Evidence map›Paper›PMID 39322327›Full record

ArticleJournal of the American College of Cardiology2024

Quantifying Triglyceride-Rich Lipoprotein Atherogenicity, Associations With Inflammation, and Implications for Risk Assessment Using Non-HDL Cholesterol.

Elias Björnson, Martin Adiels, Anders Gummesson, Marja-Riitta Taskinen, Stephen Burgess, Chris J Packard, Jan Borén

Abstract read
In one paragraph

Article in Journal of the American College of Cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  20. Targeting Triglycerides: The Rise of Apolipoprotein C3 and Angiopoietin-Like Protein 3 Inhibitors.American journal of cardiovascular drugs : drugs, devices, and other interventions · 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

7 authors.

Elias BjörnsonDepartment of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Martin AdielsDepartment of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden; School of Public Health and Community Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden.
Anders GummessonDepartment of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden; Region Västra Götaland, Sahlgrenska University Hospital, Department of Clinical Genetics, Gothenburg, Sweden.
Marja-Riitta TaskinenResearch Program for Clinical and Molecular Metabolism, University of Helsinki, Helsinki, Finland.
Stephen BurgessMRC Biostatistics Unit, University of Cambridge, Cambridge, United Kingdom; Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom.
Chris J PackardInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.
Jan BorénDepartment of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden. Electronic address: jan.boren@wlab.gu.se.

Funding

Wellcome Trust 225790
6 · The paper itself

Abstract

backgroundTriglyceride-rich lipoproteins and remnants (TRL/remnants) have a causal, but not yet quantified, relationship with coronary heart disease (CHD): myocardial infarction plus revascularization.

objectivesThe authors sought to estimate TRL/remnant per-particle atherogenicity, investigate causal relationships with inflammation, and determine whether differences in the atherogenicity of TRL/remnants and low-density lipoprotein (LDL) impact the causal association of non-high-density lipoprotein cholesterol (non-HDL-C) with CHD.

methodsSingle nucleotide polymorphisms (SNPs) (N = 1,357) identified by genome-wide association in the UK Biobank were ranked into 10 clusters according to the effect on TRL/remnant-C vs LDL-C. Mendelian randomization analysis was used to estimate for each SNP cluster CHD ORs per 10 mg/dL apolipoprotein B (apoB) and per 0.33 mmol/L non-HDL-cholesterol, and to evaluate association of TRL/remnants with biomarkers of systemic inflammation.

resultsSNPs in cluster 1 predominantly affected LDL-C, whereas SNPs in cluster 10 predominantly affected TRL/remnant-C. CHD risk per genetically predicted increase in apoB and in non-HDL-C rose across clusters. ORs per 10 mg/dL higher apoB was 1.15 (95% CI: 1.11-1.19) in cluster 1 vs 1.70 (95% CI: 1.52-1.90) in cluster 10. Comparing ORs between these TRL/remnant-predominant and LDL-predominant clusters, we estimated that TRL/remnants were at least 3.9 (95% CI: 2.8-5.4) times more atherogenic than LDL on a per-particle basis. For non-HDL-C, CHD ORs per 0.33 mmol/L rose from 1.15 (95% CI: 1.11-1.19) for cluster 1 to 1.40 (95% CI: 1.30-1.50) for cluster 10. TRL/remnants exhibited causal relationships with inflammation, but this did not explain their greater atherogenicity.

conclusionsTRL/remnants are about 4 times more atherogenic than LDL. Variation in the causal association of non-HDL-C with CHD indicates that adjustment for percentage TRL/remnant-C may be needed for accurate risk prediction.

Indexed as

InflammationPolymorphism, Single NucleotideTriglyceridesAgedAtherosclerosisBiomarkersCholesterolCholesterol, HDLCholesterol, LDLCoronary DiseaseFemaleGenome-Wide Association StudyHumansLipoproteinsMaleMendelian Randomization AnalysisBiomarkersCholesterolCholesterol, HDLCholesterol, LDLLipoproteinsTriglyceridescardiovascular diseaseLDLMendelian randomizationTRLsUK Biobank

Identifiers

PMID39322327
PMCPMC7616757

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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.