Triglyceride-mediated pathways and coronary disease: collaborative analysis of 101 studies
Open accessAbstract
Background Whether triglyceride-mediated pathways are causally relevant to coronary heart disease is uncertain. We studied a genetic variant that regulates triglyceride concentration to help judge likelihood of causality.Methods We assessed the -1131T>C (rs662799) promoter polymorphism of the apolipoprotein A5 (APOA5) gene in relation to triglyceride concentration, several other risk factors, and risk of coronary heart disease. We compared disease risk for genetically-raised triglyceride concentration (20,842 patients with coronary heart disease, 35,206 controls) with that recorded for equivalent differences in circulating triglyceride concentration in prospective studies (302 430 participants with no history of cardiovascular disease; 12,785 incident cases of coronary heart disease during 2.79 million person-years at risk). We analysed -1131T>C in 1795 people without a history of cardiovascular disease who had information about lipoprotein concentration and diameter obtained by nuclear magnetic resonance spectroscopy.Findings The minor allele frequency of -1131T>C was 8% (95% CI 7-9). -1131T>C was not significantly associated with several non-lipid risk factors or LDL cholesterol, and it was modestly associated with lower HDL cholesterol (mean difference per C allele 3.5% [95% CI 2.6-4.6]; 0.053 mmol/L [0.039-0.068]), lower apolipoprotein AI (1.3% [0.3-2.3]; 0.023 g/L [0.005-0.041]), and higher apolipoprotein B (3.2% [1.3-5.1]; 0.027 g/L [0.011-0.043]). By contrast, for every C allele inherited, mean triglyceride concentration was 16.0% (95% CI 12.9-18.7), or 0.25 mmol/L (0.20-0.29), higher (p=4.4x10(-24)). The odds ratio for coronary heart disease was 1.18 (95% CI 1.11-1.26; p=2.6x10(-7)) per C allele, which was concordant with the hazard ratio of 1.10 (95% CI 1.08-1.12) per 16% higher triglyceride concentration recorded in prospective studies. -1131T>C was significantly associated with higher VLDL particle concentration (mean difference per C allele 12.2 nmol/L [95% CI 7.7-16.7]; p=9.3x10(-8)) and smaller HDL particle size (0.14 nm [0.08-0.20]; p=7.0x10(-5)), factors that could mediate the effects of triglyceride.Interpretation These data are consistent with a causal association between triglyceride-mediated pathways and coronary heart disease.Funding British Heart Foundation, UK Medical Research Council, Novartis.
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Triglyceride-rich remnant particles have approximately the same effect on the risk of cardiovascular disease as LDL particles, as suggested by the current study's results extending prior findings.
“The results of the current study extend those findings by suggesting that triglyceride-rich remnant particles have approximately the same effect on the risk of cardiovascular disease as LDL particles.”
From Association of Triglyceride-Lowering <i>LPL</i> Variants and LDL-C–Lowering <i>LDLR</i> Variants With Risk of Coronary Heart Disease (2019) · cites this paper as [28]
The Discussion (page unavailable) describes VLDL and remnant lipoproteins as potentially proatherogenic, and reports findings consistent with a causal role for triglyceride-mediated pathways in coronary heart disease. It does not compare the effect of remnant particles with that of LDL particles or establish approximately equal effects; its reported outcome is coronary heart disease rather than cardiovascular disease broadly. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe association between triglycerides and cardiovascular risk is well established from epidemiological studies, genome-wide analyses, and Mendelian randomization studies.
“The association between triglycerides and cardiovascular (CV) risk is well established from epidemiological studies,1-5 genome-wide analyses,6-8 and Mendelian randomization studies.9,10”
Clinical benefit of therapies that lower LDL-C by reducing LDL particle mass is proportional to the absolute reduction in LDL-C, because on average reductions in LDL-C and LDL particles are concordant.
“Therefore, the clinical benefit of therapies that lower LDL-C by reducing LDL particle mass will be proportional to the absolute reduction in LDLC, because-on average-the reduction in LDL-C and LDL particles will be concordant [34,50,54,55].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [55]
Genetic studies of NPC1L1 mutations support ezetimibe's benefit: naturally occurring inactivating mutations are associated with reduced plasma LDL-C and reduced coronary artery disease risk.
