Abstract
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a life-threatening infectious disease that, 4 years after its initial identification in early 2019, has now reached
endemic proportions. Since then, the clinical course of the disease has certainly attenuated, with cumulative age-adjusted death rates in immunocompetent and
non-fragile patients that are now only slightly higher than those caused by other infectious diseases such as influenza and respiratory syncytial virus (RSV) [1]. Nevertheless, the increased risk of thrombosis that characterizes patients with SARS-CoV-2 infection is an aspect that characterized the early phase of the infection, and has also remained an important threat four years thereafter. To this end, a recent study published by Wada et al. [2] has shown that the incidence of pulmonary embolism has not changed significantly over the periods of prevalence of the different SARS-CoV-2 variants (Ancestral: 12%; Alpha: 8%; Delta: 11%; Omicron: 9%), suggesting that the interaction of the virus with the hemostasis system has remained significant throughout the course of the pandemic. Further evidence suggests that the risk of developing venous thrombosis, which may include deep vein thrombosis (DVT), pulmonary embolism and even in-situ pulmonary thrombosis is higher in patients with COVID-19 than that observed in those with common strains of Influenza virus (H1N1 may represent a limited exception) [3]. Therefore, any cost effective
strategies that could be adopted to reduce the thrombotic risk of SARS-CoV-2 must be welcomed.
endemic proportions. Since then, the clinical course of the disease has certainly attenuated, with cumulative age-adjusted death rates in immunocompetent and
non-fragile patients that are now only slightly higher than those caused by other infectious diseases such as influenza and respiratory syncytial virus (RSV) [1]. Nevertheless, the increased risk of thrombosis that characterizes patients with SARS-CoV-2 infection is an aspect that characterized the early phase of the infection, and has also remained an important threat four years thereafter. To this end, a recent study published by Wada et al. [2] has shown that the incidence of pulmonary embolism has not changed significantly over the periods of prevalence of the different SARS-CoV-2 variants (Ancestral: 12%; Alpha: 8%; Delta: 11%; Omicron: 9%), suggesting that the interaction of the virus with the hemostasis system has remained significant throughout the course of the pandemic. Further evidence suggests that the risk of developing venous thrombosis, which may include deep vein thrombosis (DVT), pulmonary embolism and even in-situ pulmonary thrombosis is higher in patients with COVID-19 than that observed in those with common strains of Influenza virus (H1N1 may represent a limited exception) [3]. Therefore, any cost effective
strategies that could be adopted to reduce the thrombotic risk of SARS-CoV-2 must be welcomed.
Original language | English |
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Pages (from-to) | 225-226 |
Number of pages | 2 |
Journal | Blood Coagulation and Fibrinolysis: international journal in haemostasis and thrombosis |
Volume | 35 |
Issue number | 5 |
DOIs | |
Publication status | Published - 01 Jul 2024 |