Microvascular Thrombosis as a Critical Factor in Severe COVID-19

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.

Keywords: capillaries; coronavirus disease 2019; glycocalyx; microcirculation; platelets; thromboinflammation; thrombosis.

Figure 1

Endothelial dysfunction with glycocalyx degradation is postulated as the central mechanism induced through and facilitating viral entry. The resulting inflammatory and procoagulative processes initiate a complex cascade destabilizing the equilibrium of Virchow’s triad resulting in (micro-) thrombosis and tissue necrosis. The concept of the figure is modified after Ataga et al.—‘Hypercoagulability and thrombotic complications in hemolytic anemias.’ [23].