Evidence map›Paper›PMID 42006434›Full record

ArticleAmerican journal of preventive cardiology2026

Polygenic risk scores enhance LDL cholesterol-based risk stratification for coronary artery disease.

Colin Harper, Anika Misra, Aniruddh P Patel, So Mi Cho, Satoshi Koyama, Gina M Peloso, Whitney Hornsby, Tetsushi Nakao, Pradeep Natarajan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of preventive cardiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–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

5 citing papers in PubMed.

  1. 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

9 authors.

Colin HarperMedical and Population Genetics Program and Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Anika MisraMedical and Population Genetics Program and Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Aniruddh P PatelMedical and Population Genetics Program and Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
So Mi ChoMedical and Population Genetics Program and Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Satoshi KoyamaMedical and Population Genetics Program and Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Gina M PelosoDepartment of Biostatistics, Boston University School of Public Health, Boston, MA, USA.
Whitney HornsbyMedical and Population Genetics Program and Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Tetsushi NakaoMedical and Population Genetics Program and Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Pradeep NatarajanMedical and Population Genetics Program and Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA, USA.

Funding

Integration of novel contextual and genomic blood pressure measures to enhance cardiovascular disease prediction and management in young adultsK99HL177340 · NHLBI · BROAD INSTITUTE, INC. · PI So Mi Cho · 2025 to 2026
$331k
NHLBI NIH HHS K99 HL177340
6 · The paper itself

Abstract

Background: Genetic risk for coronary artery disease (CAD) can be estimated using polygenic risk scores (PRS), but greater clarity is needed on how PRS might inform clinical risk assessment and prevention. We assessed the risk for CAD jointly conferred by LDL-C and CAD PRS relative to established treatment thresholds. Methods: This study followed 257,158 UK Biobank (UKBB) participants and 67,668 from the Results: Over a median (IQR) follow-up of 13.5 (12.8-14.2) years, 13,886 (5.4%) participants developed CAD in UKBB. Higher CAD PRS was associated with CAD risk that was comparable to, or in some strata exceeding, that associated with LDL-C ≥ 190 mg/dL by pairwise Wald tests at progressively lower LDL-C concentrations in both cohorts. Conclusions: Individuals with high genetic risk and moderate LDL-C elevations, representing 14.8% of the study population, have CAD risk comparable to or greater than that of SH. Consideration of dynamic LDL-C thresholds among those with high CAD PRS may identify individuals with risk sufficiently high to warrant preventive therapy.

Indexed as

Coronary artery diseaseLow-density lipoprotein cholesterolPolygenic risk score

Identifiers

PMID42006434
PMCPMC13084133

What OpenQuestion holds

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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.