Evidence map›Paper›PMID 33181158›Full record

SynthesisInternational journal of cardiology2021

From angiotensin-converting enzyme 2 disruption to thromboinflammatory microvascular disease: A paradigm drawn from COVID-19.

R Vinci, D Pedicino, F Andreotti, G Russo, A D'Aiello, R De Cristofaro, F Crea, G Liuzzo

Abstract readSystematic Review
In one paragraph

Synthesis in International journal of cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Retinal microvascular morphology versus COVID-19: What to anticipate?Photodiagnosis and photodynamic therapy · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. The state of complement in COVID-19.Nature reviews. Immunology · 2022
    Review
  11. Neurological update: COVID-19.Journal of neurology · 2021
    Review
  12. Review
  13. COVID 19: in the eye of the cytokine storm.European heart journal · 2021
    Article
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

8 authors.

R VinciDepartment of Cardiovascular and Pulmonary Sciences, Catholic University of the Sacred Heart, Rome, Italy.
D PedicinoDepartment of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.
F AndreottiDepartment of Cardiovascular and Pulmonary Sciences, Catholic University of the Sacred Heart, Rome, Italy; Department of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy. Electronic address: felicita.andreotti@unicatt.it.
G RussoDepartment of Cardiovascular and Pulmonary Sciences, Catholic University of the Sacred Heart, Rome, Italy.
A D'AielloDepartment of Cardiovascular and Pulmonary Sciences, Catholic University of the Sacred Heart, Rome, Italy.
R De CristofaroHaemorrhagic and Thrombotic Diseases, Fondazione Policlinico Universitario "A. Gemelli", IRCCS, Rome, Italy; Institute of Internal Medicine and Geriatrics, Catholic University School of Medicine, Rome, Italy.
F CreaDepartment of Cardiovascular and Pulmonary Sciences, Catholic University of the Sacred Heart, Rome, Italy; Department of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.
G LiuzzoDepartment of Cardiovascular and Pulmonary Sciences, Catholic University of the Sacred Heart, Rome, Italy; Department of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We concisely review clinical, autopsy, experimental and molecular data of 2019 coronavirus disease (COVID-19). Angiotensin-converting enzyme 2 disruption and thromboinflammatory microangiopathy emerge as distinctive features. Briefly, entry of the virus into microvessels can profoundly disrupt the local renin-angiotensin system, cause endothelial injury, activate the complement cascade and induce powerful thromboinflammatory reactions, involving, in particular, von Willebrand factor, that, if widespread, may lead to microvascular plugging, ischemia and, ultimately, organ failure. We believe the current COVID-19 data consolidate a widely unrecognised paradigm of potentially fatal thromboinflammatory microvascular disease.

Indexed as

Angiotensin-Converting Enzyme 2COVID-19HumansInflammation MediatorsMicrovesselsRenin-Angiotensin SystemThrombosisACE2 protein, humanAngiotensin-Converting Enzyme 2Inflammation Mediators2019 coronavirusComplementRenin-angiotensin systemThromboinflammatory microangiopathyvon Willebrand factor

Identifiers

PMID33181158
PMCPMC7654294

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.