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      Long COVID: The Nature of Thrombotic Sequelae Determines the Necessity of Early Anticoagulation

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          Abstract

          Many discharged COVID-19 patients affected by sequelae experience reduced quality of life leading to an increased burden on the healthcare system, their families and society at large. Possible pathophysiological mechanisms of long COVID include: persistent viral replication, chronic hypoxia and inflammation. Ongoing vascular endothelial damage promotes platelet adhesion and coagulation, resulting in the impairment of various organ functions. Meanwhile, thrombosis will further aggravate vasculitis contributing to further deterioration. Thus, long COVID is essentially a thrombotic sequela. Unfortunately, there is currently no effective treatment for long COVID. This article summarizes the evidence for coagulation abnormalities in long COVID, with a focus on the pathophysiological mechanisms of thrombosis. Extracellular vesicles (EVs) released by various types of cells can carry SARS-CoV-2 through the circulation and attack distant tissues and organs. Furthermore, EVs express tissue factor and phosphatidylserine (PS) which aggravate thrombosis. Given the persistence of the virus, chronic inflammation and endothelial damage are inevitable. Pulmonary structural changes such as hypertension, embolism and fibrosis are common in long COVID. The resulting impaired lung function and chronic hypoxia again aggravates vascular inflammation and coagulation abnormalities. In this article, we also summarize recent research on antithrombotic therapy in COVID-19. There is increasing evidence that early anticoagulation can be effective in improving outcomes. In fact, persistent systemic vascular inflammation and dysfunction caused by thrombosis are key factors driving various complications of long COVID. Early prophylactic anticoagulation can prevent the release of or remove procoagulant substances, thereby protecting the vascular endothelium from damage, reducing thrombotic sequelae, and improving quality of life for long-COVID patients.

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          Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19

          Progressive respiratory failure is the primary cause of death in the coronavirus disease 2019 (Covid-19) pandemic. Despite widespread interest in the pathophysiology of the disease, relatively little is known about the associated morphologic and molecular changes in the peripheral lung of patients who die from Covid-19.
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            Persistent Symptoms in Patients After Acute COVID-19

            This case series describes COVID-19 symptoms persisting a mean of 60 days after onset among Italian patients previously discharged from COVID-19 hospitalization.
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              COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-up

              Coronavirus disease 2019 (COVID-19), a viral respiratory illness caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), may predispose patients to thrombotic disease, both in the venous and arterial circulations, due to excessive inflammation, platelet activation, endothelial dysfunction, and stasis. In addition, many patients receiving antithrombotic therapy for thrombotic disease may develop COVID-19, which can have implications for choice, dosing, and laboratory monitoring of antithrombotic therapy. Moreover, during a time with much focus on COVID-19, it is critical to consider how to optimize the available technology to care for patients without COVID-19 who have thrombotic disease. Herein, we review the current understanding of the pathogenesis, epidemiology, management and outcomes of patients with COVID-19 who develop venous or arterial thrombosis, and of those with preexisting thrombotic disease who develop COVID-19, or those who need prevention or care for their thrombotic disease during the COVID-19 pandemic.
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                Author and article information

                Contributors
                Journal
                Front Cell Infect Microbiol
                Front Cell Infect Microbiol
                Front. Cell. Infect. Microbiol.
                Frontiers in Cellular and Infection Microbiology
                Frontiers Media S.A.
                2235-2988
                05 April 2022
                2022
                05 April 2022
                : 12
                : 861703
                Affiliations
                [1] 1 Department of Hematology, The First Hospital of Harbin, Harbin Medical University , Harbin, China
                [2] 2 Department of Nephrology, The First Hospital of Harbin, Harbin Medical University , Harbin, China
                [3] 3 Department of Geriatric, Shenzhen People’s Hospital, The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology , Shenzhen, China
                [4] 4 Department of Research, Veterans Affairs (VA) Boston Healthcare System, Harvard Medical School , Boston, MA, United States
                [5] 5 Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School , Boston, MA, United States
                Author notes

                Edited by: Leo Pruimboom, Pontifical University of Salamanca, Spain

                Reviewed by: Younes Zaid, Université de Montréal, Canada; Kavitha Mukund, University of California, San Diego, United States

                *Correspondence: Rujuan Xie, rujuan2021@ 123456163.com ; Jialan Shi, jialan_shi@ 123456dfci.harvard.edu

                This article was submitted to Clinical Microbiology, a section of the journal Frontiers in Cellular and Infection Microbiology

                Article
                10.3389/fcimb.2022.861703
                9016198
                35449732
                2b773a74-0830-48af-8975-6df0364bd66a
                Copyright © 2022 Wang, Yu, Jing, Wu, Novakovic, Xie and Shi

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 25 January 2022
                : 15 March 2022
                Page count
                Figures: 3, Tables: 3, Equations: 0, References: 90, Pages: 14, Words: 6986
                Categories
                Cellular and Infection Microbiology
                Review

                Infectious disease & Microbiology
                long covid,thrombosis,extracellular vesicles,endothelial injury,chronic hypoxia,inflammation,phosphatidylserine,early anticoagulation

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