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Triglyceride-rich lipoprotein remnants, low-density lipoproteins, and risk of coronary heart disease: a UK Biobank study
Open accessAbstract
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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![Figure 4 Association of apoB with TRL-C and ASCVD risk in clusters 1 and 2. Panel A shows for Tier 1 SNPs the association of TRL-C with apoB in each cluster with the exposure allele defined as the variant raising apoB. As for the Tier 3 set in Figure 3, the 380 Tier 1 SNPs were assigned to clusters on the basis of the ratio of effects on apoB relative to TRL/remnant-C; 205 SNPs were allocated to cluster 1, and 135 to cluster 2. Panels B and C show for cluster 1 and 2 respectively each SNPs’ effect on apoB and on ASCVD (prevalent + incident) outcome (note that the x-axis for cluster 1 in Panel B has been truncated to allow better visual comparison with the apoB range for cluster 2 in Panel C). Mendelian randomisation modelling (inverse-variance weighted method) was used to determine for each cluster the odds ratio per population SD change in apoB (0.23 g/L). The ASCVD outcome effect estimates per SD apoB differed for cluster 1 and cluster 2 with non-overlapping 95%CIs as shown. Results were similar for Mendelian randomisation analysis using the contamination mixture method which accommodates potential pleiotropic effects; odds ratio per SD apoB were for cluster 1 SNPs 1.32 [95%CI 1.26-1.42] and for cluster 2 SNPs 1.65 [1.47-1.90] (Supplementary Table 3). The genetic effect on apoB has units of g/L and on TRL/remnant-C (Panel A) has units of mmol/L.](/paper-figures/14e058ddeb504e40a405f5d352db54ed/triglyceride-rich-lipoprotein-remnants-low-density-lipoproteins-and-risk-of-figure-4.jpg)
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“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]
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“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]
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“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]
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“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]
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“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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Citations
Cites
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Interpreting findings from Mendelian randomization using the MR-Egger method.
Burgess, S., & Thompson, S. G. (2017) · European Journal of Epidemiology · doi:10.1007/s10654-017-0255-x · Cited by 4,571 · cited 2×
“The possible impact of pleiotropic effects (SNP variants influencing the outcome out with their effect on the exposure) was examined using the MR-Egger 19 and the MR ‘contamination mixture’ methods (see Supplementary Tables 3 and 4 for a fuller discussion).”
Self-citationWiller (2013) · doi:10.1038/ng.2797 · Cited by 2,983
Major lipids, apolipoproteins, and risk of vascular disease
The Emerging Risk Factors Collaboration* (2009) · JAMA · doi:10.1001/jama.2009.1619 · Cited by 2,731
Guidelines for performing Mendelian randomization investigations
Burgess, S., Smith, G. D., Davies, N. M., Dudbridge, F., Gill, D., Glymour, M. M., Hartwig, F. P., Holmes, M. V., Minelli, C., Relton, C. L., et al. (2019) · Wellcome Open Research · doi:10.12688/wellcomeopenres.15555.1 · Cited by 1,828
Self-citationBorén, J., Chapman, M. J., Krauss, R. M., Packard, C. J., Bentzon, J. F., Binder, C. J., Daemen, M. J., Demer, L. L., Hegele, R. A., Nicholls, S. J., et al. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehz962 · Cited by 1,601 · cited 2×
“29, 30 Remnant particles contain more cholesterol per apoB and so if the ‘atherogenicity’ of TRL/remnant-C is higher than LDL-C then this implies that the per-particle (per apoB) impact on atherosclerotic processes must be even greater.”
Self-citationTriglycerides and cardiovascular disease
Nordestgaard, B. G., & Varbo, A. (2014) · The Lancet · doi:10.1016/s0140-6736(14)61177-6 · Cited by 1,419 · cited 4×
“27, 28, 1, 2, 11, 29 The key question that arises from the present and earlier investigations is what is the basis of a remnant particle’s enhanced atherogenicity?”
