Evidence map›Paper›PMID 39113913›Full record

ReviewJACC. Advances2024

COVID-19 in the Initiation and Progression of Atherosclerosis: Pathophysiology During and Beyond the Acute Phase.

Vignesh Chidambaram, Amudha Kumar, Murrium I Sadaf, Emily Lu, Subhi J Al'Aref, Tushar Tarun, Panagis Galiatsatos, Martha Gulati, Roger S Blumenthal, Thorsten M Leucker and 2 more

Abstract readReview
In one paragraph

Review in JACC. Advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

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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

12 authors.

Vignesh ChidambaramDepartment of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Amudha KumarDivision of Cardiology, Department of Medicine, Loyola University Medical Center, Maywood, Illinois, USA.
Murrium I SadafDivision of Cardiovascular Medicine, Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Emily LuDivision of Infectious Diseases, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Subhi J Al'ArefDivision of Cardiovascular Medicine, Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Tushar TarunDivision of Cardiovascular Medicine, Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Panagis GaliatsatosDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Martha GulatiBarbra Streisand Women's Heart Center, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Roger S BlumenthalCiccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Thorsten M LeuckerCiccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Petros C KarakousisDivision of Infectious Diseases, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Jawahar L MehtaDivision of Cardiovascular Medicine, Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of atherosclerotic cardiovascular disease is increasing globally, especially in low- and middle-income countries, despite significant efforts to reduce traditional risk factors. Premature subclinical atherosclerosis has been documented in association with several viral infections. The magnitude of the recent COVID-19 pandemic has highlighted the need to understand the association between SARS-CoV-2 and atherosclerosis. This review examines various pathophysiological mechanisms, including endothelial dysfunction, platelet activation, and inflammatory and immune hyperactivation triggered by SARS-CoV-2 infection, with specific attention on their roles in initiating and promoting the progression of atherosclerotic lesions. Additionally, it addresses the various pathogenic mechanisms by which COVID-19 in the post-acute phase may contribute to the development of vascular disease. Understanding the overlap of these syndromes may enable novel therapeutic strategies. We further explore the need for guidelines for closer follow-up for the often-overlooked evidence of atherosclerotic cardiovascular disease among patients with recent COVID-19, particularly those with cardiometabolic risk factors.

Indexed as

atherosclerotic cardiovascular diseaseendothelial dysfunctioninflammationplatelet activationSARS-CoV-2

Identifiers

PMID39113913
PMCPMC11304887

What OpenQuestion holds

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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.