Evidence map›Paper›PMID 40808652›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2025

Estimated Small, Dense LDL Cholesterol and Atherosclerotic Cardiovascular Risk in the UK Biobank.

Rafael Zubiran, Maureen Sampson, Anna Wolska, Alan T Remaley

Abstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
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  11. Patterns of lipid profile and genetic variations in South Asians.Cardiovascular diabetology. Endocrinology reports · 2025
    Review
  12. Review
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

4 authors.

Rafael ZubiranLipoprotein Metabolism Laboratory, National Heart, Lung, and Blood Institute (R.Z., A.W., A.T.R.), National Institutes of Health, Bethesda, MD.ORCID 0000-0003-4274-3585
Maureen SampsonDepartment of Laboratory Medicine, Clinical Center (M.S.), National Institutes of Health, Bethesda, MD.ORCID 0000-0003-0885-250X
Anna WolskaLipoprotein Metabolism Laboratory, National Heart, Lung, and Blood Institute (R.Z., A.W., A.T.R.), National Institutes of Health, Bethesda, MD.ORCID 0000-0001-9479-0741
Alan T RemaleyLipoprotein Metabolism Laboratory, National Heart, Lung, and Blood Institute (R.Z., A.W., A.T.R.), National Institutes of Health, Bethesda, MD.ORCID 0000-0003-2473-5549

Funding

Intramural NIH HHS Z99 HL999999
6 · The paper itself

Abstract

backgroundA key step in primary prevention is the assessment of atherosclerotic cardiovascular disease (ASCVD) risk. Risk enhancer tests are additional tools used to further improve ASCVD risk assessment over conventional risk markers. Our objective was to determine whether estimated small, dense low-density lipoprotein cholesterol (E-sdLDL-C) can improve risk assessment and serve as a new risk enhancer test.

methodsWe used a prospective cohort analysis of participants in the UK Biobank study with a median (interquartile range) follow-up of 10 (6.7-12.3) years. We included 271 760 individuals who were not on lipid-lowering medication at baseline and did not have incident ASCVD. The primary study outcome was the incidence of all-cause ASCVD.

resultsE-sdLDL-C was strongly associated with ASCVD events with a hazard ratio (HR) of 1.23 (95% CI, 1.22-1.24). After multivariable adjustment for age, sex, systolic blood pressure, hypertension, type 2 diabetes, and blood pressure medications, E-sdLDL-C and ApoB (apolipoprotein B) remained the most significant lipid risk factors (HR, 1.18 [95% CI, 1.16-1.19] and 1.17 [95% CI, 1.16-1.18] per SD, respectively). After further adjustment for ApoB, the association between low-density lipoprotein cholesterol (LDL-C) with all-cause ASCVD was completely reversed with an HR of 0.84 (95% CI, 0.81-0.86), but E-sdLDL-C continued to have a significant positive association with an HR of 1.11 (95% CI, 1.08-1.13). When E-sdLDL-C was discordantly higher than either LDL-C or ApoB, the risk for ASCVD was higher (LDL-C, 31% higher; ApoB, 17% higher). When elevated E-sdLDL-C is coupled with other risk enhancer tests, there is a greater risk for developing ASCVD.

conclusionsIn a UK Biobank cohort for primary prevention, the risk of all-cause ASCVD was better captured by E-sdLDL-C than LDL-C. It was also more predictive than LDL-C and ApoB when discordant with these 2 measures. E-sdLDL-C, which can be freely and automatically calculated from a standard lipid panel, can potentially improve ASCVD risk assessment without additional laboratory testing.

Indexed as

AtherosclerosisCholesterol, LDLAgedApolipoprotein B-100Biological Specimen BanksBiomarkersFemaleHeart Disease Risk FactorsHumansIncidenceMaleMiddle AgedPredictive Value of TestsPrognosisProspective StudiesRisk AssessmentAPOB protein, humanApolipoprotein B-100BiomarkersCholesterol, LDLlipidsmorbiditymortalityproteinsrisk factors

Identifiers

PMID40808652
PMCPMC12369564

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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.