Triglyceride-rich lipoprotein remnants, low-density lipoproteins, and risk of coronary heart disease: a UK Biobank study

Björnson, Elias; Adiels, Martin; Taskinen, Marja-Riitta; Burgess, Stephen; Rawshani, Aidin; Borén, Jan; Packard, Chris J

doi:10.1093/eurheartj/ehad337

Cited by 183Lipoproteins and Cardiovascular HealthLipid metabolism and disordersGenetic Associations and Epidemiology

Triglyceride-rich lipoprotein remnants, low-density lipoproteins, and risk of coronary heart disease: a UK Biobank study

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Björnson, Elias, Adiels, Martin, Taskinen, Marja-Riitta, Burgess, Stephen, Rawshani, Aidin, Borén, Jan, Packard, Chris J·2023·European Heart Journal

DOI 10.1093/eurheartj/ehad337PMC PMC10576615

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Abstract

Aims: The strength of the relationship of triglyceride-rich lipoproteins (TRL) with risk of coronary heart disease (CHD) compared with low-density lipoprotein (LDL) is yet to be resolved. Methods and results: Single-nucleotide polymorphisms (SNPs) associated with TRL/remnant cholesterol (TRL/remnant-C) and LDL cholesterol (LDL-C) were identified in the UK Biobank population. In a multivariable Mendelian randomization analysis, TRL/remnant-C was strongly and independently associated with CHD in a model adjusted for apolipoprotein B (apoB). Likewise, in a multivariable model, TRL/remnant-C and LDL-C also exhibited independent associations with CHD with odds ratios per 1 mmol/L higher cholesterol of 2.59 [95% confidence interval (CI): 1.99–3.36] and 1.37 [95% CI: 1.27–1.48], respectively. To examine the per-particle atherogenicity of TRL/remnants and LDL, SNPs were categorized into two clusters with differing effects on TRL/remnant-C and LDL-C. Cluster 1 contained SNPs in genes related to receptor-mediated lipoprotein removal that affected LDL-C more than TRL/remnant-C, whereas cluster 2 contained SNPs in genes related to lipolysis that had a much greater effect on TRL/remnant-C. The CHD odds ratio per standard deviation (Sd) higher apoB for cluster 2 (with the higher TRL/remnant to LDL ratio) was 1.76 (95% CI: 1.58–1.96), which was significantly greater than the CHD odds ratio per Sd higher apoB in cluster 1 [1.33 (95% CI: 1.26–1.40)]. A concordant result was obtained by using polygenic scores for each cluster to relate apoB to CHD risk. Conclusion: Distinct SNP clusters appear to impact differentially on remnant particles and LDL. Our findings are consistent with TRL/remnants having a substantially greater atherogenicity per particle than LDL.

