Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Interrelationship between COVID-19 and coagulopathy: pathophysiological and clinical evidence

Version 1 : Received: 26 April 2023 / Approved: 27 April 2023 / Online: 27 April 2023 (04:14:52 CEST)

A peer-reviewed article of this Preprint also exists.

Ragnoli, B.; Da Re, B.; Galantino, A.; Kette, S.; Salotti, A.; Malerba, M. Interrelationship between COVID-19 and Coagulopathy: Pathophysiological and Clinical Evidence. Int. J. Mol. Sci. 2023, 24, 8945. Ragnoli, B.; Da Re, B.; Galantino, A.; Kette, S.; Salotti, A.; Malerba, M. Interrelationship between COVID-19 and Coagulopathy: Pathophysiological and Clinical Evidence. Int. J. Mol. Sci. 2023, 24, 8945.

Abstract

Since the first description of COVID-19 infection, among clinical manifestations of the disease including fever, dispnea, cough, fatigue, it was observed a high incidence of thromboembolic events potentially evolving towars ARDS and COVID-associated-coagulopathy (CAC).The hypercoagulation state is based on an interaction between thrombosis and inflammation. The so-called CAC represents a key aspect in the genesis of organ damage from SARS-CoV-2. The prothrombotic status in COVID-19 disease can be explained by the increase of coagulation levels of D-dimer, lymphocytes, fibrinogen, IL-6 and prothrombin time. Several mechanisms have been hypothesized to explain this hypercoagulable process such as inflammatory cytokine storm, platelet activation, endothelial dysfunction and stasis for a long time. The purpose of this narrative review is to provide an overview of the current knowledge on the pathogenic mechanisms of coagulopathy that may characterize COVID-19 infection and inform on new areas of research. New vascular therapeutic strategies are also reviewed.

Keywords

COVID-19 infection; coagulopathy; endothelial dysfunction; platelet activation; citokine storm; anticoagulant therapy

Subject

Medicine and Pharmacology, Pulmonary and Respiratory Medicine

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