Abstract

Background. A prothrombotic state, attributable to excessive inflammation, cytokine storm, hypoxia, and immobilization, is a feature of SARS-CoV-2 infection. Up to 30% of patients with severe COVID-19 remain at high risk of thromboembolic events despite anticoagulant administration, with adverse impact on in-hospital prognosis. Methods. We retrospectively studied 4742 patients with acute infectious respiratory disease (AIRD); 2579 were diagnosed to have COVID-19 and treated with heparin, whereas 2163 had other causes of AIRD. We compared the incidence and predictors of total, arterial, and venous thrombosis, both in the whole population and in a propensity score-matched subpopulation of 3036 patients (1518 in each group). Results. 271 thrombotic events occurred in the whole population: 121 (4.7%) in the COVID-19 group and 150 (6.9%) in the no-COVID-19 group (p < 0.001). No differences in the incidence of total (p = 0.11), arterial (p = 0.26), and venous (p = 0.38) thrombosis were found between the two groups after adjustment for confounding clinical variables and in the propensity score-matched subpopulation. Likewise, there were no significant differences in bleeding rates between the two groups. Clinical predictors of arterial thrombosis included age (p = 0.006), diabetes mellitus (p = 0.034), peripheral artery disease (p < 0.001), and previous stroke (p < 0.001), whereas history of solid cancer (p < 0.001) and previous deep vein thrombosis (p = 0.007) were associated with higher incidence of venous thrombosis. Conclusions. Hospitalized patients with COVID-19 treated with heparin do not seem to show significant differences in the cumulative incidence of thromboembolic events as well as in the incidence of arterial and venous thrombosis separately, compared with AIRD patients with different etiological diagnosis.

Highlights

  • SARS-CoV-2 is a novel coronavirus that is causing a pandemic outbreak of respiratory disease from the end of 2019 (COVID-19) [1,2]

  • COVID-19 patients were younger (p < 0.001) and included a higher proportion of male (p = 0.005) and hypertensive (p < 0.001) subjects compared to no-COVID-19 patients

  • chronic obstructive pulmonary disease (COPD) (p < 0.001), chronic kidney disease (p = 0.016), cognitive impairment (p < 0.001), connective tissue disease (p = 0.001), solid tumor (p < 0.001), and HIV infection (p = 0.008) were more frequent in the no-COVID-19 group compared with COVID-19 patients

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Summary

Introduction

SARS-CoV-2 is a novel coronavirus that is causing a pandemic outbreak of respiratory disease from the end of 2019 (COVID-19) [1,2]. A few studies have suggested that a prothrombotic state, attributable to excessive inflammation, cytokine storm, hypoxia, and prolonged immobilization, is a feature of severe COVID-19 infection and may predispose to both venous and arterial thromboembolic events, with adverse impact on in-hospital prognosis [7,8,9,10,11]. The exact prevalence of arterial and venous thrombosis in hospitalized COVID-19 patients remains uncertain and limited evidence exists to guide the prophylactic antithrombotic regimen [17,18,19,20]. International guidelines recommend that hospitalized patients with COVID-19 and respiratory failure or severe comorbidities, as well as those requiring prolonged immobilization and intensive care, should receive pharmacological prophylaxis against venous thromboembolism (VTE), in the absence of contraindications [21,22,23]

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