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

Wang，Chengyue1,2; Yu，Chengyuan1,3; Jing，Haijiao1; Wu，Xiaoming1; Novakovic，Valerie A.4; Xie，Rujuan2; Shi，Jialan1,4,5

2022-04-05

10.3389/fcimb.2022.861703

Frontiers in Cellular and Infection Microbiology   影响因子和分区

2235-2988

2235-2988

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.

chronic hypoxia early anticoagulation endothelial injury extracellular vesicles inflammation long COVID phosphatidylserine thrombosis

SCI

英语

ESI高被引

其他

Immunology ; Microbiology

Immunology ; Microbiology

WOS:000789324100001

FRONTIERS MEDIA SA

2-s2.0-85128521954

Scopus

1.Department of Hematology,The First Hospital of Harbin,Harbin Medical University,Harbin,China
2.Department of Nephrology,The First Hospital of Harbin,Harbin Medical University,Harbin,China
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.Department of Research,Veterans Affairs (VA) Boston Healthcare System,Harvard Medical School,Boston,United States
5.Department of Medical Oncology,Dana-Farber Cancer Institute,Harvard Medical School,Boston,United States

Wang，Chengyue,Yu，Chengyuan,Jing，Haijiao,et al. Long COVID: The Nature of Thrombotic Sequelae Determines the Necessity of Early Anticoagulation[J]. Frontiers in Cellular and Infection Microbiology,2022,12.

Wang，Chengyue.,Yu，Chengyuan.,Jing，Haijiao.,Wu，Xiaoming.,Novakovic，Valerie A..,...&Shi，Jialan.(2022).Long COVID: The Nature of Thrombotic Sequelae Determines the Necessity of Early Anticoagulation.Frontiers in Cellular and Infection Microbiology,12.

Wang，Chengyue,et al."Long COVID: The Nature of Thrombotic Sequelae Determines the Necessity of Early Anticoagulation".Frontiers in Cellular and Infection Microbiology 12(2022).