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Moderate elevations in triglyceride levels are associated with an increased risk of atherosclerotic cardiovascular disease.
“Moderate elevations in triglyceride levels are associated with an increased risk of atherosclerotic cardiovascular disease, 1,2,19,20”
From Targeting APOC3 with Olezarsen in Moderate Hypertriglyceridemia (2025) · cites this paper as [19]
The Results (page not specified) report that triglycerides were a significant predictor of ASCVD in Mendelian-randomisation models, supporting the general association. The paper does not establish the claim specifically for moderate elevations; its observational triglyceride-to-LDL-C association also became non-significant after adjustment for HDL-C. (LLM, conf=0.84)
Experimental — accuracy not yet measured
When lipid metabolism is imbalanced, elevated levels of RC can lead to its infiltration into the arterial wall, causing cholesterol deposition beneath the endothelium and accelerating the formation of foam cells and lipid plaques, while provoking a low-grade inflammatory response, significantly increasing the risk of AS.
“In summary, when lipid metabolism is imbalanced, elevated levels of RC can lead to its infiltration into the arterial wall, causing cholesterol deposition beneath the endothelium and accelerating the formation of foam cells and lipid plaques, while provoking a low-grade inflammatory response. These processes significantly increase the risk of AS.”
From Remnant cholesterol, lipid ratios, and the severity of coronary artery lesions: a retrospective cohort study in patients with coronary heart disease (2025) · cites this paper as [16]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measured
Mendelian randomization analyses confirm a causal relationship between lifelong TRL elevation and ASCVD.
“Observational cohorts demonstrate that higher TG and remnant cholesterol predict cardiovascular events independently of LDL-C, while Mendelian randomization analyses confirm a causal relationship between lifelong TRL elevation and ASCVD.”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [56]
The Results report that genetically defined increases in TRL/remnant cholesterol predict ASCVD outcomes in multivariable Mendelian randomisation models. However, the Introduction describes the association as “likely causal,” not confirmed, and the cited passages do not establish that TRL elevation was lifelong. Page numbers are unavailable in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measured
RC may have a stronger atherogenic effect than LDL-C.
“Thus, RC may have a stronger atherogenic effect than LDL-C.”
From Remnant cholesterol, lipid ratios, and the severity of coronary artery lesions: a retrospective cohort study in patients with coronary heart disease (2025) · cites this paper as [16]
Triglyceride-rich lipoproteins are thought to be at least as atherogenic as LDL cholesterol on a per-particle basis.
“triglyceride-rich lipoproteins are thought to be at least as atherogenic as LDL cholesterol on a perparticle basis. 19,21”
From Targeting APOC3 with Olezarsen in Moderate Hypertriglyceridemia (2025) · cites this paper as [19]

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Authors: Björnson, E., Adiels, M., Taskinen, M.-R., Burgess, S., Rawshani, A., Borén, J., & Packard, C. J.
Affiliations: Sahlgrenska University Hospital (SE)
University of Helsinki (FI)
University of Cambridge (GB)
University of Glasgow (GB)
Corresponding author: Borén, Jan
ORCID: Björnson, Elias
Adiels, Martin
Taskinen, Marja-Riitta
Burgess, Stephen
Rawshani, Aidin
Borén, Jan
Packard, Chris J
Venue: European Heart Journal
Publisher: Oxford University Press (OUP)
Published: 2023-06-26
Volume: 44
Issue: 39
Pages: 4186-4195
ISSN: 0195-668X (ISSN-L)
1522-9645
DOI: 10.1093/eurheartj/ehad337
PMC: PMC10576615
OpenAlex: W4382011883
Cited by: 183
References: 28
Citations by year: 2026: 47 · 2025: 76 · 2024: 50 · 2023: 9
FWCI: 48.59
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc
creativecommons.org/licenses/by-nc/4.0/ (vor)
Locations: European Heart Journal (publishedVersion, cc-by-nc)
PubMed Central (publishedVersion, cc-by-nc)
PubMed (publishedVersion)
Apollo (University of Cambridge) (submittedVersion, cc-by-nc)
Informationszentrum Lebenswissenschaften (ZB MED) (submittedVersion, cc-by-nc)
Työväentutkimus Vuosikirja (submittedVersion)
Funders: Swedish Research Council
Swedish Heart–Lung Foundation (ALFGBG-965404)
Sigrid Juselius Foundation
Finnish Foundation for Cardiovascular Research
Wellcome Trust and the Royal Society (204623/Z/16/Z)
United Kingdom Research and Innovation Medical Research Council (MC_UU_00002/7)
National Institute for Health Research Cambridge Biomedical Research Centre (BRC-1215-20014)
National Institute for Health Research
Department of Health and Social Care
Topics: Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
Keywords: remnant cholesterol, LDL cholesterol, coronary heart disease risk, apolipoprotein B, atherogenicity, lipoprotein particle size, lipolysis, single nucleotide polymorphisms, polygenic risk score, Mendelian randomization
MeSH terms: Apolipoproteins B, Cholesterol, Coronary Disease, United Kingdom, Humans, Lipoproteins, Cholesterol, LDL, Triglycerides, Biological Specimen Banks

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Triglyceride-rich lipoprotein remnants, low-density lipoproteins, and risk of coronary heart disease: a UK Biobank study

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