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      Venous Thromboembolism Complicated with COVID-19: What Do We Know So Far?

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          Abstract

          Coronavirus disease (COVID-19) is caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is responsible for the ongoing 2019–2020 pandemic. Venous thromboembolism (VTE), a frequent cardiovascular and/or respiratory complication among hospitalized patients, is one of the known sequelae of the illness. Hospitalized COVID-19 patients are often elderly, immobile, and show signs of coagulopathy. Therefore, it is reasonable to assume a high incidence of VTE among these patients. Presently, the incidence of VTE is estimated at around 25% of patients hospitalized in the intensive care unit for COVID-19 even under anticoagulant treatment at prophylactic doses. In this review, we discuss present knowledge of the topic, the unique challenges of diagnosis and treatment of VTE, as well as some of the potential mechanisms of increased risk for VTE during the illness. Understanding the true impact of VTE on patients with COVID-19 will potentially improve our ability to reach a timely diagnosis and initiate proper treatment, mitigating the risk for this susceptible population during a complicated disease.

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          Most cited references 18

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          Thrombosis: a major contributor to global disease burden.

          Thrombosis is the common pathology underlying ischemic heart disease, ischemic stroke, and venous thromboembolism (VTE). The Global Burden of Disease Study 2010 (GBD 2010) documented that ischemic heart disease and stroke collectively caused 1 in 4 deaths worldwide. GBD 2010 did not report data for VTE as a cause of death and disability.
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            Difference of coagulation features between severe pneumonia induced by SARS-CoV2 and non-SARS-CoV2

            Severe coronavirus disease 2019 (COVID-19) is commonly complicated with coagulopathy, the difference of coagulation features between severe pneumonia induced by SARS-CoV2 and non-SARS-CoV2 has not been analyzed. Coagulation results and clinical features of consecutive patients with severe pneumonia induced by SARS-CoV2 (COVID group) and non-SARS-CoV2 (non-COVID group) in Tongji hospital were retrospectively analyzed and compared. Whether patients with elevated D-dimer could benefit from anticoagulant treatment was evaluated. There were 449 COVID patients and 104 non-COVID patients enrolled into the study. The 28-day mortality in COVID group was approximately twofold of mortality in non-COVID group (29.8% vs. 15.4%, P = 0.003), COVID group were older (65.1 ± 12.0 vs. 58.4 ± 18.0, years, P   3.0 μg/mL (32.8% vs. 52.4%, P = 0.017). Patients with severe pneumonia induced by SARS-CoV2 had higher platelet count than those induced by non-SARS-CoV2, and only the former with markedly elevated D-dimer may benefit from anticoagulant treatment.
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              The stimulation of thrombosis by hypoxia

              Thrombus formation is increased under conditions of hypoxia in animal models of thrombosis and in human populations, but current therapies for thrombosis do not directly target hypoxia-responsive signaling pathways. The vascular response to hypoxia is controlled primarily by the hypoxia-inducible transcription factors (HIFs), whose target genes include several factors that regulate thrombus formation. In this article, we review the HIF-dependent and HIF-independent signaling pathways that regulate thrombus formation under hypoxic conditions. A better understanding of hypoxia-induced thrombus formation could lead to the development of novel prophylactic therapies for thrombosis.
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                Author and article information

                Journal
                Acta Haematol
                Acta Haematol
                AHA
                Acta Haematologica
                S. Karger AG (Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH-4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, karger@karger.com )
                0001-5792
                1421-9662
                12 May 2020
                : 1-8
                Affiliations
                aCardiology Department, Rabin Medical Center, Petah Tikva, Israel
                bHematology Department, Rabin Medical Center, Petah Tikva, Israel
                cSackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
                Author notes
                *Shir Tal, Cardiology Department, Rabin Medical Center, 39 Ze'ev Jabotinsky Street, Petah Tikva 49100 (Israel), shir_hazan@ 123456yahoo.com
                Article
                aha-0001
                10.1159/000508233
                7270063
                32396903
                Copyright © 2020 by S. Karger AG, Basel

                This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

                Page count
                Figures: 1, References: 49, Pages: 8
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