Evidence map›Paper›PMID 27655226›Full record

SynthesisEuropean heart journal2016

Genomic prediction of coronary heart disease.

Gad Abraham, Aki S Havulinna, Oneil G Bhalala, Sean G Byars, Alysha M De Livera, Laxman Yetukuri, Emmi Tikkanen, Markus Perola, Heribert Schunkert, Eric J Sijbrands and 5 more

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in European heart journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
176citing papers in PubMed, 5 pooled it
36.6field-weighted citation impact, top 1% 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

176 citing papers in PubMed, 5 syntheses or guidelines pooled it, 347 citations in OpenAlex.

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116 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 8 institutions in 6 countries.

Gad AbrahamCentre for Systems Genomics, School of BioSciences, The University of Melbourne, Parkville, Victoria 3010, Australia.
Aki S HavulinnaNational Institute for Health and Welfare, Helsinki FI-00271, Finland.
Oneil G BhalalaCentre for Systems Genomics, School of BioSciences, The University of Melbourne, Parkville, Victoria 3010, Australia.
Sean G ByarsCentre for Systems Genomics, School of BioSciences, The University of Melbourne, Parkville, Victoria 3010, Australia.
Alysha M De LiveraCentre for Systems Genomics, School of BioSciences, The University of Melbourne, Parkville, Victoria 3010, Australia.
Laxman YetukuriInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki FI-00014, Finland.
Emmi TikkanenInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki FI-00014, Finland.
Markus PerolaNational Institute for Health and Welfare, Helsinki FI-00271, Finland.
Heribert SchunkertDeutsches Herzzentrum München, and Technische Universität München, Munich 80636, Germany.
Eric J SijbrandsDepartment of Internal Medicine, Erasmus Medical Center, Rotterdam, CA 3000, The Netherlands.
Aarno PalotieInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki FI-00014, Finland.
Nilesh J SamaniDepartment of Cardiovascular Sciences, University of Leicester, BHF Cardiovascular Research Centre, Glenfield Hospital, Groby Rd, Leicester, LE3 9QP, United Kingdom minouye@unimelb.edu.au samuli.ripatti@helsinki.fi veikko.salomaa@thl.fi njs@leicester.ac.uk.
Veikko SalomaaNational Institute for Health and Welfare, Helsinki FI-00271, Finland minouye@unimelb.edu.au samuli.ripatti@helsinki.fi veikko.salomaa@thl.fi njs@leicester.ac.uk.
Samuli RipattiInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki FI-00014, Finland minouye@unimelb.edu.au samuli.ripatti@helsinki.fi veikko.salomaa@thl.fi njs@leicester.ac.uk.
Michael InouyeCentre for Systems Genomics, School of BioSciences, The University of Melbourne, Parkville, Victoria 3010, Australia minouye@unimelb.edu.au samuli.ripatti@helsinki.fi veikko.salomaa@thl.fi njs@leicester.ac.uk.
The University of Melbourne · AUUniversity of Helsinki · FIFinnish Institute for Health and Welfare · FIInstitute for Molecular Medicine Finland · FIBroad Institute · USErasmus MC · NLGerman Centre for Cardiovascular Research · DEGlenfield Hospital · GB

Funding

A Genome-wide Association Study for Early-Onset Myocardial InfarctionR01HL087676 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ALTSHULER, DAVID · 2007 to 2009
$4.7M
NHLBI NIH HHS R01 HL087676Wellcome TrustWellcome Trust 076113Wellcome Trust 085475
6 · The paper itself

Abstract

aimsGenetics plays an important role in coronary heart disease (CHD) but the clinical utility of genomic risk scores (GRSs) relative to clinical risk scores, such as the Framingham Risk Score (FRS), is unclear. Our aim was to construct and externally validate a CHD GRS, in terms of lifetime CHD risk and relative to traditional clinical risk scores. METHODS AND

resultsWe generated a GRS of 49 310 SNPs based on a CARDIoGRAMplusC4D Consortium meta-analysis of CHD, then independently tested it using five prospective population cohorts (three FINRISK cohorts, combined n = 12 676, 757 incident CHD events; two Framingham Heart Study cohorts (FHS), combined n = 3406, 587 incident CHD events). The GRS was associated with incident CHD (FINRISK HR = 1.74, 95% confidence interval (CI) 1.61-1.86 per S.D. of GRS; Framingham HR = 1.28, 95% CI 1.18-1.38), and was largely unchanged by adjustment for known risk factors, including family history. Integration of the GRS with the FRS or ACC/AHA13 scores improved the 10 years risk prediction (meta-analysis C-index: +1.5-1.6%, P < 0.001), particularly for individuals ≥60 years old (meta-analysis C-index: +4.6-5.1%, P < 0.001). Importantly, the GRS captured substantially different trajectories of absolute risk, with men in the top 20% of attaining 10% cumulative CHD risk 12-18 y earlier than those in the bottom 20%. High genomic risk was partially compensated for by low systolic blood pressure, low cholesterol level, and non-smoking.

conclusionsA GRS based on a large number of SNPs improves CHD risk prediction and encodes different trajectories of lifetime risk not captured by traditional clinical risk scores.

Indexed as

Coronary DiseaseFemaleGenomicsHeart DiseasesHumansMalePolymorphism, Single NucleotideRisk AssessmentRisk FactorsCoronary heart diseaseFramingham risk scoreGenomic risk scoreMyocardial infarctionPrimary prevention

Identifiers

PMID27655226
PMCPMC5146693
OpenAlexW2521147375

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.