Evidence map›Paper›PMID 20691829›Full record

ArticleAmerican heart journal2010

Joint effects of common genetic variants from multiple genes and pathways on the risk of premature coronary artery disease.

Jeffrey L Anderson, Benjamin D Horne, Nicola J Camp, Joseph B Muhlestein, Paul N Hopkins, Lisa A Cannon-Albright, Chrissa P Mower, James J Park, Jessica L Clarke, Zachary P Nicholas and 2 more

Open access · greenAbstract read
In one paragraph

Article in American heart journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Genetic Risk Score for Coronary Heart Disease: Review.Journal of personalized medicine · 2020
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. The sense and nonsense of direct-to-consumer genetic testing for cardiovascular disease.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2011
    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

12 authors at 2 institutions in 1 country.

Jeffrey L AndersonCardiovascular Department, Intermountain Medical Center, Murray, UT 84107, USA. jeffrey.anderson@imail.org
Benjamin D Horne
Nicola J Camp
Joseph B Muhlestein
Paul N Hopkins
Lisa A Cannon-Albright
Chrissa P Mower
James J Park
Jessica L Clarke
Zachary P Nicholas
Jason T McKinney
John F Carlquist
Intermountain Medical Center · USUniversity of Utah · US

Funding

Risk Burden of Lipoprotein Metabolic Gene HaplotypesR01HL071878 · NHLBI · IHC HEALTH SERVICES, INC. · PI ANDERSON, JEFFREY LANCE · 2004 to 2007
$2.3M
NHLBI NIH HHS R01 HL071878
6 · The paper itself

Abstract

objectiveThe aim of this study is to discover common variants in 6 lipid metabolic genes and construct and validate a genetic risk score (GRS) based on the joint effects of genetic variants in multiple genes from lipid and other pathobiologic pathways.

backgroundExplaining the genetic basis of coronary artery disease (CAD) is incomplete. Discovery and aggregation of genetic variants from multiple pathways may advance this objective.

methodsPremature CAD cases (n = 1,947) and CAD-free controls (n = 1,036) were selected from our angiographic registry. In a discovery phase, single nucleotide polymorphisms (SNPs) at 56 loci from internal discovery and external reports were tested for associations with biomarkers and CAD: 28 promising SNPs were then tested jointly for CAD associations, and a GRS consisting of SNPs contributing independently was constructed and validated in a replication set of familial cases and population-based controls (n = 1,320).

resultsFive variants contributed jointly to CAD prediction in a multigenic GRS model: odds ratio 1.24 (95% CI 1.16-1.33) per risk allele, P = 8.2 x 10(-11), adjusted OR 2.03 (1.53-2.70), fourth versus first quartile. 5-SNP genetic risk score had minor impact on area under the receiver operating characteristic curve (P > .05) but resulted in substantial net reclassification improvement: 0.16 overall, 0.28 in intermediate-risk patients (both P < .0001). GRS(5) predicted familial CAD with similar magnitude in the validation set.

conclusionsThe Intermountain Healthcare's Coronary Genetics study demonstrates the ability of a multigenic, multipathway GRS to improve discrimination of angiographic CAD. Genetic risk scores promise to increase understanding of the genetic basis of CAD and improve identification of individuals at increased CAD risk.

Indexed as

AdultAge of OnsetChromosomes, Human, Pair 9Coronary AngiographyCoronary Artery DiseaseFemaleGenetic Predisposition to DiseaseGenetic VariationHumansLogistic ModelsMaleMiddle AgedPolymorphism, Single NucleotideRisk AssessmentROC Curve

Identifiers

PMID20691829
PMCPMC2919893
OpenAlexW1965904227

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.