Elevated remnant cholesterol causes both low-grade inflammation and ischemic heart disease, whereas elevated low-density lipoprotein cholesterol causes ischemic heart disease without inflammation
Open accessAbstract
Background—: Elevated nonfasting remnant cholesterol and low-density lipoprotein (LDL) cholesterol are causally associated with ischemic heart disease (IHD), but whether elevated nonfasting remnant cholesterol and LDL cholesterol both cause low-grade inflammation is currently unknown. Methods and Results—: We studied 60 608 individuals from the Copenhagen General Population Study, the Copenhagen City Heart Study, and the Copenhagen Ischemic Heart Disease study, of whom 10 668 had IHD diagnosed between 1977 and 2011. We genotyped for variants affecting levels of nonfasting remnant cholesterol, LDL cholesterol, C-reactive protein by CRP alleles, and C-reactive protein by IL6R alleles. Using a multidirectional mendelian randomization design, we investigated possible causal associations between the lipoproteins and C-reactive protein and between the lipoproteins and IHD. A 1-mmol/L(39 mg/dL) higher level of nonfasting remnant cholesterol was associated observationally with a 37% (95% confidence interval, 35–39) higher C-reactive protein level and causally with a 28% (95% confidence interval, 10–48) higher level. For LDL cholesterol, a 1-mmol/L (39-mg/dL) higher level was associated observationally with a 7% (95% confidence interval, 6–7) higher C-reactive protein level, but we found no causal association. Likewise, higher levels of C-reactive protein did not associate causally with elevated nonfasting remnant cholesterol or LDL cholesterol. Finally, the causal risk ratio for IHD for a 1-mmol/L (39-mg/dL) higher level was 3.3 (95% confidence interval, 2.1–5.2) for nonfasting remnant cholesterol and 1.8 (95% confidence interval, 1.5–2.2) for LDL cholesterol. The causal associations for remnant cholesterol were present even in those without diabetes mellitus and obesity. Conclusions—: Elevated nonfasting remnant cholesterol is causally associated with low-grade inflammation and with IHD, whereas elevated LDL cholesterol is associated causally with IHD without inflammation.
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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 [31]
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 measuredMendelian 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 [22]
In “Risk of IHD: Observational and Causal Associations,” the paper reports a higher estimated risk of ischemic heart disease with genetically higher remnant cholesterol. That supports the causal-inference point, but the study measures remnant cholesterol rather than TRL elevation generally, and its clinical outcome is ischemic heart disease rather than ASCVD broadly. (LLM, conf=0.84)
Experimental — accuracy not yet measuredSystemically, TRLs and their remnants have been linked to markers of low-grade inflammation, including hs-CRP, circulating cytokines such as IL-6 and TNF-α, and immune cell activation.
“Systemically, TRLs and their remnants have been linked to markers of low-grade inflammation, including hs-CRP, circulating cytokines such as IL-6 and TNF-α, and immune cell activation [22–28].”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [22]
The Laboratory Analyses section (page unavailable) says CRP was measured as high-sensitivity CRP, and the Observational Associations section links higher remnant cholesterol to higher CRP. The cited paper does not establish the claimed links to circulating IL-6, TNF-α, or immune cell activation; its use of IL6R genetic variants is not a measurement of circulating IL-6. (LLM, conf=0.88)
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”
From Association Between Triglyceride Lowering and Reduction of Cardiovascular Risk Across Multiple Lipid-Lowering Therapeutic Classes: A Systematic Review and Meta-Regression Analysis of Randomized Controlled Trials (2019) · cites this paper as [10]
The Abstract describes a Mendelian randomization study and reports that triglycerides and remnant cholesterol are highly correlated. The Risk of IHD: Observational and Causal Associations section reports increased ischemic heart disease risk with genetically higher remnant cholesterol. The study tests remnant cholesterol, however, rather than a direct triglyceride–cardiovascular risk association; it therefore supports the Mendelian-randomization portion of the claim only indirectly. (LLM, conf=0.83)
Experimental — accuracy not yet measuredStudies suggest that elevated TG and remnant cholesterol levels are causally related to whole body low-grade inflammation, in contrast to LDL-C.
“Studies suggest that elevated TG and remnant cholesterol levels are causally related to whole body low-grade inflammation, in contrast to LDL-C.12,142”
A multidirectional mendelian randomization study including 60,608 individuals demonstrated that elevated remnant cholesterol (directly related to serum TG) was associated with both low-grade inflammation and ischemic heart disease, whereas elevated LDL-C was associated with ischemic heart disease without inflammation.
“A multidirectional mendelian randomization study including 60,608 individuals demonstrated that elevated remnant cholesterol (directly related to serum TG) was associated with both low-grade inflammation and ischemic heart disease, whereas elevated LDL-C was associated with ischemic heart disease without inflammation (23).”
From Triglycerides and residual atherosclerotic risk (2021) · cites this paper as [23]
TG-rich lipoproteins (TRLs) and their cholesterol-enriched remnants play a causative role in disease.
“some proposing that TG-rich lipoproteins (TRLs; e.g., very low density lipoprotein) and their cholesterol-enriched remnants play a causative role in disease.20,21”
From Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?: New Insights From the Framingham Offspring Study (2016) · cites this paper as [21]
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Remnant cholesterol and long-term incidence of death in coronary artery disease patients
Drexel, H., Mader, A., Larcher, B., Festa, A., Vonbank, A., Fraunberger, P., Leiherer, A., & Saely, C. H. (2025) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2024.119048 · Cited by 17 · see citing works
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Targeting triglycerides for cardiovascular risk reduction
Maiorca, C., Tramontano, D., Di Costanzo, A., & D’Erasmo, L. (2026) · Internal and Emergency Medicine · doi:10.1007/s11739-026-04383-1
- Authors
- Varbo, A., Benn, M., Tybjærg-Hansen, A., & Nordestgaard, B. G.
- Affiliations
- University of Copenhagen (DK)
- From the Department of Clinical Biochemistry ( A.V., B.G.N.) and Copenhagen General Population Study (A.V., M.B., A.T.-H., B.G.N.), Herlev Hospital, Copenhagen University Hospital, Copenhagen, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark (A.V., M.B., A.T.-H., B.G.N.); Department of Clinical Biochemistry, Gentofte Hospital, Copenhagen University Hospital, Copenhagen, Denmark (M.B.); Copenhagen City Heart Study, Frederiksberg Hospital, Copenhagen...
- Venue
- Circulation
- Published
- 2013-09-17
- Volume
- 128
- Issue
- 12
- Pages
- 1298-1309
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2150100875
- Cited by
- 692
- References
- 28
- Citations by year
- 2026: 84 · 2025: 98 · 2024: 112 · 2023: 79 · 2022: 59 · 2021: 47 · 2020: 42 · 2019: 25 · 2018: 26 · 2017: 26 · 2016: 36 · 2015: 26 · 2014: 25 · 2013: 6
- FWCI
- 30.53
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- remnant cholesterol, LDL cholesterol, ischemic heart disease, low-grade inflammation, C-reactive protein, IL-6 receptor, Mendelian randomization, causal relationship, dyslipidemia, cardiovascular risk
- MeSH terms
- Adult, C-Reactive Protein, Cholesterol, Denmark, Diabetes Mellitus, Female, Genotype, Humans, Inflammation, Lipoproteins, Cholesterol, LDL, Male, Middle Aged, Risk Factors, Triglycerides, Myocardial Ischemia
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