Evidence map›Paper›PMID 35449732›Full record

ReviewFrontiers in cellular and infection microbiology2022

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

Chengyue Wang, Chengyuan Yu, Haijiao Jing, Xiaoming Wu, Valerie A Novakovic, Rujuan Xie, Jialan Shi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular and infection microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
13.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Observational
  10. Review
  11. Article
  12. Article
  13. Article
  14. Observational
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Chengyue WangDepartment of Hematology, The First Hospital of Harbin, Harbin Medical University, Harbin, China.
Chengyuan YuDepartment of Hematology, The First Hospital of Harbin, Harbin Medical University, Harbin, China.
Haijiao JingDepartment of Hematology, The First Hospital of Harbin, Harbin Medical University, Harbin, China.
Xiaoming WuDepartment of Hematology, The First Hospital of Harbin, Harbin Medical University, Harbin, China.
Valerie A NovakovicDepartment of Research, Veterans Affairs (VA) Boston Healthcare System, Harvard Medical School, Boston, MA, United States.
Rujuan XieDepartment of Nephrology, The First Hospital of Harbin, Harbin Medical University, Harbin, China.
Jialan ShiDepartment of Hematology, The First Hospital of Harbin, Harbin Medical University, Harbin, China.
First Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CNSouthern University of Science and Technology · CNVA Boston Healthcare System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

COVID-19COVID-19 Drug TreatmentThrombosisAnticoagulantsHumansHypoxiaInflammationPost-Acute COVID-19 SyndromeQuality of LifeSARS-CoV-2Anticoagulantschronic hypoxiaearly anticoagulationendothelial injuryextracellular vesiclesinflammationlong COVIDphosphatidylserinethrombosis

Identifiers

PMID35449732
PMCPMC9016198
OpenAlexW4226514831

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.