IMR Press / RCM / Volume 22 / Issue 2 / DOI: 10.31083/j.rcm2202035
Open Access Review
Thrombotic risk in patients with COVID-19
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1 Cardiology Unit, Department of Medical and Surgical Specialities, Radiological Sciences and Public Health, University of Brescia, 23123 Brescia, Italy
These authors contributed equally.
Rev. Cardiovasc. Med. 2021, 22(2), 277–286;
Submitted: 29 November 2020 | Revised: 28 March 2021 | Accepted: 31 March 2021 | Published: 30 June 2021
(This article belongs to the Special Issue Utilizing Technology in the COVID 19 era)

Emerging evidences prove that the ongoing pandemic of coronavirus disease 2019 (COVID-19) is strictly linked to coagulopathy even if pneumonia appears as the major clinical manifestation. The exact incidence of thromboembolic events is largely unknown, so that a relative significant number of studies have been performed in order to explore thrombotic risk in COVID-19 patients. Cytokine storm, mediated by pro-inflammatory interleukins, tumor necrosis factor α and elevated acute phase reactants, is primarily responsible for COVID-19-associated hypercoagulopathy. Also comorbidities, promoting endothelial dysfunction, contribute to a higher thromboembolic risk. In this review we aim to investigate epidemiology and clarify the pathophysiological pathways underlying hypercoagulability in COVID-19 patients, providing indications on the prevention of thromboembolic events in COVID-19. Furthermore we aim to reassume the pathophysiological paths involved in COVID-19 infection.

Pulmonary embolism
Fig. 1.
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