Evidence map›Paper›PMID 37013573›Full record

ArticleCardiovascular diabetology2023

Visceral adipose tissue is an independent predictor and mediator of the progression of coronary calcification: a prospective sub-analysis of the GEA study.

Neftali Eduardo Antonio-Villa, Juan Gabriel Juárez-Rojas, Rosalinda Posadas-Sánchez, Juan Reyes-Barrera, Aida Medina-Urrutia

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 37 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Neftali Eduardo Antonio-VillaDepartamento de Endocrinología, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1, Col. Sección XVI, C.P. 14080, Ciudad de Mexico, Tlalpan, México.
Juan Gabriel Juárez-RojasDepartamento de Endocrinología, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1, Col. Sección XVI, C.P. 14080, Ciudad de Mexico, Tlalpan, México.
Rosalinda Posadas-SánchezDepartamento de Endocrinología, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1, Col. Sección XVI, C.P. 14080, Ciudad de Mexico, Tlalpan, México.
Juan Reyes-BarreraDepartamento de Endocrinología, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1, Col. Sección XVI, C.P. 14080, Ciudad de Mexico, Tlalpan, México.
Aida Medina-UrrutiaDepartamento de Endocrinología, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1, Col. Sección XVI, C.P. 14080, Ciudad de Mexico, Tlalpan, México. aidaxm@yahoo.com.
Instituto Nacional de Cardiología · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCoronary artery calcium (CAC) improves cardiovascular event prediction. Visceral adipose tissue (VAT) is a cardiometabolic risk factor that may directly or through its related comorbidities determine the obesity-related risk. A clinical VAT estimator could allow an efficient evaluation of obesity-related risk. We aimed to analyze the effect of VAT and its related cardiometabolic risk factors on CAC progression.

methodsCAC was quantified at baseline and after 5 years by computed tomography (CT), determining its progression. VAT and pericardial fat were measured by CT and estimated by a clinical surrogate (METS-VF). Considered cardiometabolic risk factors were: peripheral insulin resistance (IR), HOMA-IR, adipose tissue IR (ADIPO-IR), and adiponectin. Factors independently associated to CAC progression were analyzed by adjusted Cox proportional hazard models, including statin use and ASCVD risk score as covariates. We performed interaction and mediation models to propose possible pathways for CAC progression.

resultsThe study included 862 adults (53 ± 9 years, 53% women), incidence CAC progression rate: 30.2 (95% CI 25.3-35.8)/1000 person-years. VAT (HR: 1.004, 95% CI 1.001-1.007, p < 0.01) and METS-VF (HR: 1.001, 95% CI 1.0-1.001, p < 0.05) independently predicted CAC progression. VAT-associated CAC progression risk was evident among low-risk ASCVD subjects, and attenuated among medium-high-risk subjects, suggesting that traditional risk factors overcome adiposity in the latter. VAT mediates 51.8% (95% CI 44.5-58.8%) of the effect attributable to IR together with adipose tissue dysfunction on CAC progression.

conclusionsThis study supports the hypothesis that VAT is a mediator of the risk conferred by subcutaneous adipose tissue dysfunction. METS-VF is an efficient clinical surrogate that could facilitate the identification of at-risk adiposity subjects in daily clinical practice.

Indexed as

Coronary Artery DiseaseInsulin ResistanceAdipose TissueAdiposityAdultFemaleHumansIntra-Abdominal FatMaleObesityProspective StudiesRisk FactorsCardiovascular riskCoronary artery calcium progressionDysfunctional adiposityVisceral abdominal fat

Identifiers

PMID37013573
PMCPMC10071707
OpenAlexW4362523320

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.