Evidence map›Paper›PMID 21127300›Full record

ArticleStroke2011

Genetic variation in LPAL2, LPA, and PLG predicts plasma lipoprotein(a) level and carotid artery disease risk.

James Ronald, Ramakrishnan Rajagopalan, Felecia Cerrato, Alex S Nord, Thomas Hatsukami, Ted Kohler, Santica Marcovina, Patrick Heagerty, Gail P Jarvik

Open access · bronzeAbstract readMulticenter Study
In one paragraph

Article in Stroke, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.

  1. Genome-Wide Association Study HighlightsArteriosclerosis, thrombosis, and vascular biology · 2021
    Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Review
  7. Review
  8. Lipoprotein(a): Just an Innocent Bystander in Arterial Hypertension?International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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  17. Article
  18. Article
  19. Review
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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

9 authors at 1 institution in 1 country.

James RonaldDepartment of Medicine, Division of Medical Genetics, University of Washington Medical Center Box 357720, Seattle, WA 98195-7720, USA.
Ramakrishnan Rajagopalan
Felecia Cerrato
Alex S Nord
Thomas Hatsukami
Ted Kohler
Santica Marcovina
Patrick Heagerty
Gail P Jarvik
VA Puget Sound Health Care System · US

Funding

Serum Amyloid and Inflammation in AtherogenesisP01HL030086 · NHLBI · UNIVERSITY OF WASHINGTON · PI HEINECKE, JAY W · 1985 to 2009
$14.7M
Prediction and Progression of Carotid Artery DiseaseR01HL067406 · NHLBI · UNIVERSITY OF WASHINGTON · PI JARVIK, GAIL PAIRITZ · 2002 to 2009
$5.1M
NHLBI NIH HHS P01 HL030086NHLBI NIH HHS P01 HL 30086NHLBI NIH HHS R01 HL067406NHLBI NIH HHS R01 HL67406
6 · The paper itself

Abstract

background and purposelipoprotein(a) [Lp(a)] level is an established risk factor for coronary artery disease and has been implicated in carotid artery disease (CAAD). The relationship between genetic variation in the LPA gene region and CAAD risk remains unknown.

methodswe genotyped single nucleotide polymorphisms (SNPs) in the LPAL2, LPA, and PLG regions in 530 individuals with severe CAAD and 770 controls and kringle IV type 2 (KIV2) repeat length in a subset of 90 individuals.

resultsnine SNPs collectively accounted for 30% of the variance in Lp(a) level. Six SNPs were associated with Lp(a) level after accounting for KIV2 copy number, and the dominant KIV2 allele combined with these markers explained 60% of the variance in Lp(a) level. Five SNPs, including rs10455872, which had an odds ratio of 2.1 per minor allele and haplotypes formed by rs10455872, rs6919346, and rs3123629, were significant predictors of CAAD. After accounting for Lp(a) level, all evidence of CAAD-genotype association in the LPA region was eliminated.

conclusionsLPA region SNPs capture some but not all of the effect of KIV2 repeat length on Lp(a) level. There are associations between LPA region SNPs and CAAD that appear to be attributable to effects on Lp(a) level.

Indexed as

Apolipoprotein A-IIGenetic Predisposition to DiseasePolymorphism, Single NucleotideAgedAllelesCarotid Artery DiseasesFemaleGenes, DominantHumansLipoprotein(a)MaleProtein Structure, TertiaryRepetitive Sequences, Amino AcidAPOA2 protein, humanApolipoprotein A-IILipoprotein(a)

Identifiers

PMID21127300
PMCPMC3020902
OpenAlexW2130440394

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.