Non-HDL Cholesterol and Triglycerides: Implications for Coronary Atheroma Progression and Clinical Events
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Objectives—: Non–high-density lipoprotein cholesterol (non-HDLC) levels reflect the full burden of cholesterol transported in atherogenic lipoproteins. Genetic studies suggest a causal association between elevated triglycerides (TGs)-rich lipoproteins and atherosclerosis. We evaluated associations between achieved non-HDLC and TG levels on changes in coronary atheroma volume. Approach and Results—: Data were analyzed from 9 clinical trials involving 4957 patients with coronary disease undergoing serial intravascular ultrasonography to assess changes in percent atheroma volume (ΔPAV) and were evaluated against on-treatment non-HDLC and TG levels. The effects of lower (<100 mg/dL) versus higher (≥100 mg/dL) achieved non-HDLC levels and lower (<200 mg/dL) versus higher (≥200 mg/dL) achieved TG levels were evaluated in populations with variable on-treatment low-density lipoprotein cholesterol (LDLC) </≥70 mg/dL and C-reactive protein </≥2 mg/L and in patients with or without diabetes mellitus. On-treatment non-HDLC levels linearly associated with ΔPAV. Overt PAV progression (ΔPAV>0) was associated with achieved TG levels >200 mg/dL, respectively. Lower on-treatment non-HDLC and TG levels associated with significant PAV regression compared with higher non-HDLC and TG levels across all levels of LDLC and C-reactive protein and irrespective of diabetic status ( P <0.001 across all comparisons). ΔPAV were more strongly influenced by changes in non-HDLC (β=0.62; P <0.001) compared with changes in LDLC (β=0.51; P <0.001). Kaplan–Meier sensitivity analyses demonstrated significantly greater major adverse cardiovascular event rates in those with higher versus lower non-HDLC and TG levels, with an earlier separation of the non-HDLC compared with the LDLC curve. Conclusions—: Achieved non-HDLC levels seem more closely associated with coronary atheroma progression than LDLC. Plaque progression associates with achieved TGs, but only above levels of 200 mg/dL. These observations support a more prominent role for non-HDLC (and possibly TG) lowering in combating residual cardiovascular risk.
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Elevated levels of triglyceride-rich lipoproteins and remnant lipoproteins contribute directly to atherosclerosis by promoting endothelial dysfunction, inflammation, and foam cell formation.
“Elevated levels of TRLs and remnant lipoproteins contribute directly to atherosclerosis by promoting endothelial dysfunction, inflammation, and foam cell formation [8, 9].”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [9]
The Discussion (page not provided) says cholesterol-rich remnants cross the endothelial barrier and promote foam-cell accumulation and plaque progression; it also describes genetic evidence suggesting a causal role for triglyceride-rich lipoproteins. It does not say these lipoproteins promote endothelial dysfunction or inflammation, and its own analysis reports associations rather than directly establishing those mechanisms. (LLM, conf=0.87)
Experimental — accuracy not yet measuredRemnant lipoproteins are causal contributors to atherogenesis.
“Genetic studies and epidemiologic data increasingly implicate remnant lipoproteins as causal contributors to atherogenesis, providing a strong mechanistic and clinical rationale for targeted intervention [8–12].”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [9]
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“…LDL-C of 1.8 mmol/L (70 mg/dl), with a further 50% – 55% reduction after treatment, 20% did not have regression in atheroma volume despite achieving very low LDL-C (86), thereby suggesting a role of TG-rich lipoproteins and other factors (Figure 1) in atheroma development and progression (87).”
BackgroundInfluentialAssociation between vitamin D status and metabolic syndrome risk factors
Barbalho, S. M., Tofano, R. J., de Campos, A. L., Rodrigues, A. S., Quesada, K. R., Bechara, M. D., Goulart, R. D. Á., & Oshiiwa, M. (2018) · Diabetes & Metabolic Syndrome Clinical Research & Reviews · doi:10.1016/j.dsx.2018.03.011 · Cited by 40 · see citing works
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“even more strongly linked to the development of coronary atheroma [27].”
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Is it possible to predict the complexity of peripheral artery disease with atherogenic index?
