Evidence map›Paper›PMID 33124029›Full record

ReviewThrombosis and haemostasis2020

Immunoinflammatory, Thrombohaemostatic, and Cardiovascular Mechanisms in COVID-19.

Selin Gencer, Michael Lacy, Dorothee Atzler, Emiel P C van der Vorst, Yvonne Döring, Christian Weber

Abstract readReview
In one paragraph

Review in Thrombosis and haemostasis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

  1. Observational
  2. Article
  3. Article
  4. Observational
  5. Alterations of whole body glucose metabolism in a feline SARS-CoV-2 infection model.American journal of physiology. Regulatory, integrative and comparative physiology · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Retinal microvascular morphology versus COVID-19: What to anticipate?Photodiagnosis and photodynamic therapy · 2022
    Article
  12. Review
  13. Article
  14. Crizanlizumab: A CRITICAL Drug During a CRITICAL Time?JACC. Basic to translational science · 2021
    Article
  15. Review
  16. Article
  17. COVID-19 and ischemic stroke.European journal of neurology · 2021
    Review
  18. Article
  19. Article
  20. Review
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

6 authors.

Selin Gencer *Institute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany.
Michael LacyInstitute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany.
Dorothee AtzlerInstitute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany.
Emiel P C van der VorstInstitute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany.
Yvonne DöringInstitute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany.
Christian WeberInstitute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany.

Funding

SFB1123 Deutsche Forschungsgemeinschaft
6 · The paper itself

Abstract

The global coronavirus disease 2019 (COVID-19) pandemic has deranged the recent history of humankind, afflicting more than 27 million individuals to date. While the majority of COVID-19 patients recuperate, a considerable number of patients develop severe complications. Bilateral pneumonia constitutes the hallmark of severe COVID-19 disease but an involvement of other organ systems, namely the cardiovascular system, kidneys, liver, and central nervous system, occurs in at least half of the fatal COVID-19 cases. Besides respiratory failure requiring ventilation, patients with severe COVID-19 often display manifestations of systemic inflammation and thrombosis as well as diffuse microvascular injury observed postmortem. In this review, we survey the mechanisms that may explain how viral entry and activation of endothelial cells by severe acute respiratory syndrome coronavirus 2 can give rise to a series of events including systemic inflammation, thrombosis, and microvascular dysfunction. This pathophysiological scenario may be particularly harmful in patients with overt cardiovascular disease and may drive the fatal aspects of COVID-19. We further shed light on the role of the renin-angiotensin aldosterone system and its inhibitors in the context of COVID-19 and discuss the potential impact of antiviral and anti-inflammatory treatment options. Acknowledging the comorbidities and potential organ injuries throughout the course of severe COVID-19 is crucial in the clinical management of patients affecting treatment approaches and recovery rate.

Indexed as

Renin-Angiotensin SystemCardiovascular DiseasesCOVID-19HemostasisHumansImmunityInflammationMicrocirculationPandemicsSARS-CoV-2Thrombosis

Identifiers

PMID33124029
PMCPMC7869061

What OpenQuestion holds

Textmetadata
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.