Evidence map›Paper›PMID 22632920›Full record

ArticleAtherosclerosis2012

Apo E4 and lipoprotein-associated phospholipase A2 synergistically increase cardiovascular risk.

Zeynep Gungor, Erdembileg Anuurad, Byambaa Enkhmaa, Wei Zhang, Kyoungmi Kim, Lars Berglund

Open access · greenAbstract read
In one paragraph

Article in Atherosclerosis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  17. An overview of the genomics of metabolic syndrome.Journal of nursing scholarship : an official publication of Sigma Theta Tau International Honor Society of Nursing · 2013
    Review
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

6 authors at 3 institutions in 2 countries.

Zeynep GungorDepartment of Biochemistry, Cerrahpasa Medical School, University of Istanbul, Turkey.
Erdembileg Anuurad
Byambaa Enkhmaa
Wei Zhang
Kyoungmi Kim
Lars Berglund
University of California, Davis · USIstanbul University · TRVA Northern California Health Care System · US

Funding

UC DAVIS CLINICAL AND TRANSLATIONAL SCIENCE CENTER: BPCAUL1RR024146 · NCRR · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2006 to 2011
$27.0M
UC Davis Clinical and Translational Science CenterUL1TR000002 · NCATS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2012 to 2015
$12.2M
UC Davis Clinical and Translational Science CenterKL2TR000134 · NCATS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2012 to 2015
$3.1M
UC Davis Clinical and Translational Science CenterKL2RR024144 · NCRR · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2006 to 2011
$3.1M
Regulation of Lipoprotein(a) Metabolism in Humans with Reference to EthnicityR01HL062705 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI BERGLUND, LARS F · 2000 to 2011
$2.9M
NCATS NIH HHS KL2 TR000134NCATS NIH HHS UL1 TR000002NCRR NIH HHS K12RR024144NCRR NIH HHS KL2 RR024144NCRR NIH HHS RR024146NCRR NIH HHS UL1 RR024146NHLBI NIH HHS HL 62705NHLBI NIH HHS R01 HL062705
6 · The paper itself

Abstract

objectiveApolipoprotein E (apoE) has been implicated as conveying increased risk for coronary artery disease (CAD). Previous studies suggest a role of apoE as a modulator of immune response and inflammatory properties. We hypothesized that the presence of apo E4 is associated with an increased inflammatory burden in subjects with CAD as compared to subjects without CAD.

methodsApoE genotypes, systemic (C-reactive protein [CRP], fibrinogen, serum amyloid-A [SAA]) and vascular inflammatory markers (Lipoprotein-associated phospholipase A(2) [Lp-PLA(2)] and pentraxin-3 [PTX-3]) were assessed in 324 Caucasians and 208 African Americans, undergoing coronary angiography.

resultsFor both ethnic groups, Lp-PLA(2) index, an integrated measure of Lp-PLA(2) mass and activity, increased significantly and stepwise across apoE isoforms (P = 0.009 and P = 0.026 for African Americans and Caucasians respectively). No differences were found for other inflammatory markers tested (CRP, fibrinogen, SAA and PTX-3). For the top cardiovascular score tertile, apo E4 carriers had a significantly higher level of Lp-PLA(2) index in both ethnic groups (P = 0.027 and P = 0.010, respectively).

conclusionThe presence of the apo E4 isoform was associated with a higher level of Lp-PLA(2) index, a marker of vascular inflammation. Our results suggest that genetic variation at the apoE locus may impact cardiovascular disease risk through enhanced vascular inflammation.

Indexed as

1-Alkyl-2-acetylglycerophosphocholine EsteraseAnalysis of VarianceApolipoprotein E4BiomarkersBlack or African AmericanCoronary AngiographyCoronary Artery DiseaseC-Reactive ProteinCross-Sectional StudiesFibrinogenGene FrequencyGenetic Predisposition to DiseaseHumansInflammationInflammation MediatorsPentraxins1-Alkyl-2-acetylglycerophosphocholine EsteraseApolipoprotein E4BiomarkersC-Reactive ProteinFibrinogenInflammation MediatorsPentraxinsPhospholipases A2PLA2G7 protein, humanSerum Amyloid A ProteinSerum Amyloid P-Component

Identifiers

PMID22632920
PMCPMC3389284
OpenAlexW1982607102

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.