Evidence map›Paper›PMID 40164586›Full record

ArticleNature communications2025

A genome-wide association study of imaging-defined atherosclerosis.

Anders Gummesson, Per Lundmark, Qiao Sen Chen, Elias Björnson, Koen F Dekkers, Ulf Hammar, Martin Adiels, Yunzhang Wang, Therese Andersson, Göran Bergström and 15 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
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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

25 authors.

Anders GummessonRegion Västra Götaland, Sahlgrenska University Hospital, Department of Clinical Genetics and Genomics, Gothenburg, Sweden. anders.gummesson@vgregion.se.ORCID http://orcid.org/0000-0003-0024-960X
Per LundmarkDepartment of Medical Sciences, Molecular Epidemiology, Uppsala University, Uppsala, Sweden.ORCID http://orcid.org/0009-0006-2334-8802
Qiao Sen ChenDivision of Cardiology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-5864-7574
Elias BjörnsonDepartment of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Koen F DekkersDepartment of Medical Sciences, Molecular Epidemiology, Uppsala University, Uppsala, Sweden.ORCID http://orcid.org/0000-0002-4074-7235
Ulf HammarDepartment of Medical Sciences, Molecular Epidemiology, Uppsala University, Uppsala, Sweden.
Martin AdielsSchool of Public Health and Community Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden.
Yunzhang WangDepartment of Clinical Sciences, Danderyd University Hospital, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-1165-3595
Therese AnderssonDepartment of Public Medicine and Clinical Health, Umeå University, Umeå, Sweden.
Göran BergströmDepartment of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0003-4289-5722
Carl-Johan CarlhällCenter for Medical Image Science and Visualization (CMIV), Linköping University, Linköping, Sweden.
David ErlingeDepartment of Clinical Sciences Lund, Cardiology, Lund University, Lund, Sweden.
Tomas JernbergDepartment of Clinical Sciences, Danderyd University Hospital, Karolinska Institutet, Stockholm, Sweden.
Fredrik LandforsDepartment of Public Medicine and Clinical Health, Umeå University, Umeå, Sweden.ORCID http://orcid.org/0000-0002-5695-2276
Lars LindDepartment of Medical Sciences, Clinical Epidemiology, Uppsala University, Uppsala, Sweden.
Maria MannilaDepartment of Cardiology, Karolinska University Hospital, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-6189-2901
Olle MelanderDepartment of Clinical Sciences in Malmö, Lund University, Malmö, Sweden.
Carlo PirazziRegion Västra Götaland, Sahlgrenska University Hospital, Department of Cardiology, Gothenburg, Sweden.
Johan SundströmDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Carl Johan ÖstgrenCenter for Medical Image Science and Visualization (CMIV), Linköping University, Linköping, Sweden.ORCID http://orcid.org/0000-0003-1617-3179
Cecilia GunnarssonDepartment of Biomedical and Clinical Sciences, Division of Clinical Genetics, Linköping University, Linköping, Sweden.ORCID http://orcid.org/0000-0001-9474-6820
Marju Orho-MelanderDepartment of Clinical Sciences in Malmö, Lund University, Malmö, Sweden.ORCID http://orcid.org/0000-0002-3578-2503
Stefan SöderbergDepartment of Public Medicine and Clinical Health, Umeå University, Umeå, Sweden.ORCID http://orcid.org/0000-0001-9225-1306
Tove FallDepartment of Medical Sciences, Molecular Epidemiology, Uppsala University, Uppsala, Sweden.ORCID http://orcid.org/0000-0003-2071-5866
Bruna GiganteDivision of Cardiology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-4508-7990

Funding

Hjärt-Lungfonden (Swedish Heart-Lung Foundation) 2023-0439Hjärt-Lungfonden (Swedish Heart-Lung Foundation) 2024-1135 and 2024-1137Vetenskapsrådet (Swedish Research Council) 2023-02177
6 · The paper itself

Abstract

Imaging-defined atherosclerosis represents an intermediate phenotype of atherosclerotic cardiovascular disease (ASCVD). Genome-wide association studies (GWAS) on directly measured coronary plaques using coronary computed tomography angiography (CCTA) are scarce. In the so far largest population-based cohort with CCTA data, we performed a GWAS on coronary plaque burden as determined by the segment involvement score (SIS) in 24,811 European individuals. We identified 20 significant independent genetic markers for SIS, three of which were found in loci not implicated in ASCVD before. Further GWAS on coronary artery calcification showed similar results to that of SIS, whereas a GWAS on ultrasound-assessed carotid plaques identified both shared and non-shared loci with SIS. In two-sample Mendelian randomization studies using SIS-associated markers in UK Biobank and CARDIoGRAMplusC4D, one extra coronary segment with atherosclerosis corresponded to 1.8-fold increased odds of myocardial infarction. This GWAS data can aid future studies of causal pathways in ASCVD.

Indexed as

AtherosclerosisCoronary Artery DiseaseGenome-Wide Association StudyPlaque, AtheroscleroticAgedCohort StudiesComputed Tomography AngiographyCoronary AngiographyCoronary VesselsFemaleGenetic MarkersGenetic Predisposition to DiseaseHumansMaleMendelian Randomization AnalysisMiddle AgedGenetic Markers

Identifiers

PMID40164586
PMCPMC11958696

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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.