Evidence map›Paper›PMID 32882706›Full record

ReviewEuropean heart journal2020

COVID-19 is, in the end, an endothelial disease.

Peter Libby, Thomas Lüscher

Registry-linked trialOpen access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in European heart journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04631536 (Managing Endothelial Dysfunction in COVID-19), which is not on this map. Cited by 567 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
567citing papers in PubMed, 6 pooled it
20.2field-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.

NCT04631536 phase3unknown statusnot on this mapstarted 2021, after this paper: background citation

Managing Endothelial Dysfunction in COVID-19 : A Randomized Controlled Trial at the Lebanese American University Medical Center- Rizk Hospital

TypeinterventionalSponsorLebanese American University Medical CenterRan2021 to 2022Enrolled42ConditionsCovid19ArmsAtorvastatin + L-arginine + Folic acid + Nicorandil + Nebivolol, Placebo
3 · Its place in the literature

Who cites it

567 citing papers in PubMed, 6 syntheses or guidelines pooled it, 982 citations in OpenAlex.

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  18. Regional inequities in myocardial infarction burden in Brazil's public healthcare system.Archives of public health = Archives belges de sante publique · 2026
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507 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Peter LibbyDivision of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Thomas LüscherHeart Division, Royal Brompton & Harefield Hospital and National Heart and Lung Institute, Imperial College, London, UK.
Brigham and Women's Hospital · USHarefield Hospital · GB

Funding

Novel mechanisms of the thrombotic complications of atherosclerosisR01HL134892 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIBBY, PETER · 2019 to 2022
$1.7M
NHLBI NIH HHS R01 HL134892
6 · The paper itself

Abstract

The vascular endothelium provides the crucial interface between the blood compartment and tissues, and displays a series of remarkable properties that normally maintain homeostasis. This tightly regulated palette of functions includes control of haemostasis, fibrinolysis, vasomotion, inflammation, oxidative stress, vascular permeability, and structure. While these functions participate in the moment-to-moment regulation of the circulation and coordinate many host defence mechanisms, they can also contribute to disease when their usually homeostatic and defensive functions over-reach and turn against the host. SARS-CoV-2, the aetiological agent of COVID-19, causes the current pandemic. It produces protean manifestations ranging from head to toe, wreaking seemingly indiscriminate havoc on multiple organ systems including the lungs, heart, brain, kidney, and vasculature. This essay explores the hypothesis that COVID-19, particularly in the later complicated stages, represents an endothelial disease. Cytokines, protein pro-inflammatory mediators, serve as key danger signals that shift endothelial functions from the homeostatic into the defensive mode. The endgame of COVID-19 usually involves a cytokine storm, a phlogistic phenomenon fed by well-understood positive feedback loops that govern cytokine production and overwhelm counter-regulatory mechanisms. The concept of COVID-19 as an endothelial disease provides a unifying pathophysiological picture of this raging infection, and also provides a framework for a rational treatment strategy at a time when we possess an indeed modest evidence base to guide our therapeutic attempts to confront this novel pandemic.

Indexed as

BetacoronavirusOxidative StressCoronavirus InfectionsCOVID-19CytokinesEndothelium, VascularHumansPandemicsPneumonia, ViralSARS-CoV-2ThrombosisCytokinesCytokineEndotheliumInflammationMicrovasculatureThrombosis

Identifiers

PMID32882706
PMCPMC7470753
OpenAlexW3082240102

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.