Evidence map›Paper›PMID 24965026›Full record

ArticleJournal of the American Heart Association2014

HDL-3 is a superior predictor of carotid artery disease in a case-control cohort of 1725 participants.

Daniel Seung Kim, Amber A Burt, Elisabeth A Rosenthal, Jane E Ranchalis, Jason F Eintracht, Thomas S Hatsukami, Clement E Furlong, Santica Marcovina, John J Albers, Gail P Jarvik

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
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  6. Fish-Derived Omega-3 Fatty Acids: Guardians of High-Density Lipoprotein?Journal of atherosclerosis and thrombosis · 2023
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  8. Review
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  12. HDL subclasses and mortality in acute heart failure patients.Clinica chimica acta; international journal of clinical chemistry · 2019
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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

10 authors at 3 institutions in 1 country.

Daniel Seung KimDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA (D.S.K., A.A.B., E.A.R., J.E.R., C.E.F., G.P.J.) Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA (D.S.K., C.E.F., G.P.J.).
Amber A BurtDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA (D.S.K., A.A.B., E.A.R., J.E.R., C.E.F., G.P.J.).
Elisabeth A RosenthalDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA (D.S.K., A.A.B., E.A.R., J.E.R., C.E.F., G.P.J.).
Jane E RanchalisDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA (D.S.K., A.A.B., E.A.R., J.E.R., C.E.F., G.P.J.).
Jason F EintrachtDepartment of General Medicine, Virginia Mason Medical Center, Seattle, WA (J.F.E.).
Thomas S HatsukamiDivision of Vascular Surgery, Department of Surgery, University of Washington School of Medicine, Seattle, WA (T.S.H.).
Clement E FurlongDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA (D.S.K., A.A.B., E.A.R., J.E.R., C.E.F., G.P.J.) Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA (D.S.K., C.E.F., G.P.J.).
Santica MarcovinaNorthwest Lipid Metabolism and Diabetes Research Laboratories, Seattle, WA (S.M., J.J.A.) Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA (S.M., J.J.A.).
John J AlbersNorthwest Lipid Metabolism and Diabetes Research Laboratories, Seattle, WA (S.M., J.J.A.) Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA (S.M., J.J.A.).
Gail P JarvikDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA (D.S.K., A.A.B., E.A.R., J.E.R., C.E.F., G.P.J.) Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA (D.S.K., C.E.F., G.P.J.).
University of Washington · USUniversity of Washington Medical Center · USVirginia Mason Medical Center · US

Funding

INTERDISCIPLINARY TRAINING IN GENOMIC SCIENCEST32HG000035 · NHGRI · UNIVERSITY OF WASHINGTON · PI Bruce Colston Trapnell · 1995 to 2026
$24.2M
Prediction and Progression of Carotid Artery DiseaseR01HL067406 · NHLBI · UNIVERSITY OF WASHINGTON · PI JARVIK, GAIL PAIRITZ · 2002 to 2009
$5.1M
Pharmacogenomics of serotonin-specific reuptake inhibitorsF31MH101905 · NIMH · UNIVERSITY OF WASHINGTON · PI KIM, DANIEL SEUNG · 2013 to 2014
$70k
NHGRI NIH HHS 5T31HG000035-18NHGRI NIH HHS T32 HG000035NHLBI NIH HHS R01 HL067406NHLBI NIH HHS R01 HL67406NIMH NIH HHS 1F31MH101905-01NIMH NIH HHS F31 MH101905
6 · The paper itself

Abstract

backgroundRecent data suggest that high-density lipoprotein cholesterol (HDL-C) levels are likely not in the causative pathway of atheroprotection, shifting focus from HDL-C to its subfractions and associated proteins. This study's goal was to determine which HDL phenotype was the better predictor of carotid artery disease (CAAD). METHODS AND

resultsHDL-2 and HDL-3 were measured in 1725 participants of European ancestry in a prevalent case-control cohort study of CAAD. Stratified analyses were conducted for men (n=1201) and women (n=524). Stepwise linear regression was used to determine whether HDL-C, HDL-2, HDL-3, or apolipoprotein A1 was the best predictor of CAAD, while adjusting for the confounders of censored age, diabetes, and current smoking status. In both men and women, HDL-3 was negatively associated with CAAD (P=0.0011 and 0.033 for men and women, respectively); once HDL-3 was included in the model, no other HDL phenotype was significantly associated with CAAD. Addition of paraoxonase 1 activity to the aforementioned regression model showed a significant and independent (of HDL-3) association with CAAD in men (P=0.001) but not in the smaller female subgroup.

conclusionsThis study is the first to contrast the associations of HDL-2 and HDL-3 with CAAD. We found that HDL-3 levels were more predictive of CAAD status than HDL-2, HDL-C, or apolipoprotein A1. In addition, for men, paraoxonase 1 activity improved the overall model prediction for CAAD independently and additively with HDL-3 levels. Further investigation into the molecular mechanisms through which HDL-3 is associated with protection from CAAD is warranted.

Indexed as

AgedApolipoprotein A-ICarotid Artery DiseasesCase-Control StudiesCholesterol, HDLFemaleHumansLinear ModelsLipoproteins, HDL2Lipoproteins, HDL3MaleMiddle AgedPredictive Value of TestsApolipoprotein A-ICholesterol, HDLLipoproteins, HDL2Lipoproteins, HDL3atherosclerosiscarotid arterieshigh‐density lipoproteinlipidslipoproteins

Identifiers

PMID24965026
PMCPMC4309059
OpenAlexW2167540690

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.