Beyond LDL-C: unravelling the residual atherosclerotic cardiovascular disease risk landscape—focus on hypertriglyceridaemia
Open accessAbstract
Aims: Historically, atherosclerotic cardiovascular disease (ASCVD) risk profile mitigation has had a predominant focus on low density lipoprotein cholesterol (LDL-C). In this narrative review we explore the residual ASCVD risk profile beyond LDL-C with a focus on hypertriglyceridaemia, recent clinical trials of therapeutics targeting hypertriglyceridaemia and novel modalities addressing other residual ASCVD risk factors. Findings: Hypertriglyceridaemia remains a significant ASCVD risk despite low LDL-C in statin or proprotein convertase subtilisin/kexin type 9 inhibitor-treated patients. Large population-based observational studies have consistently demonstrated an association between hypertriglyceridaemia with ASCVD. This relationship is complicated by the co-existence of low high-density lipoprotein cholesterol. Despite significantly improving atherogenic dyslipidaemia, the most recent clinical trial outcome has cast doubt on the utility of pharmacologically lowering triglyceride concentrations using fibrates. On the other hand, purified eicosapentaenoic acid (EPA), but not in combination with docosahexaenoic acid (DHA), has produced favourable ASCVD outcomes. The outcome of these trials suggests alternate pathways involved in ASCVD risk modulation. Several other pharmacotherapies have been proposed to address other ASCVD risk factors targeting inflammation, thrombotic and metabolic factors. Implications: Hypertriglyceridaemia poses a significant residual ASCVD risk in patients already on LDL-C lowering therapy. Results from pharmacologically lowering triglyceride are conflicting. The role of fibrates and combination of EPA and DHA is under question but there is now convincing evidence of ASCVD risk reduction with pure EPA in a subgroup of patients with hypertriglyceridaemia. Clinical guidelines should be updated in line with recent clinical trials evidence. Novel agents targeting non-conventional ASCVD risks need further evaluation.
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Benefits of traditional TG-lowering agents in outcome studies appear limited to subgroups with high TG and low HDL-C.
“Benefits in outcome studies appear limited to subgroups with high TG and low HDL-C, highlighting the complexity of translating TG reduction into ASCVD risk reduction [61, 74–77].”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [74]
The Therapeutic targets > Fibrates section says cardiovascular benefits were greatest, and in meta-analyses observed only, in people with high TG and low HDL-C. But the paper does not extend that pattern to traditional TG-lowering agents as a whole: its Niacin section reports no benefit even in a high-TG, low-HDL-C trial, while its Omega 3 fatty acids section reports benefit in a trial with normal mean baseline TG. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredTraditional TG-lowering agents, such as fibrates and niacin, have demonstrated inconsistent CVD benefits in randomized trials, even when lipid changes were robust.
“Conversely, traditional TG-lowering agents, such as fibrates and niacin, have demonstrated inconsistent CVD benefits in randomized trials, even when lipid changes were robust.”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [74]
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Soran, H., Kwok, S., Adam, S., Ho, J. H., & Durrington, P. N. (2017) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000433 · Cited by 16 · see citing works
Self-citationYamashita, S., Hirano, T., Shimano, H., Tsukamoto, K., Yoshida, M., & Yoshida, H. (2024) · European Journal of Clinical Investigation · doi:10.1111/eci.14227 · Cited by 14 · see citing works
Hirano, T., & Ito, Y. (2023) · Journal of Diabetes Investigation · doi:10.1111/jdi.14013 · Cited by 11 · see citing works
Bashir, B., Adam, S., Ho, J. H., Linn, Z., Durrington, P. N., & Soran, H. (2023) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000889 · Cited by 7 · see citing works
Self-citationThe Reaven syndrome: An historical perspective
Soran, H., Adam, S., Ho, J. H., & Durrington, P. N. (2019) · Diabetes and Vascular Disease Research · doi:10.1177/1479164119828899 · Cited by 6 · see citing works
Self-citationHumbert, X., Dolladille, C., Sassier, M., Valnet‐Rabier, M., Vial, T., Bondon‐Guitton, E., Page, A., Solé, E., Auriche, P., Coquerel, A., et al. (2017) · Therapies · doi:10.1016/j.therap.2017.07.002 · Cited by 5 · see citing works
Bashir, B., Iqbal, Z., Schofield, J. D., & Soran, H. (2023) · Elsevier eBooks · doi:10.1016/b978-0-323-99991-5.00012-7 · Cited by 1 · see citing works
Self-citation
Flagged first, then by citations
3 of the 183 references couldn’t be matched to a known paper.
