Evidence map›Paper›PMID 26117401›Full record

ArticleAtherosclerosis2015

Lipoprotein associated phospholipase A2 activity, apolipoprotein C3 loss-of-function variants and cardiovascular disease: The Atherosclerosis Risk In Communities Study.

Yashashwi Pokharel, Wensheng Sun, Linda M Polfus, Aaron R Folsom, Gerardo Heiss, A Richey Sharrett, Eric Boerwinkle, Christie M Ballantyne, Ron C Hoogeveen

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

Article in Atherosclerosis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Observational
  7. Article
  8. Article
  9. Article
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

9 authors at 6 institutions in 1 country.

Yashashwi PokharelSection of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, TX, USA; Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart and Vascular Center, Houston, TX, USA. Electronic address: yashashwi.pokharel@bcm.edu.
Wensheng SunSection of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, TX, USA. Electronic address: wsun@bcm.edu.
Linda M PolfusUniversity of Texas Health Science Center at Houston, Houston, TX, USA. Electronic address: Linda.M.Whitaker@uth.tmc.edu.
Aaron R FolsomSchool of Public Health, Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN, USA. Electronic address: folso001@umn.edu.
Gerardo HeissGillings School of Global Public Health, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. Electronic address: gerardo_heiss@unc.edu.
A Richey SharrettBloomberg School of Public Health, Department of Epidemiology, Johns Hopkins University, Baltimore, MD, USA. Electronic address: rsharret@jhu.edu.
Eric BoerwinkleUniversity of Texas Health Science Center at Houston, Houston, TX, USA; Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX, USA. Electronic address: Eric.Boerwinkle@uth.tmc.edu.
Christie M BallantyneSection of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, TX, USA; Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart and Vascular Center, Houston, TX, USA. Electronic address: cmb@bcm.edu.
Ron C HoogeveenSection of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, TX, USA; Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart and Vascular Center, Houston, TX, USA. Electronic address: ronh@bcm.edu.
Houston Methodist · USBaylor College of Medicine · USJohns Hopkins University · USThe University of Texas Health Science Center · USUniversity of Minnesota · USUniversity of North Carolina at Chapel Hill · US

Funding

The Human Genome Sequencing CenterU54HG003273 · NHGRI · BAYLOR COLLEGE OF MEDICINE · PI GIBBS, RICHARD A · 2004 to 2015
$341.3M
Building on GWAS for NHLBI-disease: the CHARGE consortiumRC2HL102419 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BOERWINKLE, ERIC A. · 2009 to 2010
$27.6M
FIELD CENTER FOR CCSPN01HC055019 · HC · UNIVERSITY OF MINNESOTA TWIN CITIES · PI FOLSOM, AARON R · 1985 to 2000
$748k
NHGRI NIH HHS U54 HG003273NHGRI NIH HHS U54HG003273NHLBI NIH HHS HHSN268201100005CNHLBI NIH HHS HHSN268201100005GNHLBI NIH HHS HHSN268201100005INHLBI NIH HHS HHSN268201100006CNHLBI NIH HHS HHSN268201100007CNHLBI NIH HHS HHSN268201100007INHLBI NIH HHS HHSN268201100008CNHLBI NIH HHS HHSN268201100008INHLBI NIH HHS HHSN268201100009CNHLBI NIH HHS HHSN268201100009INHLBI NIH HHS HHSN268201100010CNHLBI NIH HHS HHSN268201100011CNHLBI NIH HHS HHSN268201100011INHLBI NIH HHS HHSN268201100012CNHLBI NIH HHS RC2 HL102419NHLBI NIH HHS RC2HL102419
6 · The paper itself

Abstract

objectiveLipoprotein-associated phospholipase A2 (LpPLA2) activity was associated with higher CHD risk in a meta-analysis, which was partly dependent on circulating lipid levels. Apolipoprotein C3 loss-of-function (ApoC3 LOF) mutations were related with reduced postprandial lipemia and CHD risk. However, the association of LpPLA2 activity with ApoC3 LOF is not known.

methodsWe examined the association of LpPLA2 activity and ApoC3 LOF mutations and incident cardiovascular disease (CVD) (defined as coronary heart disease [CHD] plus ischemic stroke) and all-cause mortality in the biracial longitudinal Atherosclerosis Risk In Communities (ARIC) study.

resultsThe mean LpPLA2 activity was 229.3 nmol/min/mL and was higher in men and whites. LpPLA2 activity correlated positively with atherogenic dyslipidemia. ApoC3 LOF carriers had lower LpPLA2 activity levels compared to non-carriers, and there was inverse association between LpPLA2 activity and ApoC3 LOF mutations in whites. In a fully adjusted model, greater LpPLA2 activity was independently associated with incident CVD (HR 1.35, 1.09-1.68 for highest vs. lowest quintile), which was mainly explained by its association with CHD, and was also associated with all-cause mortality (HR 1.65, 1.38-1.98).

conclusionsGreater LpPLA2 activity was associated with increased CHD and all-cause mortality in both whites and African-Americans in the ARIC study. The inverse relation between LpPLA2 activity and ApoC3 LOF mutations suggests that delayed lipoprotein clearance may at least in part explain the observed association of LpPLA2 activity with increased CVD risk.

Indexed as

1-Alkyl-2-acetylglycerophosphocholine EsteraseAgedAllelesApolipoprotein C-IIIAtherosclerosisCardiovascular DiseasesDyslipidemiasFemaleHumansLipoprotein LipaseMaleMiddle AgedMutationPostprandial PeriodProportional Hazards ModelsProspective Studies1-Alkyl-2-acetylglycerophosphocholine EsteraseApolipoprotein C-IIILipoprotein LipaseApolipoprotein C3 loss-of-functionAtherogenic dyslipidemiaAtherosclerosis Risk In Communities StudyCardiovascular diseaseCoronary heart diseaseIschemic strokeLipoprotein-associated phospholipase A(2) activity

Identifiers

PMID26117401
PMCPMC4731876
OpenAlexW2131261486

What OpenQuestion holds

Textmetadata
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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.