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Zhao, Q., Zhang, T., Cheng, Y., Ma, Y., Xu, Y.-K., Yang, J., & Zhou, Y.-J. (2020) · Lipids in Health and Disease · doi:10.1186/s12944-020-01355-y · Cited by 20 · see citing works
Triglyceride-Rich Lipoproteins and Novel Targets for Anti-atherosclerotic Therapy
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β-Aminoisobutyric Acid Suppresses Atherosclerosis in Apolipoprotein E-Knockout Mice
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Gómez-Delgado, F., Alcala-Diaz, J. F., Leon‐Acuña, A., López-Moreno, J., Delgado‐Lista, J., Gomez‐Marin, B., Roncero‐Ramos, I., Yubero‐Serrano, E. M., Rangel-Zúñiga, O. A., Vals‐Delgado, C., et al. (2019) · European Journal of Clinical Investigation · doi:10.1111/eci.13146 · Cited by 18 · see citing works
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Endothelial Dysfunction in Type 2 Diabetes: Targeting Inflammation
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“It has been reported that among individuals with prior coronary artery disease with LDL-C less than 70 mg/dL, lowering triglyceride to less than 200 mg/dL was associated with a lessening of coronary atheroma progression and a lowering of the residual risk of cardiovascular disease events 37 .”
BackgroundRecent Advances in the Development of Cardiovascular Biomarkers
Satoh, K., & Shimokawa, H. (2018) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.118.310226 · Cited by 15 · see citing works
“They concluded that their findings provide mechanistic support for the possible roles of non-HDL cholesterol and triglycerides to more definitively emerge as future therapeutic targets, especially in statin-treated patients requiring secondary prevention.(89) Kockx et al(90) reported on the LDLr (LDL receptor)–”
BackgroundDo triglyceride-lowering drugs decrease risk of cardiovascular disease?
Maki, K. C., & Dicklin, M. R. (2017) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000424 · Cited by 14 · see citing works
Vallejo‐Vaz, A. J., Leiter, L. A., Prato, S. D., Taskinen, M., Müller‐Wieland, D., Bujas‐Bobanovic, M., Letierce, A., Mandel, J., Samuel, R., & Ray, K. K. (2020) · European Journal of Preventive Cardiology · doi:10.1177/2047487320905185 · Cited by 14 · see citing works
KEECH, A. C., & Jenkins, A. J. (2017) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000465 · Cited by 14 · see citing works
“Clinically available drugs are italicized: HMG CoA reductase inhibition via HMG CoA reductase inhibitors (statins); [1] intestinal cholesterol absorption inhibition via inhibitor of Niemann Pick Like protein-1 transporter, ezetimibe; [2] binding and excretion of cholesterol rich bile acids by bile acid binding resins;…”
MethodAnti-atherogenic properties of vitamin E, aspirin, and their combination
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Impact of triglyceride levels on plaque characteristics in patients with coronary artery disease
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“20 Also, TG concentrations are directly related to residual lipoproteins that are highly atherogenic and have a high risk of penetrating the arterial wall.”
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“…and CVDs, there are some other delegate inflammatory markers, such as GDF-15 (growth differentiation factor-15), myeloid-related protein 8/14, pentraxin3, galectin-3 and LOX-1, these would be better called as dyslipidemia markers (Krintus et al. 2014; Papapanagiotou et al. 2015; Puri et al. 2016).”
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Relationship between remnant cholesterol and short‐term prognosis in acute ischemic stroke patients
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“Furthermore, an IVUS study demonstrated that coronary plaque volume changes increased with the increase of serum TG levels [29].”
BackgroundDiabetes mellitus and heart disease
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Ascaso, J. F., Millán, J., Hernández‐Mijares, A., Blasco, M., Brea, Á., Díaz, Á., Pedro‐Botet, J., & Pintó, X. (2020) · Clínica e Investigación en Arteriosclerosis (English Edition) · doi:10.1016/j.artere.2020.05.002 · Cited by 10 · see citing works
“Estos efectos son dependien-tes de las concentraciones basales 11 y vienen recogidos en la tabla 3 26 .”
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New Approaches to Lipoproteins for the Prevention of Cardiovascular Events
Fujino, M., Giovanni, G. D., & Nicholls, S. J. (2024) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.rv22031 · Cited by 8 · see citing works
“Hypertriglyceridemia contributes to residual risk, even when low LDL-C levels are achieved through intensive statin therapy 60) .”
Self-citationLipoprotein cholesterol ratios and cardiovascular disease risk in US adults: a cross-sectional study
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Non-HDL Cholesterol and Atherosclerotic Cardiovascular Disease.
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“reported that an increase in TG levels was significantly associated with coronary atheroma progression as evaluated by IVUS [27].”
