Evidence map›Paper›PMID 40218941›Full record

ArticleNutrients2025

High-Density Lipoprotein Particles, Inflammation, and Coronary Heart Disease Risk.

Eveline O Stock, Bela F Asztalos, John M Miller, Lihong He, Kate Townsend Creasy, Rachel Schwemberger, Alexander Quinn, Clive R Pullinger, Mary J Malloy, Margaret R Diffenderfer and 1 more

Abstract read
In one paragraph

Article in Nutrients, 2025. 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

11 authors.

Eveline O StockCardiovascular Research Institute (CVRI) and Department of Medicine, University of California, San Francisco, CA 94143, USA.ORCID 0000-0001-7085-5790
Bela F AsztalosCardiovascular Research Laboratory, Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111, USA.
John M MillerJ2 Health, New York, NY 10006, USA.
Lihong HeBoston Heart Diagnostics, Framingham, MA 01702, USA.
Kate Townsend CreasyCardiovascular Research Institute (CVRI) and Department of Medicine, University of California, San Francisco, CA 94143, USA.ORCID 0000-0003-1870-4586
Rachel SchwembergerCardiovascular Research Institute (CVRI) and Department of Medicine, University of California, San Francisco, CA 94143, USA.
Alexander QuinnCardiovascular Research Institute (CVRI) and Department of Medicine, University of California, San Francisco, CA 94143, USA.
Clive R PullingerCardiovascular Research Institute (CVRI) and Department of Medicine, University of California, San Francisco, CA 94143, USA.
Mary J MalloyCardiovascular Research Institute (CVRI) and Department of Medicine, University of California, San Francisco, CA 94143, USA.
Margaret R DiffenderferBoston Heart Diagnostics, Framingham, MA 01702, USA.
John P KaneCardiovascular Research Institute (CVRI) and Department of Medicine, University of California, San Francisco, CA 94143, USA.

Funding

Boston Heart Diagnostics Research contract from Boston Heart Diagnostics (Framingham, MA, USA) to the Cardiovascular Research Institute, University of California, San Francisco (San Francisco, CA, USA)
6 · The paper itself

Abstract

backgroundCoronary heart disease (CHD) remains a leading cause of death and has been associated with alterations in plasma lipoprotein particles and inflammation markers. This study aimed to evaluate and compare standard and advanced lipid parameters and inflammatory biomarkers in CHD cases and matched control subjects. We hypothesized that incorporating advanced lipid and inflammatory biomarkers into risk models would improve CHD risk prediction beyond the standard lipid measures.

methodsCHD cases (

resultsThe most significant percent differences between male and female cases versus controls were for hsCRP (+78%, +200%), MPO (+109%, +106%), SAA (+84%, +33%), sdLDL-C (+48%; +43%), Lp(a) (+43%,+70%), apoA-I in very large α-1 HDL (-34%, -26%), HDL-C (-24%, -27%), and apoA-I in very small preβ-1 HDL (+17%; +16%). Total C, non-HDL-C, and direct and calculated LDL-C levels were only modestly higher in the cases. Multivariate models incorporating advanced parameters were statistically superior to a standard model (C statistic: men: 0.913 vs. 0.856; women: 0.903 versus 0.838). Machine learning identified apoA-I in preβ-1-HDL, α-2-HDL, α-1-HDL, α-3-HDL, MPO, and sdLDL-C as the top predictors of CHD.

conclusionsThis study introduces a novel approach to CHD risk assessment by integrating advanced HDL particle analysis and machine learning. By assessing HDL subpopulations (α-1, α-2, preβ-1 HDL), inflammatory biomarkers (MPO, SAA), and small dense LDL, we provide a more refined stratification model. Notably, preβ-1 HDL, an independent risk factor reflecting impaired cholesterol efflux from the artery wall, is highlighted as a critical marker of CHD risk. Our approach allows for earlier identification of high-risk individuals, particularly those with subtle lipid or inflammatory abnormalities, supporting more personalized interventions. These findings demonstrate the potential of advanced lipid profiling and machine learning to enhance CHD risk prediction.

Indexed as

Coronary DiseaseInflammationLipoproteins, HDLAgedApolipoprotein A-IBiomarkersCase-Control StudiesC-Reactive ProteinFemaleHumansMaleMiddle AgedPeroxidaseRisk FactorsSerum Amyloid A ProteinTriglyceridesApolipoprotein A-IBiomarkersC-Reactive ProteinLipoproteins, HDLPeroxidaseSerum Amyloid A ProteinTriglyceridesCHDHDLinflammation

Identifiers

PMID40218941
PMCPMC11990870

What OpenQuestion holds

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Registered trials

None linked

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.