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Review

Thrombotic and Hypercoagulability Complications of COVID-19: An Update

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Pages 785-793 | Published online: 31 Aug 2021

Figures & data

Figure 1 Schematic representation of SARS-CoV-2 structure.

Figure 1 Schematic representation of SARS-CoV-2 structure.

Figure 2 Activation of the spike protein by TMPRSS2 at (or close to) the cell surface, leading to fusion of the viral membrane with the plasma membrane.

Figure 2 Activation of the spike protein by TMPRSS2 at (or close to) the cell surface, leading to fusion of the viral membrane with the plasma membrane.

Table 1 Incidence of Thrombotic Complications Among COVID-19 Patients

Figure 3 Pathogenesis of thrombotic complications of COVID-19. SARS-CoV2 infection induces endothelial damage triggering endothelial release of cytokines, increasing capillary permeability. PAMPs and DAMPs induced activation of neutrophils, and macrophages results in localized production of cytokines, procoagulants, and complement activation, leading to further endothelial damage and tissue factor release. Endothelial damage exposes collagen and other prothrombotic mediators leading to thrombus formation.

Notes: Adapted from Brosnahan SB, Jonkman AH, Kugler MC, Munger JS, Kaufman DA. COVID-19 and Respiratory System Disorders: Current Knowledge, Future Clinical and Translational Research Questions. Arterioscler Thromb Vasc Biol. 2020;40(11):2586–2597.Citation64 © 2020 The Authors. Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/legalcode). https://www.ahajournals.org/doi/pdf/10.1161/ATVBAHA.120.314515?download=true.
Figure 3 Pathogenesis of thrombotic complications of COVID-19. SARS-CoV2 infection induces endothelial damage triggering endothelial release of cytokines, increasing capillary permeability. PAMPs and DAMPs induced activation of neutrophils, and macrophages results in localized production of cytokines, procoagulants, and complement activation, leading to further endothelial damage and tissue factor release. Endothelial damage exposes collagen and other prothrombotic mediators leading to thrombus formation.