InfluentialTabas, I., Williams, K. J., & Borén, J. (2007) · Circulation · doi:10.1161/circulationaha.106.676890 · Cited by 1,399
Self-citationGuidelines for performing Mendelian randomization investigations
Burgess, S., Davey Smith, G., Davies, N. M., Dudbridge, F., Gill, D., Glymour, M. M., Hartwig, F. P., Holmes, M. V., Minelli, C., Relton, C. L., et al. (2020) · Wellcome Open Research · doi:10.12688/wellcomeopenres.15555.2 · Cited by 1,273 · cited 4×
“21 It is worthwhile noting that the two SNP clusters were defined empirically based on the observed effect size for apoB relative to TRL/remnant-C rather than any preconception as to which SNPs/genes should be grouped together based on their role in lipid metabolism or their relationship to ASCVD…”
InfluentialSelf-citationChapman, M. J., Ginsberg, H. N., Amarenco, P., Andreotti, F., Borén, J., Catapano, A. L., Descamps, O. S., Fisher, E., Kovanen, P. T., Kuivenhoven, J. A., et al. (2011) · European Heart Journal · doi:10.1093/eurheartj/ehr112 · Cited by 1,227 · cited 2×
“27, 28, 1, 2, 11, 29 The key question that arises from the present and earlier investigations is what is the basis of a remnant particle’s enhanced atherogenicity?”
Self-citationNordestgaard, B. G. (2016) · Circulation Research · doi:10.1161/circresaha.115.306249 · Cited by 1,116 · cited 6×
“10, 22 In contrast, extensive reports from the Copenhagen General Population Study 1, 11–13, 23,21 and other cohorts 12 indicated that TRL cholesterol or remnant cholesterol was associated with a higher CHD risk per mmol/l increase than LDL-C, and since remnants have a higher cholesterol/apoB ratio…”
InfluentialRemnant Cholesterol as a Causal Risk Factor for Ischemic Heart Disease
Varbo, A., Benn, M., Tybjærg-Hansen, A., Jørgensen, A. B., Frikke-Schmidt, R., & Nordestgaard, B. G. (2013) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2012.08.1026 · Cited by 1,115 · cited 2×
“However, the broad agreement between the present results and those from the Copenhagen General Population Study 1, 11–13 , 23 do In conclusion, we have shown that choice of lipoprotein biomarker (exposure) to reflect the abundance of TRL/remnants has a substantial impact on the perceived…”
Ginsberg, H. N., Packard, C. J., Chapman, M. J., Borén, J., Aguilar-Salinas, C. A., Averna, M., Ference, B. A., Gaudet, D., Hegele, R. A., Kersten, S., et al. (2021) · European Heart Journal · doi:10.1093/eurheartj/ehab551 · Cited by 979 · cited 5×
“2 The issue has been addressed in a number of recent reports and differing conclusions have been drawn.”
InfluentialSelf-citationFerence, B. A., Kastelein, J. J. P., Ray, K. K., Ginsberg, H. N., Chapman, M. J., Packard, C. J., Laufs, U., Oliver-Williams, C., Wood, A. M., Butterworth, A. S., et al. (2019) · JAMA · doi:10.1001/jama.2018.20045 · Cited by 703 · cited 4×
“…combined cohort E u r op e P M C F und e r s A u t ho r M a nu s c r i p t s E u r op e P M C F und e r s A u t ho r M a nu s c r i p t s analysis 8 which showed that SNPs linked to the lipoprotein lipase (LPL) gene with effects on TG, and SNPs linked to the LDL receptor gene (LDLR) with effects…”
InfluentialSelf-citationA robust and efficient method for Mendelian randomization with hundreds of genetic variants
Burgess, S., Foley, C. N., Allara, E., Staley, J. R., & Howson, J. M. M. (2020) · Nature Communications · doi:10.1038/s41467-019-14156-4 · Cited by 681 · cited 3×
“18 However, close agreement in the results from the range of SNP sets examined, and E u r op e P M C F und e r s A u t ho r M a nu s c r i p t s E u r op e P M C F und e r s A u t ho r M a nu s c r i p t s from the different statistical methods of conducting Mendelian randomisation analyses that…”
Self-citationApolipoprotein B Particles and Cardiovascular Disease: A Narrative Review
Sniderman, A. D., Thanassoulis, G., Glavinovic, T., Navar, A. M., Pencina, M., Catapano, A., & Ference, B. A. (2019) · JAMA Cardiology · doi:10.1001/jamacardio.2019.3780 · Cited by 593 · cited 1×
“9, 10 11–13 Resolving these discordant findings is important since it impacts on risk assessment, and the design and interpretation of intervention trials.”