“The beneficial effect of ezetimibe is also supported by genetic studies of mutations in NPC1L1; naturally occurring mutations that inactivate the protein were found to be associated with reduced plasma LDL-C and reduced risk for CAD [55,269,270].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [55]
Recent data strongly support triglyceride-rich lipoproteins as a cardiovascular risk factor, although the role of triglycerides has been debated.
“Although the role of TG as a risk factor for CVD has been strongly debated, recent data strongly favour the role of TG-rich lipoproteins as a risk factor for CVD.121”
From ESC/EAS Guidelines for the management of dyslipidaemias (2011) · cites this paper as [121]
The causative protective role of HDL-C against cardiovascular disease has been questioned by Mendelian randomization studies.
“The causative role of HDL-C for protection against CVD has been questioned in several studies utilizing Mendelian randomization. 87,89,91,92”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [87]
Non-HDL-C includes atherogenic TG-rich lipoproteins, which is essential considering recent information from GWAS and Mendelian randomization supporting TGs and remnant particles as causative factors in atherogenesis.
“Non-HDL-C also includes the atherogenic TG-rich lipoproteins (VLDL, IDL and remnants), which is essential considering the recent information from genome-wide association studies (GWASs) and Mendelian randomization 76,86 - 89 supporting TGs and remnant particles as causative factors in atherogenesis.”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [87]
CVD risk is increased if fasting TGs > 1.7 mmol/L; drug treatment to lower TGs may be considered in high-risk subjects when TGs > 2.3 mmol/L and not lowered by lifestyle.
“Although the CVD risk is increased if fasting TGs are . 1.7 mmol/ L (150 mg/dL), 87 the use of drugs to lower TGs may only be considered in high-risk subjects when TGs are . 2.3 mmol/L (200 mg/dL) and cannot be lowered by lifestyle measures.”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [87]
Recent data favor TG-rich lipoproteins as a risk factor for CVD.
“Although the role of TGs as a risk factor for CVD has been strongly debated, recent data favour the role of TG-rich lipoproteins as a risk factor for CVD.”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [87]
The causative role of HDL-C for protection against CVD has been questioned in several Mendelian randomization studies.
“The causative role of HDL-C for protection against CVD has been questioned in several studies utilizing Mendelian randomization.87,89,91,92”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [87]
TG-rich lipoproteins are a risk factor for cardiovascular disease.
“recent data favour the role of TG-rich lipoproteins as a risk factor for CVD.87”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [87]
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- Authors
- ‡
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- ‡
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2010-05
- Volume
- 375
- Issue
- 9726
- Pages
- 1634-1639
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- PMC
- PMC2867029
- OpenAlex
- W2144516660
- Cited by
- 716
- References
- 37
- Citations by year
- 2026: 10 · 2025: 24 · 2024: 29 · 2023: 29 · 2022: 47 · 2021: 49 · 2020: 53 · 2019: 55 · 2018: 50 · 2017: 36 · 2016: 51 · 2015: 51 · 2014: 48 · 2013: 45 · 2012: 47
- FWCI
- 62.17
- Type
- journal article
- Language
- en
- Update notices
- erratum (2010-07-10)
- Open access
- bronze
- doi.org
- Licence
- Locations
- The Lancet (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- University of Birmingham Research Portal (University of Birmingham) (publishedVersion, other-oa)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Bristol Research (University of Bristol) (publishedVersion)
- Socio-Environmental Systems Modeling (acceptedVersion)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Figshare (submittedVersion)
- Leicester Research Archive (University of Leicester) (submittedVersion, other-oa)
- Explore Bristol Research (submittedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- British Heart Foundation
- Novartis
- Medical Research Council
- 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
- triglycerides, coronary artery disease, APOA5, APOA5 -1131T>C polymorphism, genetic association, triglyceride concentration, HDL cholesterol, apolipoprotein A-I, apolipoprotein B, lipoprotein concentration, lipoprotein particle size, causal inference, genetic risk factors
- MeSH terms
- Apolipoprotein A-V, Apolipoproteins, Apolipoproteins A, Coronary Disease, Gene Frequency, Genotype, Humans, Lipids, Lipoproteins, HDL, Lipoproteins, LDL, Lipoproteins, VLDL, Particle Size, Promoter Regions, Genetic, Risk Factors, Triglycerides, Polymorphism, Single Nucleotide, Mendelian Randomization Analysis
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