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Dirajlal‐Fargo, S., Jacobson, D. L., Yu, W., Mirza, A., Geffner, M. E., McComsey, G. A., Jao, J. K., & (PHACS), F. T. P. H. C. S. (2023) · HIV Medicine · doi:10.1111/hiv.13566 · Cited by 7 · see citing works
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“Non-HDL-c encompasses all cholesterol with atherogenic potential in the bloodstream, and elevated levels of non-HDL-c have been linked to damage in vascular endothelial function (54, 55).”
BackgroundKataoka, Y., Kitahara, S., Funabashi, S., Makino, H., Matsubara, M., Matsuo, M., Omura‐Ohata, Y., Koezuka, R., Tochiya, M., Tamanaha, T., et al. (2024) · Atherosclerosis Plus · doi:10.1016/j.athplu.2024.03.001 · Cited by 7 · see citing works
“Observational and intravascular imaging studies have consistently reported the association of triglyceride-rich lipoproteins with atherosclerosis [29 – 32], suggesting they are a potential therapeutic target.”
BackgroundSelf-citationEvsen, A., Aktan, A., Altunova, M., & Özbek, M. (2024) · Vascular · doi:10.1177/17085381241260203 · Cited by 7 · see citing works
“16 In the study conducted by Salazar et al., it was demonstrated that the TG/HDL-C ratio predicts the extent of atherosclerosis more sensitively compared to a single blood lipid parameter.”
Triglycerides and the Risk of Atherosclerotic Cardiovascular Events Across Different Risk Categories
Mizuta, H., Ishii, M., Ikebe, S., Otsuka, Y., Yamanouchi, Y., Nakamura, T., & Tsujita, K. (2024) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.65334 · Cited by 8 · see citing works
“Previous reports have shown that in patients receiving secondary prevention on statin therapy for LDL-C management, TG levels ＞ 200 mg/dL was associated with an increased presence of coronary artery plaques 40) .”
Cardiovascular Risk Factors and Markers
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Targeting triglycerides to lower residual cardiovascular risk
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“of cardiovascular events in the statin trials [22].”
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Cardiovascular Immunotherapy and the Role of Imaging
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“adverse cardiovascular events, that is, myocardial infarctions or stroke, within the first 5 years.(30,34) Consistent with this find-”
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Triglycerides and T Cells in Cardiovascular Risk
Reilly, N. A., Mulder, J. W. C. M., Dekkers, K. F., Kuipers, T. B., der Zee, L. C. V. V., Mulder, M. T., van Lennep, J. E. R., Jukema, J. W., & Heijmans, B. T. (2025) · JACC Basic to Translational Science · doi:10.1016/j.jacbts.2025.101359 · Cited by 5 · see citing works
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“18 Unlike TG, HDL-C has effects that inhibit the atherosclerotic process mainly by providing cholesterol transport from macrophages in the vascular wall toward the liver.”
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- Authors
- Puri, R., Nissen, S. E., Shao, M., Elshazly, M. B., Kataoka, Y., Kapadia, S. R., Tuzcu, E. M., & Nicholls, S. J.
- Affiliations
- Cleveland Clinic (US)
- ORCID
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2016-11
- Volume
- 36
- Issue
- 11
- Pages
- 2220-2228
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2509381650
- Cited by
- 143
- References
- 46
- Citations by year
- 2026: 7 · 2025: 4 · 2024: 17 · 2023: 18 · 2022: 8 · 2021: 11 · 2020: 17 · 2019: 24 · 2018: 20 · 2017: 14 · 2016: 3
- FWCI
- 22.51
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Funders
- Eli Lilly and Company
- Pfizer
- Sanofi
- Cleveland Clinic
- InfraRedx
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Surgery › Coronary Interventions and Diagnostics
- Keywords
- non-HDL cholesterol, triglycerides, atherosclerosis progression, LDL cholesterol, triglyceride-rich lipoproteins, residual cardiovascular risk, major adverse cardiovascular events, intravascular ultrasound, coronary artery disease, diabetes mellitus, C-reactive protein
- MeSH terms
- Aged, Hypolipidemic Agents, Cholesterol, Clinical Trials as Topic, Coronary Artery Disease, Coronary Vessels, Female, Humans, Male, Middle Aged, Predictive Value of Tests, Risk Factors, Time Factors, Triglycerides, Biomarkers, Multivariate Analysis, Linear Models, Treatment Outcome, Ultrasonography, Interventional, Disease Progression, Kaplan-Meier Estimate, Plaque, Atherosclerotic
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