Evidence map›Paper›PMID 25682028›Full record

SynthesisAtherosclerosis2015

GWAS-identified loci for coronary heart disease are associated with intima-media thickness and plaque presence at the carotid artery bulb.

Marcel den Hoed, Rona J Strawbridge, Peter Almgren, Stefan Gustafsson, Tomas Axelsson, Gunnar Engström, Ulf de Faire, Bo Hedblad, Steve E Humphries, Cecilia M Lindgren and 8 more

Open access · greenAbstract readMeta-Analysis
In one paragraph

Synthesis in Atherosclerosis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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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

18 authors at 8 institutions in 3 countries.

Marcel den HoedDepartment of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden. Electronic address: marcel.den_hoed@medsci.uu.se.
Rona J StrawbridgeAtherosclerosis Research Unit, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital Solna, Stockholm, Sweden.
Peter AlmgrenDepartment of Clinical Sciences, Diabetes and Endocrinology, Lund University and Lund University Diabetes Centre, Malmö, Sweden.
Stefan GustafssonDepartment of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
Tomas AxelssonDepartment of Medical Sciences, SNP&SEQ Technology Platform, Uppsala University, Uppsala, Sweden.
Gunnar EngströmDepartment of Clinical Sciences, Diabetes and Endocrinology, Lund University and Lund University Diabetes Centre, Malmö, Sweden.
Ulf de FaireDivision of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Bo HedbladDepartment of Clinical Sciences, Diabetes and Endocrinology, Lund University and Lund University Diabetes Centre, Malmö, Sweden.
Steve E HumphriesCentre for Cardiovascular Genetics, University College London, London, UK.
Cecilia M LindgrenGenetic and Genomic Epidemiology Unit, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.
Andrew P MorrisGenetic and Genomic Epidemiology Unit, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK; Department of Biostatistics, University of Liverpool, Liverpool, UK.
Gerd ÖstlingDepartment of Clinical Sciences, Diabetes and Endocrinology, Lund University and Lund University Diabetes Centre, Malmö, Sweden.
Ann-Christine SyvänenDepartment of Medical Sciences, SNP&SEQ Technology Platform, Uppsala University, Uppsala, Sweden; Department of Medical Sciences, Molecular Medicine, Uppsala University, Uppsala, Sweden.
Elena TremoliDipartimento di Scienze Farmacologiche e Biomolecolari, Università di Milano & Centro Cardiologico Monzino, IRCCS, Milan, Italy.
Anders HamstenAtherosclerosis Research Unit, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital Solna, Stockholm, Sweden.
Erik IngelssonDepartment of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
Olle MelanderDepartment of Clinical Sciences, Diabetes and Endocrinology, Lund University and Lund University Diabetes Centre, Malmö, Sweden.
Lars LindDepartment of Medical Sciences, Cardiovascular Epidemiology and EpiHealth, Uppsala University, Akademiska Sjukhuset, Uppsala, Sweden.
Lund University · SEUppsala University · SECentre for Human Genetics · GBKarolinska University Hospital · SECentro Cardiologico Monzino · ITKarolinska Institutet · SEUniversity College London · GBUppsala University Hospital · SE

Funding

British Heart Foundation RG/08/008British Heart Foundation RG/08/008/25291British Heart Foundation RG/10/12/28456European Research Council 282255European Research Council 335395Wellcome Trust
6 · The paper itself

Abstract

backgroundLarge-scale genome-wide association studies (GWAS) have so far identified 45 loci that are robustly associated with coronary heart disease (CHD) in data from adult men and women of European descent.

objectivesTo examine whether the CHD-associated loci are associated with measures of atherosclerosis in data from up to 9582 individuals of European ancestry.

methodsForty-five SNPs representing the CHD-associated loci were genotyped in middle-aged to elderly individuals of European descent from four independent population-based studies (IMPROVE, MDC-CC, ULSAM and PIVUS). Intima-media thickness (IMT) was measured by external B-mode ultrasonography at the far wall of the bulb (sinus) and common carotid artery. Plaque presence was defined as a maximal IMT of the bulb >1.5 mm. We meta-analysed single-SNP associations across the four studies, and combined them in a genetic predisposition score. We subsequently examined the association of the genetic predisposition score with prevalent CHD and the three indices of atherosclerosis, adjusting for sex, age and Framingham risk factors.

resultsAs anticipated, the genetic predisposition score was associated with prevalent CHD, with each additional risk allele increasing the odds of disease by 5.5% (p = 4.1 × 10(-6)). Moreover, each additional CHD-risk allele across the 45 loci was associated with a 0.24% increase in IMT (p = 4.0 × 10(-3)), and with a 2.8% increased odds of plaque presence (p = 7.4 × 10(-6)) at the far wall of the bulb. The genetic predisposition score was not associated with IMT of the common carotid artery (p = 0.47).

conclusionsOur results suggest that the association between the 45 previously identified loci and CHD at least partly acts through atherosclerosis.

Indexed as

Carotid Intima-Media ThicknessGenome-Wide Association StudyAgedAllelesCarotid Artery, CommonCoronary DiseaseEuropeFemaleGenetic Predisposition to DiseaseGenotypeHumansMaleMiddle AgedOdds RatioPlaque, AtheroscleroticPolymorphism, Single NucleotideAtherogenic plaqueAtherosclerosisCarotid arteryGenome-wide associationIntima-media thickness

Identifiers

PMID25682028
PMCPMC5526440
OpenAlexW2154169092

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.