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Major Lipids, Apolipoproteins, and Risk of Vascular Disease
Open accessAbstract
CONTEXT: Associations of major lipids and apolipoproteins with the risk of vascular disease have not been reliably quantified. OBJECTIVE: To assess major lipids and apolipoproteins in vascular risk. DESIGN, SETTING, AND PARTICIPANTS: Individual records were supplied on 302,430 people without initial vascular disease from 68 long-term prospective studies, mostly in Europe and North America. During 2.79 million person-years of follow-up, there were 8857 nonfatal myocardial infarctions, 3928 coronary heart disease [CHD] deaths, 2534 ischemic strokes, 513 hemorrhagic strokes, and 2536 unclassified strokes. MAIN OUTCOME MEASURES: Hazard ratios (HRs), adjusted for several conventional factors, were calculated for 1-SD higher values: 0.52 log(e) triglyceride, 15 mg/dL high-density lipoprotein cholesterol (HDL-C), 43 mg/dL non-HDL-C, 29 mg/dL apolipoprotein AI, 29 mg/dL apolipoprotein B, and 33 mg/dL directly measured low-density lipoprotein cholesterol (LDL-C). Within-study regression analyses were adjusted for within-person variation and combined using meta-analysis. RESULTS: The rates of CHD per 1000 person-years in the bottom and top thirds of baseline lipid distributions, respectively, were 2.6 and 6.2 with triglyceride, 6.4 and 2.4 with HDL-C, and 2.3 and 6.7 with non-HDL-C. Adjusted HRs for CHD were 0.99 (95% CI, 0.94-1.05) with triglyceride, 0.78 (95% CI, 0.74-0.82) with HDL-C, and 1.50 (95% CI, 1.39-1.61) with non-HDL-C. Hazard ratios were at least as strong in participants who did not fast as in those who did. The HR for CHD was 0.35 (95% CI, 0.30-0.42) with a combination of 80 mg/dL lower non-HDL-C and 15 mg/dL higher HDL-C. For the subset with apolipoproteins or directly measured LDL-C, HRs were 1.50 (95% CI, 1.38-1.62) with the ratio non-HDL-C/HDL-C, 1.49 (95% CI, 1.39-1.60) with the ratio apo B/apo AI, 1.42 (95% CI, 1.06-1.91) with non-HDL-C, and 1.38 (95% CI, 1.09-1.73) with directly measured LDL-C. Hazard ratios for ischemic stroke were 1.02 (95% CI, 0.94-1.11) with triglyceride, 0.93 (95% CI, 0.84-1.02) with HDL-C, and 1.12 (95% CI, 1.04-1.20) with non-HDL-C. CONCLUSION: Lipid assessment in vascular disease can be simplified by measurement of either total and HDL cholesterol levels or apolipoproteins without the need to fast and without regard to triglyceride.
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The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“fasting and nonfasting TG levels were associated with increased risk of coronary heart disease”
From The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk (2019) · cites this paper as [72]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“However, the association was attenuated after adjustment for HDL-C”
From The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk (2019) · cites this paper as [72]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“was nonsignificant after adjustment for non-HDL-C”
From The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk (2019) · cites this paper as [72]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The hazard ratio for coronary heart disease with triglycerides was 1.37 (95% CI, 1.31-1.42)after adjustment for nonlipid factors, but was reduced to 0.99 (95% CI, 0.94 -1.05) after adjustment for HDL cholesterol and non-HDL cholesterol (9).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [9]
The cited source says what the claim attributes to it.
In the citing paper
“Risk associations are similar in nonfasting study populations than in those who did fast [72,74].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [72]
The cited source says what the claim attributes to it.
In the citing paper
“TGs were not associated with stroke after adjustment for lipids”
From The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk (2019) · cites this paper as [72]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“A serum triglyceride level of 150 mg/dl (1.7 mmol/liter) usually falls below the 75th percentile in various populations, although there have been well-established differences identified between racial and ethnic groups (6 -9).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [9]
Experimental — accuracy not yet measuredIn the citing paper
“Recent advances in human genetics, together with a large body of epidemiologic, preclinical, and clinical trial results, provide strong support for a causal association between triglycerides (TG), TG-rich lipoproteins (TRL), and TRL remnants, and increased risk of myocardial infarction, ischaemic stroke, and aortic valve stenosis.”
In the citing paper
“Over the past three decades, epidemiologic and genetic evidence has accumulated to support the concept that elevated levels of plasma TG, TRL, and TRL remnants are causally related to an increased risk of ASCVD-related events—myocardial infarction (MI), stroke, and aortic valve stenosis—and all-cause mortality.1,2,17,19,20,24–28”
In the citing paper
“Recent data from a meta-analysis by the Emerging Risk Factor Collaboration 42 indicate that apo B does not provide any benefit beyond non-HDL-C or traditional lipid ratios.”
From ESC/EAS Guidelines for the management of dyslipidaemias (2011) · cites this paper as [42]
In the citing paper
“Alternatively apo B and the apo B/apo A1 ratio can be used, which have been found to be at least as good risk markers compared with traditional lipid parameters.42”
From ESC/EAS Guidelines for the management of dyslipidaemias (2011) · cites this paper as [42]
In the citing paper
“Recently, non-HDL-C has turned out to be a good surrogate marker of TG and remnants.42”
From ESC/EAS Guidelines for the management of dyslipidaemias (2011) · cites this paper as [42]
In the citing paper
“After adjustment for HDL cholesterol, there is no significant association between triglycerides and CVD.52”
From European Guidelines on cardiovascular disease prevention in clinical practice (version 2012) (2012) · cites this paper as [52]
In the citing paper
“Very high levels of HDL-C have consistently not been found to be associated with atheroprotection. 90”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [90]
In the citing paper
“Very high levels of HDL-C have consistently not been found to be associated with atheroprotection.90”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [90]
In the citing paper
“Recent data from a meta-analysis 83,90 indicate that apoB does not provide any benefit beyond non-HDL-C or traditional lipid ratios.101”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [90]
In the citing paper
“The relationship between HDL-C and cardiovascular risk is not linear; for instance, no further improvement in prognosis is seen with HDL-C levels above ~60 mg/dl (1.5 mmol/l) (Fig. 1) [3].”
