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Review
. 2020 Aug:77:100735.
doi: 10.1016/j.jbior.2020.100735. Epub 2020 Jun 17.

Thromboembolic events and Covid-19

Agnès Ribes  1 , Fanny Vardon-Bounes  2 , Vincent Mémier  3 , Michael Poette  2 , Jonathan Au-Duong  2 , Cédric Garcia  1 , Vincent Minville  4 , Pierre Sié  1 , Alessandra Bura-Rivière  5 , Sophie Voisin  1 , Bernard Payrastre  6
Affiliations
Review

Thromboembolic events and Covid-19

Agnès Ribes et al. Adv Biol Regul. 2020 Aug.

Abstract

The novel Corona virus infection (Covid-19) first identified in China in December 2019 has rapidly progressed in pandemic leading to significant mortality and unprecedented challenge for healthcare systems. Although the clinical spectrum of Covid-19 is variable, acute respiratory failure and systemic coagulopathy are common in severe Covid-19 patients. Lung is an important target of the SARS-CoV-2 virus causing eventually acute respiratory distress syndrome associated to a thromboinflammatory state. The cytokinic storm, thromboinflammation and pulmonary tropism are the bedrock of tissue lesions responsible for acute respiratory failure and for prolonged infection that may lead to multiple organ failure and death. The thrombogenicity of this infectious disease is illustrated by the high frequency of thromboembolic events observed even in Covid-19 patients treated with anticoagulation. Increased D-Dimers, a biomarker reflecting activation of hemostasis and fibrinolysis, and low platelet count (thrombocytopenia) are associated with higher mortality in Covid-19 patients. In this review, we will summarize our current knowledge on the thromboembolic manifestations, the disturbed hemostatic parameters, and the thromboinflammatory conditions associated to Covid-19 and we will discuss the modalities of anticoagulant treatment or other potential antithrombotic options.

Keywords: Acute respiratory distress syndrome; Anticoagulants; Covid-19; Platelets; Thromboembolic events; Thromboinflammation.

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Conflict of interest statement

The authors declare no competing financial interests.

Figures

Fig. 1
Fig. 1
Immunothrombosis mechanisms in pulmonary circulation during SARS-CoV-2 infection. A. Recruitment phase. SARS-CoV2 infects the alveolar epithelium and endothelial cells through binding to the ACE2 receptor (ACE Rc) exposed at the surface of these cells. Activation of endothelial cells by SARS-CoV-2 upregulates the externalization of Von Willebrand factor (vWF) and leukocytes' adhesion molecules (i.e. ICAM-1 (Intercellular Adhesion Molecule 1), VCAM-1 (Vascular cell adhesion protein-1), E-selectin) allowing adhesion of platelets and neutrophils. Activation of endothelial cells also triggers expression of tissue factor (TF) activating the extrinsic coagulation pathway and in turn α-thrombin generation leading to fibrin generation and platelets activation. B. Activation phase. Activated platelets interact with neutrophils leading to mutual amplification of neutrophil and platelet activation and eventually formation of Neutrophhils Extracelullar Traps (NETs) by DNA decondensation and externalization, allowing activation of the contact pathway. Thrombin generation through Tissue Factor (extrinsic) and contact pathways lead to clot formation and microvascular occlusion. Furthermore, clots are stabilized by the downregulation of endothelial antithrombotic properties. Meanwhile, cytokine release is triggered by platelets and leukocytes. C. Schematic representation of the systemic consequences of microvascular thromboinflammation.This figure was created using Servier Medical Art templates, which are licensed under a Creative Commons Attribution 3.0 Unported License;https://smart.servier.com.
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References

    1. Akca S., Haji-Michael P., de Mendonça A., Suter P., Levi M., Vincent J.L. Time course of platelet counts in critically ill patients. Crit. Care Med. 2002;30:753–756. - PubMed
    1. Alikhan R., Bedenis R., Cohen A.T. Heparin for the prevention of venous thromboembolism in acutely ill medical patients (excluding stroke and myocardial infarction) Cochrane Database Syst. Rev. 2014;5:1465–1858. doi: 10.1002/14651858.CD003747.pub4. - DOI - PMC - PubMed
    1. Ancrenaz V., Déglon J., Samer C., Staub C., Dayer P., Daali Y., Desmeules J. Pharmacokinetic interaction between Prasugrel and Ritonavir in healthy volunteers. Basic Clin. Pharmacol. Toxicol. 2013;112:132–137. doi: 10.1111/j.1742-7843.2012.00932.x. - DOI - PMC - PubMed
    1. Becker R.C. Covid-19-associated coagulopathy. J. Thromb. Thrombolysis. 2020 doi: 10.1007/s11239-020-02134-3. - DOI - PMC - PubMed
    1. Bikdeli B., Madhavan M.V., Jimenez D., Chuich T., Dreyfus I., Driggin E., Nigoghossian C., Ageno W., Madjid M., Guo Y., Tang L.V., Hu Y., Giri J., Cushman M., Quéré I., Dimakakos E.P., Gibson C.M., Lippi G., Favaloro E.J., Fareed J., Caprini J.A., Tafur A.J., Burton J.R., Francese D.P., Wang E.Y., Falanga A., McLintock C., Hunt B.J., Spyropoulos A.C., Barnes G.D., Eikelboom J.W., Weinberg I., Schulman S., Carrier M., Piazza G., Beckman J.A., Steg P.G., Stone G.W., Rosenkranz S., Goldhaber S.Z., Parikh S.A., Monreal M., Krumholz H.M., Konstantinides S.V., Weitz J.I., Lip G.Y.H. COVID-19 and thrombotic or thromboembolic disease: implications for prevention, antithrombotic therapy, and follow-up. J. Am. Coll. Cardiol. 2020 https://doi:10.1016/j.jacc.2020.04.031 - DOI - PMC - PubMed

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