Evidence map›Paper›PMID 29874178›Full record

ArticleCirculation. Genomic and precision medicine2018

Polygenic Contribution in Individuals With Early-Onset Coronary Artery Disease.

Sébastien Thériault, Ricky Lali, Michael Chong, James L Velianou, Madhu K Natarajan, Guillaume Paré

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Circulation. Genomic and precision medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
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  9. What Causes Premature Coronary Artery Disease?Current atherosclerosis reports · 2024
    Review
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  12. Observational
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Sébastien ThériaultFrom the Department of Pathology and Molecular Medicine (S.T., G.P.), Department of Biochemistry and Biomedical Sciences (R.L.), and Division of Cardiology, Department of Medicine (J.L.V., M.K.N.), Hamilton Health Sciences, McMaster University, Ontario; Population Health Research Institute, Hamilton, Ontario (S.T., M.C., G.P.); and Quebec Heart and Lung Institute Research Center, Department of Molecular Biology, Medical Biochemistry and Pathology, Laval University, Canada (S.T.).
Ricky LaliFrom the Department of Pathology and Molecular Medicine (S.T., G.P.), Department of Biochemistry and Biomedical Sciences (R.L.), and Division of Cardiology, Department of Medicine (J.L.V., M.K.N.), Hamilton Health Sciences, McMaster University, Ontario; Population Health Research Institute, Hamilton, Ontario (S.T., M.C., G.P.); and Quebec Heart and Lung Institute Research Center, Department of Molecular Biology, Medical Biochemistry and Pathology, Laval University, Canada (S.T.).
Michael ChongFrom the Department of Pathology and Molecular Medicine (S.T., G.P.), Department of Biochemistry and Biomedical Sciences (R.L.), and Division of Cardiology, Department of Medicine (J.L.V., M.K.N.), Hamilton Health Sciences, McMaster University, Ontario; Population Health Research Institute, Hamilton, Ontario (S.T., M.C., G.P.); and Quebec Heart and Lung Institute Research Center, Department of Molecular Biology, Medical Biochemistry and Pathology, Laval University, Canada (S.T.).
James L VelianouFrom the Department of Pathology and Molecular Medicine (S.T., G.P.), Department of Biochemistry and Biomedical Sciences (R.L.), and Division of Cardiology, Department of Medicine (J.L.V., M.K.N.), Hamilton Health Sciences, McMaster University, Ontario; Population Health Research Institute, Hamilton, Ontario (S.T., M.C., G.P.); and Quebec Heart and Lung Institute Research Center, Department of Molecular Biology, Medical Biochemistry and Pathology, Laval University, Canada (S.T.).
Madhu K NatarajanFrom the Department of Pathology and Molecular Medicine (S.T., G.P.), Department of Biochemistry and Biomedical Sciences (R.L.), and Division of Cardiology, Department of Medicine (J.L.V., M.K.N.), Hamilton Health Sciences, McMaster University, Ontario; Population Health Research Institute, Hamilton, Ontario (S.T., M.C., G.P.); and Quebec Heart and Lung Institute Research Center, Department of Molecular Biology, Medical Biochemistry and Pathology, Laval University, Canada (S.T.).
Guillaume ParéFrom the Department of Pathology and Molecular Medicine (S.T., G.P.), Department of Biochemistry and Biomedical Sciences (R.L.), and Division of Cardiology, Department of Medicine (J.L.V., M.K.N.), Hamilton Health Sciences, McMaster University, Ontario; Population Health Research Institute, Hamilton, Ontario (S.T., M.C., G.P.); and Quebec Heart and Lung Institute Research Center, Department of Molecular Biology, Medical Biochemistry and Pathology, Laval University, Canada (S.T.). pareg@mcmaster.ca.
Population Health Research Institute · CA

Funding

CIHRMedical Research Council MC_PC_17228Medical Research Council MC_QA137853
6 · The paper itself

Abstract

backgroundDespite evidence of high heritability, monogenic disorders are identified in a minor fraction of individuals with early-onset coronary artery disease (EOCAD). We hypothesized that some individuals with EOCAD carry a high number of common genetic risk variants, with a combined effect similar to Mendelian forms of coronary artery disease, such as familial hypercholesterolemia. METHODS AND

resultsTo confirm the polygenic contribution to EOCAD (age of ≤40 years for men and ≤45 years for women), we calculated in 111 418 British participants from the UK Biobank cohort a genetic risk score (GRS) based on the presence of 182 independent variants associated with coronary artery disease (GRS182). Participants with a diagnosis of EOCAD who underwent a revascularization procedure (n=96) had a significantly higher GRS182 (

conclusionsThese results suggest a significant polygenic contribution in individuals presenting with EOCAD, which could be more prevalent than familial hypercholesterolemia. Determination of the polygenic risk component could be included in the diagnostic workup of patients with EOCAD.

Indexed as

AdultAgedAllelesCohort StudiesCoronary Artery DiseaseFemaleGenotypeHumansLogistic ModelsMaleMiddle AgedOdds RatioPolymorphism, Single NucleotideProspective StudiesRisk Factorscoronary artery diseasegeneticsmolecular epidemiologyrisk assessmentrisk factors

Identifiers

PMID29874178
OpenAlexW2781693957

What OpenQuestion holds

Textmetadata
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.