Abstract

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.

Highlights

  • Coronavirus disease 2019 (COVID-19) has spread rapidly around the world, with high morbidity and mortality.The World Health Organization (WHO) has declared COVID-19 a public health emergency of international concern, and, as of 26 April 2021, with 146,689,258 global estimate laboratory confirmed cases and 3,102,410 deaths [1].In view of the rapid increase in the number of patients suffering from this unpredictable disease, the aim of physicians working on first line should be to know in depth its pathophysiology, clinical evolution and short and long-term consequences

  • Several studies attempted to examine the epidemiology of venous thromboembolism (VTE), pulmonary embolism (PE), deep venous thrombosis (DVT), arterial thrombosis and bleeding in COVID-19

  • Data reported in our review are derived from prospective, multinational and multicenter studies and could help clarify similarities and differences in the presentation and outcomes of COVID-19 disease, especially in the presence of thromboembolic disease, helping to identify strategies for better management in these patients

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Summary

Introduction

Coronavirus disease 2019 (COVID-19) has spread rapidly around the world, with high morbidity and mortality.The World Health Organization (WHO) has declared COVID-19 a public health emergency of international concern, and, as of 26 April 2021, with 146,689,258 global estimate laboratory confirmed cases and 3,102,410 deaths (https: //www.who.int) [1].In view of the rapid increase in the number of patients suffering from this unpredictable disease, the aim of physicians working on first line should be to know in depth its pathophysiology, clinical evolution and short and long-term consequences. Coronavirus disease 2019 (COVID-19) has spread rapidly around the world, with high morbidity and mortality. The World Health Organization (WHO) has declared COVID-19 a public health emergency of international concern, and, as of 26 April 2021, with 146,689,258 global estimate laboratory confirmed cases and 3,102,410 deaths (https: //www.who.int) [1]. Pneumonia remains the major clinical manifestation of COVID-19 [2] but, the onset of the disease have highlighted severe features previously unthinkable in patients, even in young patients with no previous pathology [3, 4]. Hospitalized COVID-19 patients frequently develop laboratory abnormalities compatible with hypercoagulability and clinically high prevalence of thromboembolic events [5]. Pulmonary embolism (PE) is one of the most important parts of the spectrum of clinical manifestations of these patients [6], but left ventricular thrombosis as a rare complication of Takotsubo syndrome has been reported [7], and extracorporeal circuits and arterial thrombosis [8]

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