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Current and Emerging Treatment Options for Hypertriglyceridemia: State-of-the-Art Review
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Self-citationChapman, M. J., Packard, C. J., Björnson, E., Ginsberg, H. N., & Borén, J. (2025) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2025.120529 · Cited by 32 · see citing works
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Olezarsen, a liver-directed APOC3 ASO therapy for hypertriglyceridemia
Hooper, A. J., Bell, D. A., & Burnett, J. R. (2024) · Expert Opinion on Pharmacotherapy · doi:10.1080/14656566.2024.2408369 · Cited by 15 · see citing works
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Small nerve fibre damage and cardiac autonomic dysfunction in patients with hypertriglyceridaemia
Bashir, B., Pasha, R., Kamath, A., Malik, R. A., Ferdousi, M., & Soran, H. (2025) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2025.119186 · Cited by 8 · see citing works
Self-citationLiu, H.-H., Li, S., & Li, J. (2025) · Drugs · doi:10.1007/s40265-025-02167-z · Cited by 7 · see citing works
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Šabović, M., Pejkov, H., Caraus, A., Gruev, I. T., Vintila, V., Csanádi, Z., Batjargal, S., Kovačević-Preradović, T., Kušljugić, Z., Kuprešak, D., et al. (2025) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2025.1665059 · Cited by 3 · see citing works
Srivastava, A., Dinesh, D., Bhatia, J., & Arya, D. S. (2026) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2026.119301 · Cited by 3 · see citing works
Assessing coronary artery disease severity using the TyG index in patients with LDL-C < 2.6 mmol/l
Li, J., Jia, W., Chen, Y., Liu, Y., Fang, L., Qi, X., & Wei, L. (2025) · Lipids in Health and Disease · doi:10.1186/s12944-025-02691-7 · Cited by 2 · see citing works
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Chiara, F. D., la Rubia, E. C.-D., de Bruijn, P., Pletikapic, G., Cnubben, N. H. P., Stevens, L. J., Theunissen, E., Turunen, J. J., van den Hoek, A. M., Princen, H. M. G., et al. (2026) · Molecular Therapy — Nucleic Acids · doi:10.1016/j.omtn.2026.103001 · Cited by 2 · see citing works
Emerging Pharmacological Therapies in the Management of Hyperlipidemia
Sharma, N., & Roy, S. (2026) · Current Clinical Pharmacology · doi:10.2174/0127724328440604260225063619 · Cited by 2 · see citing works
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Guo, B., Li, H.-B., Zhao, B., & Xu, P. (2025) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwaf336 · Cited by 1 · see citing works
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Lipid-lowering therapies: the arrows in the quiver and future bullets
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Challenges in achieving low-density lipoprotein targets: a cross-sectional study in statin users
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Investigation of the Effect of Topinambur Extract on Cholesterol Levels
Shahova, A. S., Chmutov, E. Y., Shkhanokova, A. R., Cherevatov, N. V., Kokozova, A. E., Isaldibirova, A. V., Oganyan, S. V., & Elmurzaev, I. I. (2024) · Archives of Pharmacy Practice · doi:10.51847/dve6fn5cvu
Apolipoprotein B48 Knockout Ameliorates High-Fat-Diet-Induced Metabolic Impairment in Mice
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Hypertriglyceridemia: Causes, Consequences, Diagnosis, and Management
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- Authors
- Bashir, B., Schofield, J., Downie, P., France, M., Ashcroft, D. M., Wright, A. K., Romeo, S., Gouni-Berthold, I., Maan, A., Durrington, P. N., & Soran, H.
- Affiliations
- University of Manchester (GB)
- Manchester University NHS Foundation Trust (GB)
- Bristol Royal Infirmary (GB)
- Sahlgrenska University Hospital (SE)
- Corresponding author
- Soran, Handrean
- ORCID
- Venue
- Frontiers in Cardiovascular Medicine
- Publisher
- Frontiers Media SA
- Published
- 2024-08-07
- Volume
- 11
- Pages
- 1389106-1389106
- ISSN
- 2297-055X (ISSN-L)
- PMC
- PMC11335737
- OpenAlex
- W4401403602
- Cited by
- 40
- References
- 183
- Citations by year
- 2026: 21 · 2025: 15 · 2024: 4
- FWCI
- 4.43
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Cardiovascular Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Funders
- Wellcome Trust
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- hypertriglyceridemia, residual cardiovascular risk, atherosclerotic cardiovascular disease, LDL-C lowering therapy, fibrates, eicosapentaenoic acid, docosahexaenoic acid, omega-3 fatty acids, triglyceride-lowering therapy, statins, PCSK9 inhibitors, low HDL cholesterol, atherogenic dyslipidemia, inflammation, thrombosis risk, metabolic risk factors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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