Evidence mapPaperPMID 41147828Full record

ArticleNEJM evidence2025

Genetics of Cholesterol and Coronary Disease Risk across Six Global Ancestries.

Sarah M Urbut, Qiuli Chen, Yang Sui, Anika Misra, Satoshi Koyama, Whitney Hornsby, Gina M Peloso, Sarah Finer, David A van Heel, Kaoro Ito and 4 more

Abstract read
In one paragraph

Article in NEJM evidence, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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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

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No citing paper in PubMed yet.

4 · The record

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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.

Sarah M UrbutDivision of Cardiovascular Disease, Massachusetts General Hospital, Boston.
Qiuli ChenNational Genomics Data Center, China National Center for Bioinformation, Beijing.
Yang SuiDivision of Cardiovascular Disease, Massachusetts General Hospital, Boston.
Anika MisraDivision of Cardiovascular Disease, Massachusetts General Hospital, Boston.
Satoshi KoyamaDivision of Cardiovascular Disease, Massachusetts General Hospital, Boston.
Whitney HornsbyDivision of Cardiovascular Disease, Massachusetts General Hospital, Boston.
Gina M PelosoDepartment of Biostatistics, Boston University, Boston.
Sarah FinerQueen Mary University of London, London.
David A van HeelQueen Mary University of London, London.
Kaoro ItoRIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Fowzan AlkurayaGenomic Medicine Center of Excellence, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia.
Akl C FahedDivision of Cardiovascular Disease, Massachusetts General Hospital, Boston.
Minxian WangNational Genomics Data Center, China National Center for Bioinformation, Beijing.
Pradeep NatarajanDivision of Cardiovascular Disease, Massachusetts General Hospital, Boston.

Funding

Integrating genomic and nongenomic risk for coronary artery diseaseK08HL161448 · MASSACHUSETTS GENERAL HOSPITAL · 2025 to 2025
$122k
NHLBI NIH HHS K08 HL161448
6 · The paper itself

Abstract

backgroundClinical trials of low-density lipoprotein cholesterol (LDL-C)-lowering medicines have shown improvement in cardiovascular disease risk. However, representation across diverse communities in such trials is limited. We set out to study whether or not more diverse human genetic studies could provide an opportunity to test whether these trial results can be generalized to poorly populations poorly represented in drug clinical trials.

methodsWe included six cohorts across 967,325 individuals (54.5% female), including 65,258 African, 45,393 admixed American, 179,521 East Asian, 616,045 European, 4686 Middle Eastern, and 56,422 South Asian individuals. Genetic ancestry was determined using genetic principal components and k-nearest neighbors. We constructed ancestry-specific LDL-C polygenic risk scores (PGS) using genome-wide association study (GWAS) summary statistics trained and externally validated on each ancestry. We associated each PGS with population LDL-C, scaled for a 40 mg/dl increase, and tested these scores against coronary artery disease (CAD) risk using hierarchical Bayesian meta-analyses.

resultsThe associations between genetically predicted LDL-C levels and observed LDL-C were consistent across ancestries, supporting the validity of our genetic proxy. When scaled to mimic a 40 mg/dl increase in LDL-C, the PGS showed positive but heterogeneous associations with CAD. Posterior odds ratios for CAD ranged from 1.35 (95% credible interval, 1.05 to 1.68) in African populations to 1.82 (95% credible interval, 1.33 to 2.97) in Middle Eastern populations. Bayesian analysis revealed that 97.9% of posterior samples showed all population means greater than 0 on a log scale with a between-ancestry posterior variance (τ

conclusionsOur findings demonstrated a consistent association between LDL-C and CAD risk across diverse ancestry groups that are often poorly represented in clinical trials, although effect magnitudes varied. (Funded by the National Institutes of Health and others.).

Indexed as

Cholesterol, LDLCoronary Artery DiseaseCoronary DiseaseBayes TheoremFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMaleRisk FactorsCholesterol, LDL

Identifiers

PMID41147828
PMCPMC13403192

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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 Socratic graph.