Evidence map›Paper›PMID 30022276›Full record

ReviewClinical research in cardiology : official journal of the German Cardiac Society2018

Genetics of coronary artery disease in the light of genome-wide association studies.

Heribert Schunkert, Moritz von Scheidt, Thorsten Kessler, Barbara Stiller, Lingyao Zeng, Baiba Vilne

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical research in cardiology : official journal of the German Cardiac Society, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
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

33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  7. The Impact of Single Nucleotide Polymorphisms and Other Mechanisms on Aspirin Resistance.Cardiovascular & hematological disorders drug targets · 2025
    Review
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  15. The Role of Mitochondrial DNA Mutations in Cardiovascular Diseases.International journal of molecular sciences · 2022
    Review
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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

6 authors at 3 institutions in 1 country.

Heribert SchunkertDeutsches Herzzentrum München, Klinik für Herz- und Kreislauferkrankungen, Technische Universität München, 80636, Munich, Germany. schunkert@dhm.mhn.de.
Moritz von ScheidtDeutsches Herzzentrum München, Klinik für Herz- und Kreislauferkrankungen, Technische Universität München, 80636, Munich, Germany.
Thorsten KesslerDeutsches Herzzentrum München, Klinik für Herz- und Kreislauferkrankungen, Technische Universität München, 80636, Munich, Germany.
Barbara StillerDeutsches Herzzentrum München, Klinik für Herz- und Kreislauferkrankungen, Technische Universität München, 80636, Munich, Germany.
Lingyao ZengDeutsches Herzzentrum München, Klinik für Herz- und Kreislauferkrankungen, Technische Universität München, 80636, Munich, Germany.
Baiba VilneDeutsches Herzzentrum München, Klinik für Herz- und Kreislauferkrankungen, Technische Universität München, 80636, Munich, Germany.
Technical University of Munich · DEDeutsches Herzzentrum München · DEMünchen Klinik · DE

Funding

European Union Seventh Framework Programme FP7/2007-2013 under grant agreement no. HEALTH-F2-2013-601456 (CVgenes-at-target)Fondation Leducq CADgenomics, 12CVD02German Federal Ministry of Education and Research (BMBF) within the framework of ERA-NET on Cardiovascular Disease, Joint Transnational Call 2017 ERA-CVD: grant JTC2017_21-040German Federal Ministry of Education and Research (BMBF) within the framework of target validation BlockCAD: 16GW0198KGerman Federal Ministry of Education and Research (BMBF) within the framework of the e:Med research and funding concept AbCD-Net: grant 01ZX1706CGerman Federal Ministry of Education and Research (BMBF) within the framework of the e:Med research and funding concept e:AtheroSysMed: grant 01ZX1313A-2014
6 · The paper itself

Abstract

As clinicians, we understand the development of atherosclerosis as a consequence of cholesterol deposition and inflammation in the arterial wall, both being triggered by traditional risk factors such as hypertension, hyperlipidaemia or diabetes mellitus. Another risk factor is genetic predisposition, as indicated by the predictive value of a positive family history. However, we had to wait until recently to appreciate the abundant contribution of genetic variation to the manifestation of atherosclerosis. Indeed, by now 164 chromosomal loci have been identified by genome-wide association studies (GWAS) to affect the risk of coronary artery disease. By design, practically all risk variants discovered by GWAS are frequently found in our population, resulting in the fact that principally every Western European individual carries between 130 and 190 risk alleles at the known, genome-wide significant loci (there are 0, 1, or 2 risk alleles per locus). One can assume that it is this widespread disposition that makes mankind susceptible to the detrimental effects of lifestyle factors, which likewise increase the risk of atherosclerosis. In this review, we summarize the recent genetic discoveries and attempt to group the multiple genetic risk variants in functional groups that may become actionable from a preventive or therapeutic perspective.

Indexed as

Genetic Predisposition to DiseaseCoronary Artery DiseaseGenetic VariationGenome-Wide Association StudyGenotypeHumansAtherosclerosisCoronary artery diseaseGeneticsGenome-wide association studiesPost-GWAS

Identifiers

PMID30022276
OpenAlexW2884359321

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.