Evidence map›Paper›PMID 33161318›Full record

ReviewAtherosclerosis2020

Endothelial dysfunction in COVID-19: Current findings and therapeutic implications.

Matthias P Nägele, Bernhard Haubner, Felix C Tanner, Frank Ruschitzka, Andreas J Flammer

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Atherosclerosis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
176citing papers in PubMed, 6 pooled it
5.9field-weighted citation impact, top 3% 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

176 citing papers in PubMed, 6 syntheses or guidelines pooled it, 299 citations in OpenAlex.

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116 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

5 authors at 1 institution in 1 country.

Matthias P NägeleDepartment of Cardiology, University Heart Center Zurich, University Hospital Zurich, Zurich, Switzerland.
Bernhard HaubnerDepartment of Cardiology, University Heart Center Zurich, University Hospital Zurich, Zurich, Switzerland.
Felix C TannerDepartment of Cardiology, University Heart Center Zurich, University Hospital Zurich, Zurich, Switzerland.
Frank RuschitzkaDepartment of Cardiology, University Heart Center Zurich, University Hospital Zurich, Zurich, Switzerland.
Andreas J FlammerDepartment of Cardiology, University Heart Center Zurich, University Hospital Zurich, Zurich, Switzerland. Electronic address: andreas.flammer@usz.ch.
University Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19) increases the risk of several non-pulmonary complications such as acute myocardial injury, renal failure or thromboembolic events. A possible unifying explanation for these phenomena may be the presence of profound endothelial dysfunction and injury. This review provides an overview on the association of endothelial dysfunction with COVID-19 and its therapeutic implications. Endothelial dysfunction is a common feature of the key comorbidities that increase risk for severe COVID-19 such as hypertension, obesity, diabetes mellitus, coronary artery disease or heart failure. Preliminary studies indicate that vascular endothelial cells can be infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and evidence of widespread endothelial injury and inflammation is found in advanced cases of COVID-19. Prior evidence has established the crucial role of endothelial cells in maintaining and regulating vascular homeostasis and blood coagulation. Aggravation of endothelial dysfunction in COVID-19 may therefore impair organ perfusion and cause a procoagulatory state resulting in both macro- and microvascular thrombotic events. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and statins are known to improve endothelial dysfunction. Data from smaller observational studies and other viral infections suggests a possible beneficial effect in COVID-19. Other treatments that are currently under investigation for COVID-19 may also act by improving endothelial dysfunction in patients. Focusing therapies on preventing and improving endothelial dysfunction could improve outcomes in COVID-19. Several clinical trials are currently underway to explore this concept.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsAnimalsBlood CoagulationCardiovascular DiseasesCOVID-19COVID-19 Drug TreatmentEndothelium, VascularHost-Pathogen InteractionsHumansHydroxymethylglutaryl-CoA Reductase InhibitorsPrognosisRenin-Angiotensin SystemRisk FactorsSARS-CoV-2Angiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsHydroxymethylglutaryl-CoA Reductase InhibitorsCoronavirusCOVID-19Endothelial dysfunctionRenin angiotensin systemSARS-CoV2Statin

Identifiers

PMID33161318
PMCPMC7554490
OpenAlexW3092997163

What OpenQuestion holds

Texttitle and abstract
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.