Evidence map›Paper›PMID 24956534›Full record

Observational studyAtherosclerosis2014

Associations between nonalcoholic fatty liver disease and subclinical atherosclerosis in middle-aged adults: the Coronary Artery Risk Development in Young Adults Study.

Lisa B VanWagner, Hongyan Ning, Cora E Lewis, Christina M Shay, John Wilkins, J Jeffrey Carr, James G Terry, Donald M Lloyd-Jones, David R Jacobs, Mercedes R Carnethon

Open access · greenAbstract readMulticenter StudyObservational Study
In one paragraph

Observational study in Atherosclerosis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 2 pooled it
12.2field-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.

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

104 citing papers in PubMed, 2 syntheses or guidelines pooled it, 146 citations in OpenAlex.

  1. Pooled it
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  13. Biomolecules & biomedicine · 2025
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44 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

10 authors at 6 institutions in 1 country.

Lisa B VanWagnerDepartment of Preventive Medicine, Division of Gastroenterology & Hepatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA; Department of Medicine, Division of Gastroenterology & Hepatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. Electronic address: lvw@northwestern.edu.
Hongyan NingDepartment of Preventive Medicine, Division of Gastroenterology & Hepatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. Electronic address: h-ning@northwestern.edu.
Cora E LewisUniversity of Alabama Birmingham, Birmingham, AL, USA. Electronic address: clewis@mail.dopm.uab.edu.
Christina M ShayUniversity of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: christina-shay@ouhsc.edu.
John WilkinsDepartment of Preventive Medicine, Division of Gastroenterology & Hepatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. Electronic address: j-wilkins@md.northwestern.edu.
J Jeffrey CarrVanderbilt University, Nashville, TN, USA. Electronic address: j.jeffreycarr@vanderbilt.edu.
James G TerryWake Forest University, Winston-Salem, NC, USA. Electronic address: jgterry@wakehealth.edu.
Donald M Lloyd-JonesDepartment of Preventive Medicine, Division of Gastroenterology & Hepatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. Electronic address: dlj@northwestern.edu.
David R JacobsDivision of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA. Electronic address: jacob004@umn.edu.
Mercedes R CarnethonDepartment of Preventive Medicine, Division of Gastroenterology & Hepatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. Electronic address: carnethon@northwestern.edu.
Northwestern University · USUniversity of Alabama at Birmingham · USUniversity of Minnesota · USUniversity of Oklahoma Health Sciences Center · USVanderbilt University · USWake Forest University · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Stuart J Frank · 2013 to 2026
$19.5M
Longitudinal Changes in Pericardial Adiposity and Subclinical AtherosclerosisR01HL098445 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CARR, JOHN JEFFREY · 2010 to 2013
$4.6M
Derivation and validation of a cardiac risk index in liver transplantationF32HL116151 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI VANWAGNER, LISA B · 2012 to 2013
$122k
NHLBI NIH HHS 1 F32HL116151-01NHLBI NIH HHS F32 HL116151NHLBI NIH HHS R01 HL098445NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

objectiveNon-alcoholic fatty liver disease (NAFLD) is an obesity-related condition associated with cardiovascular mortality. Yet, whether or not NAFLD is independently related to atherosclerosis is unclear. In a population-based cross-sectional sample of middle-aged adults free from liver or heart disease, we tested the hypothesis that NAFLD is associated with subclinical atherosclerosis (coronary artery (CAC) and abdominal aortic calcification (AAC)) independent of obesity.

methodsParticipants from the Coronary Artery Risk Development in Young Adults study with CT quantification of liver fat, CAC and AAC were included (n = 2424). NAFLD was defined as liver attenuation ≤40 Hounsfield Units after exclusion of other causes of liver fat. CAC and AAC presence was defined as Agatston score >0.

resultsMean participant age was 50.1 ± 3.6 years, (42.7% men, 50.0% black) and BMI was 30.6 ± 7.2 kg/m(2). The prevalence of NAFLD, CAC, and AAC was 9.6%, 27.1%, and 51.4%. NAFLD participants had increased prevalence of CAC (37.9% vs. 26.0%, p < 0.001) and AAC (65.1% vs. 49.9%, p < 0.001). NAFLD remained associated with CAC (OR, 1.33; 95% CI, 1.001-1.82) and AAC (OR, 1.74; 95% CI, 1.29-2.35) after adjustment for demographics and health behaviors. However, these associations were attenuated after additional adjustment for visceral adipose tissue (CAC OR, 1.05; 95% CI, 0.74-1.48, AAC OR = 1.20; 95% CI, 0.86-1.67). There was no interaction by race or sex.

conclusionIn contrast to prior research, these findings suggest that obesity attenuates the relationship between NAFLD and subclinical atherosclerosis. Further studies evaluating the role of NAFLD duration on atherosclerotic progression and cardiovascular events are needed.

Indexed as

AdultAorta, AbdominalAortic DiseasesAtherosclerosisCoronary Artery DiseaseCoronary VesselsFemaleHumansIntra-Abdominal FatMaleMiddle AgedNon-alcoholic Fatty Liver DiseaseTomography, X-Ray ComputedVascular CalcificationYoung AdultCalciumCardiovascular diseasesEpidemiologyImagingLiverObesityRisk factors

Identifiers

PMID24956534
PMCPMC4124046
OpenAlexW2029896592

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.