Sampson, M. L., Ling, C., Sun, Q., Harb, R., Ashmaig, M., Warnick, R., Sethi, A. A., Fleming, J. K., Otvos, J. D., Meeusen, J. W., et al. (2020) · JAMA Cardiology · doi:10.1001/jamacardio.2020.0013 · Cited by 593
Remnant cholesterol predicts cardiovascular disease beyond LDL and ApoB: A primary prevention study
Quispe, R., Martin, S. S., Michos, E. D., Lamba, I., Blumenthal, R. S., Saeed, A., Lima, J., Puri, R., Nomura, S., Tsai, M., et al. (2021) · European Heart Journal · doi:10.1093/eurheartj/ehab432 · Cited by 441 · cited 1×
“10, 22 In contrast, extensive reports from the Copenhagen General Population Study 1, 11–13, 23,21 and other cohorts 12 indicated that TRL cholesterol or remnant cholesterol was associated with a higher CHD risk per mmol/l increase than LDL-C, and since remnants have a higher cholesterol/apoB ratio…”
Metabolism of triglyceride-rich lipoproteins in health and dyslipidaemia
Borén, J., Taskinen, M.-R., Björnson, E., & Packard, C. J. (2022) · Nature Reviews Cardiology · doi:10.1038/s41569-022-00676-y · Cited by 315 · cited 1×
“1–5 In analogy with the pathogenic mechanisms linked to low-density lipoproteins (LDL), remnant lipoproteins can penetrate the sub-endothelial space in artery walls and bind to proteoglycans, thereby initiating cholesterol deposition and foam cell formation.”
Self-citationMarston, N. A., Giugliano, R. P., Melloni, G. E. M., Park, J.-G., Morrill, V., Blazing, M. A., Ference, B., Stein, E., Stroes, E. S., Braunwald, E., et al. (2022) · JAMA Cardiology · doi:10.1001/jamacardio.2021.5083 · Cited by 262 · cited 3×
“10, 22 In contrast, extensive reports from the Copenhagen General Population Study 1, 11–13, 23,21 and other cohorts 12 indicated that TRL cholesterol or remnant cholesterol was associated with a higher CHD risk per mmol/l increase than LDL-C, and since remnants have a higher cholesterol/apoB ratio…”
Causes and consequences of hypertriglyceridemia
Packard, C. J., Boren, J., & Taskinen, M.-R. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00252 · Cited by 239 · cited 5×
“…variable for LDL-C is compromised by the revelation from metabolic studies that the LDL receptor is involved also in TRL/remnant clearance 2, 20 – an observation that explains the increase in remnants in familial hypercholesterolemia and the reduction in TRL/remnant particle concentration…”
InfluentialSelf-citationWelsh, C., Celis-Morales, C. A., Brown, R., Mackay, D. F., Lewsey, J., Mark, P. B., Gray, S. R., Ferguson, L. D., Anderson, J. J., Lyall, D. M., et al. (2019) · Circulation · doi:10.1161/circulationaha.119.041149 · Cited by 191
Vallejo-Vaz, A. J., Fayyad, R., Boekholdt, S. M., Hovingh, G. K., Kastelein, J. J., Melamed, S., Barter, P., Waters, D. D., & Ray, K. K. (2018) · Circulation · doi:10.1161/circulationaha.117.032318 · Cited by 187 · cited 1×
“20, 24, 25 We found that SNPs affecting the receptor pathway (cluster 1 which includes SNPs in the LDL receptor gene) had little effect on plasma TG as an exposure (confirming earlier findings 8 ), but here show that they do indeed influence TRL/remnant-C.”
