• Luca Costanzo, Francesco Paolo Palumbo, Giorgio Ardita, Pier Luigi Antignani, Enrico Arosio, Giacomo Failla, and Italian Society for Vascular Investigation and the Italian Society of Vascular Medicine.
• Angiology Unit, San Marco Hospital, Department of Cardiovascular Disease, A.O.U. "Policlinico-Vittorio Emanuele", University of Catania, Catania, Italy. Electronic address: lucacost84@gmail.com.
• J Vasc Surg Venous Lymphat Disord. 2020 Sep 1; 8 (5): 711-716.

AbstractThe SARS-CoV-2 (COVID-19) is causing a pandemic and potentially fatal disease of global public health concern. Viral infections are known to be associated with coagulation impairment; thus, thrombosis, hemorrhage, or both may occur. Understanding the pathophysiologic mechanisms underlying the development of coagulation disorders during viral infection is essential for the development of therapeutic strategies. Coagulopathy in COVID-19 infection is emerging as a precipitant factor for severe respiratory complications and death. An increase in coagulation markers, such as fibrinogen and D-dimer, has been found in severe COVID-19 cases. Heparin, clinically used as an anticoagulant, also has anti-inflammatory properties, including binding of inflammatory cytokines, inhibition of neutrophil chemotaxis, and protection of endothelial cells, and a potential antiviral effect. We hypothesized that low-molecular-weight heparin may attenuate cytokine storm in COVID-19 patients; therefore, low-molecular-weight heparin could be a valid adjunctive therapeutic drug for the treatment of COVID-19 pneumopathy. In this paper, we review potential mechanisms involved in coagulation impairment after viral infection and the possible role of heparin in the treatment of COVID-19 patients.Copyright © 2020 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.

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