistry and Biotechnology, Jagiellonian University, 30-387 Krakow, Poland

3. Department of Cardiology, Wilhelminenspital, 1160 Vienna, Austria

4. Institute of Antithrombotic Therapy in Cardiovascular Disease, Karl Landsteiner Society, 3100 St. Pölten, Austria

5. Department of Internal Medicine I, Cardiology and Intensive Care Medicine, Landesklinikum Mistelbach-Gänserndorf, 2130 Mistelbach, Austria

6. Department of Blood Group Serology and Transfusion Medicine, Medical University of Vienna, 1090 Vienna, Austria

Abstract

Platelet–endothelial interactions have a critical role in microcirculatory function, which maintains tissue homeostasis. The subtle equilibrium between platelets and the vessel wall is disturbed by the coronavirus disease 2019 (COVID-19), which affects all three components of Virchow’s triad (endothelial injury, stasis and a hypercoagulable state). Endotheliitis, vasculitis, glycocalyx degradation, alterations in blood flow and viscosity, neutrophil extracellular trap formation and microparticle shedding are only few pathomechanisms contributing to endothelial damage and microthrombosis resulting in capillary plugging and tissue ischemia. In the following opinion paper, we discuss major pathological processes leading to microvascular endothelial activation and thrombosis formation as a possible major adverse factor driving the deterioration of patient disease course in severe COVID-19.

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

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