Evidence map›Paper›PMID 21658281›Full record

ArticleBMC cardiovascular disorders2011

GWAS for discovery and replication of genetic loci associated with sudden cardiac arrest in patients with coronary artery disease.

Bradley E Aouizerat, Eric Vittinghoff, Stacy L Musone, Ludmila Pawlikowska, Pui-Yan Kwok, Jeffrey E Olgin, Zian H Tseng

Registry-linked trialOpen access · goldAbstract readComparative Study
In one paragraph

Article in BMC cardiovascular disorders, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06976502 (Health eHeart BioBank), which is not on this map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
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.

NCT06976502 enrolling by invitationnot on this mapstarted 2025, after this paper: background citation

Health eHeart BioBank

Typeobservational_patient_registrySponsorUniversity of California, San FranciscoRan2025 to 2035Enrolled500,000ConditionsHeart Diseases, Cardiac Diseases, Vascular Diseases, Cardiovascular DiseasesArmsBlood Draw, Tissue Collection, DNA Collection, Medical Chart Review
3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.

  1. Pooled it
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  7. Association of a CommonJournal of personalized medicine · 2022
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  20. Interactions betweenOncotarget · 2017
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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

7 authors at 1 institution in 1 country.

Bradley E AouizeratDepartment of Physiological Nursing, Institute for Human Genetics, University of California, San Francisco, 94143, USA.
Eric Vittinghoff
Stacy L Musone
Ludmila Pawlikowska
Pui-Yan Kwok
Jeffrey E Olgin
Zian H Tseng
University of California, San Francisco · US

Funding

CTSA: K12 COMPONENTKL2RR024130 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JOHNSTON, S. CLAIBORNE · 2006 to 2011
$19.3M
Comprehensive autopsy characterization of sudden cardiac deathR01HL102090 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TSENG, ZIAN H · 2010 to 2014
$2.8M
NCRR NIH HHS KL2 RR024130NHLBI NIH HHS R01 HL102090NHLBI NIH HHS R01 HL102090-01
6 · The paper itself

Abstract

backgroundEpidemiologic evidence suggests a heritable component to risk for sudden cardiac arrest independent of risk for myocardial infarction. Recent candidate gene association studies for community sudden cardiac arrests have focused on a limited number of biological pathways and yielded conflicting results. We sought to identify novel gene associations for sudden cardiac arrest in patients with coronary artery disease by performing a genome-wide association study.

methodsTagging SNPs (n = 338,328) spanning the genome were typed in a case-control study comparing 89 patients with coronary artery disease and sudden cardiac arrest due to ventricular tachycardia or ventricular fibrillation to 520 healthy controls.

resultsFourteen SNPs including 7 SNPs among 7 genes (ACYP2, AP1G2, ESR1, DGES2, GRIA1, KCTD1, ZNF385B) were associated with sudden cardiac arrest (all p < 1.30 × 10(-7)), following Bonferroni correction and adjustment for population substructure, age, and sex; genetic variation in ESR1 (p = 2.62 × 10(-8); Odds Ratio [OR] = 1.43, 95% confidence interval [CI]:1.277, 1.596) has previously been established as a risk factor for cardiovascular disease. In tandem, the role of 9 genes for monogenic long QT syndrome (LQT1-9) was assessed, yielding evidence of association with CACNA1C (LQT8; p = 3.09 × 10(-4); OR = 1.18, 95% CI:1.079, 1.290). We also assessed 4 recently published gene associations for sudden cardiac arrest, validating NOS1AP (p = 4.50 × 10(-2), OR = 1.15, 95% CI:1.003, 1.326), CSMD2 (p = 6.6 × 10(-3), OR = 2.27, 95% CI:1.681, 2.859), and AGTR1 (p = 3.00 × 10(-3), OR = 1.13, 95% CI:1.042, 1.215).

conclusionWe demonstrate 11 gene associations for sudden cardiac arrest due to ventricular tachycardia/ventricular fibrillation in patients with coronary artery disease. Validation studies in independent cohorts and functional studies are required to confirm these associations.

Indexed as

Genome-Wide Association StudyAdultAgedAged, 80 and overCase-Control StudiesCoronary Artery DiseaseDeath, Sudden, CardiacFemaleGenetic LociHaplotypesHumansMaleMiddle AgedPilot ProjectsPolymorphism, Single Nucleotide

Identifiers

PMID21658281
PMCPMC3141757
OpenAlexW2122035554

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.