From HDL cholesterol: reappraisal of its clinical relevance (2017) · cites this paper as [3]
In the citing paper
“With adjustment for age and sex, triglycerides showed a strong, stepwise association with both CVD and ischemic stroke; however, after adjustment for standard risk factors and for HDL-C and non-HDL-C, the associations for both CVD and stroke were no longer significant.”
From Triglycerides and Cardiovascular Disease: A Scientific Statement From the American Heart Association (2011) · cites this paper as [17]
In the citing paper
“Such an effect modification could obscure a modest but significant effect, as demonstrated recently.17”
From Triglycerides and Cardiovascular Disease: A Scientific Statement From the American Heart Association (2011) · cites this paper as [17]
In the citing paper
“With adjustment for age and sex, triglycerides showed a strong, stepwise association with both CVD and ischemic stroke; however, after adjustment for standard risk factors and for HDL-C and non-HDL-C, the associations for both CVD and stroke were no longer significant.”
From Triglycerides and Cardiovascular Disease: A Scientific Statement From the American Heart Association (2011) · cites this paper as [17]
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Citations
Cites
Quantifying heterogeneity in a meta‐analysis
Higgins, J. P. T., & Thompson, S. G. (2002) · Statistics in Medicine · doi:10.1002/sim.1186 · Cited by 36,763
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Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein
Ridker, P. M., Danielson, E., Fonseca, F. A. H., Genest, J., Gotto, A. M., Kastelein, J. J. P., Koenig, W., Libby, P., Lorenzatti, A. J., MacFadyen, J. G., et al. (2008) · New England Journal of Medicine · doi:10.1056/nejmoa0807646 · Cited by 6,674
Antihyperlipidemic and Biochemical Activities of Mcy Protein in Streptozotocin Induced Diabetic Rats
Marella, S., Maddirela, D. R., Badri, K. R., Kumar, M. V. J., & Chippada, A. R. (2015) · Cellular Physiology and Biochemistry · doi:10.1159/000373954 · Cited by 5,938
High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies.
Gordon, D. J., Probstfield, J. L., Garrison, R. J., Neaton, J. D., Castelli, W. P., Knoke, J. D., Jacobs, D. R., Bangdiwala, S., & Tyroler, H. A. (1989) · Circulation · doi:10.1161/01.cir.79.1.8 · Cited by 3,162
Effects of torcetrapib in patients at high risk for coronary events
Barter, P. J., Caulfield, M., Eriksson, M., Grundy, S. M., Kastelein, J. J. P., Komajda, M., Lopez-Sendon, J., Mosca, L., Tardif, J.-C., Waters, D. D., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa0706628 · Cited by 3,139
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Kakehi, E., Kotani, K., Ishikawa, S., Gotoh, T., Kayaba, K., Nakamura, Y., & Kajii, E. (2015) · Asia Pacific Journal of Public Health · doi:10.1177/1010539513475649 · Cited by 12
Ference, B. A. (2019) · Clinical Pharmacology & Therapeutics · doi:10.1002/cpt.1163 · Cited by 8
Metadata
- Authors
- The Emerging Risk Factors Collaboration*
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 2009-11-11
- Volume
- 302
- Issue
- 18
- Pages
- 1993
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- PMC
- PMC3284229
- OpenAlex
- W2127427274
- Cited by
- 2,731
- References
- 41
- Citations by year
- 2026: 89 · 2025: 116 · 2024: 150 · 2023: 178 · 2022: 169 · 2021: 188 · 2020: 156 · 2019: 177 · 2018: 188 · 2017: 175 · 2016: 163 · 2015: 187 · 2014: 198 · 2013: 189 · 2012: 160
- FWCI
- 136.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- JAMA (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- VU Research Portal (publishedVersion, other-oa)
- University of Southern Denmark Research Portal (University of Southern Denmark) (publishedVersion)
- PubMed Central (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (submittedVersion)
- Research Portal (Queen's University Belfast) (submittedVersion)
- Bristol Research (University of Bristol) (submittedVersion)
- LSHTM Research Online (London School of Hygiene and Tropical Medicine) (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- OPUS (Augsburg University) (submittedVersion)
- Padua Research Archive (University of Padova) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Wellcome Trust
- British Heart Foundation (RG/08/013/25942, RG/08/014, RG/07/008/23674, RG/08/014/24067)
- Economic and Social Research Council (ES/G007438/1)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Risk Factors
- Keywords
- apolipoproteins, vascular risk, coronary artery disease, myocardial infarction, ischemic stroke, hemorrhagic stroke, triglycerides, HDL cholesterol, non-HDL cholesterol, LDL cholesterol, apolipoprotein A-I, apolipoprotein B, fasting state, lipid-lowering therapy, cardiovascular risk factors, prospective cohort, meta-analysis
- MeSH terms
- Apolipoproteins, Coronary Disease, Female, Humans, Lipids, Cholesterol, HDL, Male, Middle Aged, Regression Analysis, Risk Factors, Triglycerides, Vascular Diseases, Proportional Hazards Models, Stroke
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