Evidence map›Paper›PMID 28223054›Full record

ArticleThe Annals of thoracic surgery2017

Epicardial Adipose Tissue Removal Potentiates Outward Remodeling and Arrests Coronary Atherogenesis.

Mikaela L McKenney-Drake, Stacey D Rodenbeck, Rebecca S Bruning, Ayeeshik Kole, Kyle W Yancey, Mouhamad Alloosh, Harold S Sacks, Michael Sturek

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Annals of thoracic surgery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

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  8. Obesity and the risk of cardiometabolic diseases.Nature reviews. Cardiology · 2023
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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

8 authors at 4 institutions in 1 country.

Mikaela L McKenney-DrakeDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana.
Stacey D RodenbeckDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana.
Rebecca S BruningDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; College of Pharmacy and Health Sciences, Butler University, Indianapolis, Indiana.
Ayeeshik KoleDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; Covance, Inc, Greenfield, Indiana.
Kyle W YanceyWeldon School of Biomedical Engineering, Purdue University, Lafayette, Indiana.
Mouhamad AllooshDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana.
Harold S SacksEndocrinology and Diabetes Division, VA Greater Los Angeles Healthcare System, and David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.
Michael SturekDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; Covance, Inc, Greenfield, Indiana. Electronic address: msturek@iu.edu.
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · USPurdue University West Lafayette · USUniversity of California, Los Angeles · US

Funding

Translation CoreP30DK097512 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI Carmella Evans-Molina · 2015 to 2026
$17.4M
Indiana Medical Scientist/Engineer Training ProgramT32GM077229 · NIGMS · INDIANA UNIVERSITY INDIANAPOLIS · PI GASTON, BENJAMIN, HERBERT, BRITTNEY-SHEA · 2008 to 2022
$6.0M
Training in Vascular Biology and MedicineT32HL079995 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MARCH, KEITH LEONARD · 2005 to 2014
$2.2M
NHLBI NIH HHS T32 HL079995NIDDK NIH HHS P30 DK097512NIGMS NIH HHS T32 GM077229
6 · The paper itself

Abstract

backgroundPericoronary epicardial adipose tissue (cEAT) serves as a metabolic and paracrine organ that contributes to inflammation and is associated with macrovascular coronary artery disease (CAD) development. Although there is a strong correlation in humans between cEAT volume and CAD severity, there remains a paucity of experimental data demonstrating a causal link of cEAT to CAD. The current study tested the hypothesis that surgical resection of cEAT attenuates inflammation and CAD progression.

methodsFemale Ossabaw miniature swine (n = 12) were fed an atherogenic diet for 8 months and randomly allocated into sham (n = 5) or adipectomy (n = 7) groups. Both groups underwent a thoracotomy, opening of the pericardial sac, and placement of radioopaque clips to mark the proximal left anterior descending artery. Adipectomy swine underwent removal of 1 to 1.5 cm

resultsSeverity of CAD as assessed by percent stenosis was reduced in the adipectomy cohort compared with shams; however, plaque size remained unaltered, whereas larger plaque sizes developed in sham-operated swine. Adipectomy resulted in an expanded arterial diameter, similar to the Glagov phenomenon of positive outward remodeling. No differences in inflammatory marker expression were observed.

conclusionsThese data indicate that cEAT resection did not alter inflammatory marker expression, but arrested CAD progression through increased positive outward remodeling and arrest of atherogenesis.

Indexed as

Adipose TissueAnimalsBiomarkersCoronary Artery DiseaseCoronary VesselsFemaleInflammationPlaque, AtheroscleroticRandom AllocationSwineSwine, MiniatureUltrasonography, InterventionalBiomarkers

Identifiers

PMID28223054
PMCPMC5401651
OpenAlexW2590620606

What OpenQuestion holds

Textmetadata
LicenceTDM
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.