Evidence map›Paper›PMID 39152960›Full record

ArticleJACC. Cardiovascular imaging2024

Polygenic Risk Is Associated With Long-Term Coronary Plaque Progression and High-Risk Plaque.

Nick S Nurmohamed, Injeong Shim, Emilie L Gaillard, Shirin Ibrahim, Michiel J Bom, James P Earls, James K Min, R Nils Planken, Andrew D Choi, Pradeep Natarajan and 4 more

Abstract read
In one paragraph

Article in JACC. Cardiovascular imaging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

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

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  17. Advancing cardiovascular risk assessment.Cardiovascular research · 2025
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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

14 authors.

Nick S NurmohamedDepartment of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands; Department of Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands; Division of Cardiology, The George Washington University School of Medicine, Washington, DC, USA.
Injeong ShimCardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA; Department of Digital Health, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Samsung Medical Center, Seoul, Republic of South Korea.
Emilie L GaillardDepartment of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands; Department of Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Shirin IbrahimDepartment of Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Michiel J BomDepartment of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
James P EarlsCleerly Inc, Denver, Colorado, USA.
James K MinCleerly Inc, Denver, Colorado, USA.
R Nils PlankenDepartment of Radiology and Nuclear Medicine, Amsterdam UMC, Universiteit van Amsterdam, Amsterdam, the Netherlands.
Andrew D ChoiDivision of Cardiology, The George Washington University School of Medicine, Washington, DC, USA.
Pradeep NatarajanCardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA; Cardiovascular Research Center, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Erik S G StroesDepartment of Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Paul KnaapenDepartment of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Laurens F ReeskampDepartment of Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands. Electronic address: l.f.reeskamp@amsterdamumc.nl.
Akl C FahedCardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA; Cardiovascular Research Center, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA. Electronic address: afahed@mgh.harvard.edu.

Funding

Coronary plaque changes with statin and colchicine among people with high polygenic risk- a mechanistic pilot studyR01HL164629 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI Akl C Fahed, Michael TseYin Lu · 2023 to 2026
$3.3M
Integrating genomic and nongenomic risk for coronary artery diseaseK08HL161448 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI Akl C Fahed · 2022 to 2026
$751k
NHLBI NIH HHS K08 HL161448NHLBI NIH HHS R01 HL164629
6 · The paper itself

Abstract

backgroundThe longitudinal relation between coronary artery disease (CAD) polygenic risk score (PRS) and long-term plaque progression and high-risk plaque (HRP) features is unknown.

objectivesThe goal of this study was to investigate the impact of CAD PRS on long-term coronary plaque progression and HRP.

methodsPatients underwent CAD PRS measurement and prospective serial coronary computed tomography angiography (CTA) imaging. Coronary CTA scans were analyzed with a previously validated artificial intelligence-based algorithm (atherosclerosis imaging-quantitative computed tomography imaging). The relationship between CAD PRS and change in percent atheroma volume (PAV), percent noncalcified plaque progression, and HRP prevalence was investigated in linear mixed-effect models adjusted for baseline plaque volume and conventional risk factors.

resultsA total of 288 subjects (mean age 58 ± 7 years; 60% male) were included in this study with a median scan interval of 10.2 years. At baseline, patients with a high CAD PRS had a more than 5-fold higher PAV than those with a low CAD PRS (10.4% vs 1.9%; P < 0.001). Per 10 years of follow-up, a 1 SD increase in CAD PRS was associated with a 0.69% increase in PAV progression in the multivariable adjusted model. CAD PRS provided additional discriminatory benefit for above-median noncalcified plaque progression during follow-up when added to a model with conventional risk factors (AUC: 0.73 vs 0.69; P = 0.039). Patients with high CAD PRS had an OR of 2.85 (95% CI: 1.14-7.14; P = 0.026) and 6.16 (95% CI: 2.55-14.91; P < 0.001) for having HRP at baseline and follow-up compared with those with low CAD PRS.

conclusionsPolygenic risk is strongly associated with future long-term plaque progression and HRP in patients suspected of having CAD.

Indexed as

Computed Tomography AngiographyCoronary AngiographyCoronary Artery DiseaseDisease ProgressionGenetic Predisposition to DiseaseMultifactorial InheritancePlaque, AtheroscleroticPredictive Value of TestsAgedAlgorithmsArtificial IntelligenceCoronary VesselsFemaleHumansLinear ModelsMaleatherosclerosisatherosclerosis imagingatherosclerotic cardiovascular diseasecoronary artery diseasecoronary CT angiographypolygenic risk scorequantitative computed tomography

Identifiers

PMID39152960
PMCPMC12190865

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Registered trials

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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.