Varbo, A., & Nordestgaard, B. G. (2021) · European Heart Journal · doi:10.1093/eurheartj/ehab293 · Cited by 178
Robust methods in Mendelian randomization via penalization of heterogeneous causal estimates
Rees, J. M. B., Wood, A., Dudbridge, F., & Burgess, S. (2019) · PLoS ONE · doi:10.1371/journal.pone.0222362 · Cited by 177
Self-citationBroadbent, J. R., Foley, C. N., Grant, A. J., Mason, A. M., Staley, J. R., & Burgess, S. (2020) · Wellcome Open Research · doi:10.12688/wellcomeopenres.16374.2 · Cited by 148
Self-citationVarbo, A., & Nordestgaard, B. G. (2017) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000429 · Cited by 135
Triglyceride-rich lipoproteins and remnants: targets for therapy?
Dallinga-Thie, G. M., Kroon, J., Borén, J., & Chapman, M. J. (2016) · Current Cardiology Reports · doi:10.1007/s11886-016-0745-6 · Cited by 90
Self-citationRemnant lipoproteins: are they equal to or more atherogenic than LDL?
Salinas, C. A. A., & Chapman, M. J. (2020) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000682 · Cited by 87 · cited 1×
“14, 15 TRL/remnant-C was derived by subtracting LDL-C from non-HDL-C and since it was based on measured parameters, it was deemed an indirectly ‘measured’ concentration.”
Sniderman, A. D., Návar, A. M., & Thanassoulis, G. (2021) · JAMA Cardiology · doi:10.1001/jamacardio.2021.5080 · Cited by 78 · cited 1×
“10, 22 In contrast, extensive reports from the Copenhagen General Population Study 1, 11–13, 23,21 and other cohorts 12 indicated that TRL cholesterol or remnant cholesterol was associated with a higher CHD risk per mmol/l increase than LDL-C, and since remnants have a higher cholesterol/apoB ratio…”
Lotta, L. A., Stewart, I. D., Sharp, S. J., Day, F. R., Burgess, S., Luan, J., Bowker, N., Cai, L., Li, C., Wittemans, L. B. L., et al. (2018) · JAMA Cardiology · doi:10.1001/jamacardio.2018.2866 · Cited by 72 · cited 2×
“The implication of the present and earlier findings 4, 26 is that interventions to regulate TRL/remnant lipoproteins may prove disproportionately beneficial.”
Self-citationCabodevilla, A. G., Tang, S., Lee, S., Mullick, A. E., Alemán, J. O., Hussain, M. M., Sessa, W. C., Abumrad, N. A., & Goldberg, I. J. (2021) · Journal of Clinical Investigation · doi:10.1172/jci145800 · Cited by 35
Phenotypes, genotypes and response to statin therapy
CASLAKE, M. J., & Packard, C. J. (2004) · Current Opinion in Lipidology · doi:10.1097/01.mol.0000137225.46654.4d · Cited by 35 · cited 1×
“20, 24, 25 We found that SNPs affecting the receptor pathway (cluster 1 which includes SNPs in the LDL receptor gene) had little effect on plasma TG as an exposure (confirming earlier findings 8 ), but here show that they do indeed influence TRL/remnant-C.”
Self-citationHelgadottir, A., Thorleifsson, G., Snaebjarnarson, A., Stefansdottir, L., Sveinbjornsson, G., Tragante, V., Björnsson, E., Steinthorsdottir, V., Gretarsdottir, S., Helgason, H., et al. (2022) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwac219 · Cited by 30
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Metadata
- 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
- 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
- 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
- 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 › Cardiology and Cardiovascular Medicine › 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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