Key result
Carotid atherosclerosis is linked to ~0.5-point lower plasma omega-3 levels versus healthy controls.
Why the study?
The relationship between plasma fatty acid profiles, omega-3 status, and statin efficacy in carotid atherosclerosis remains poorly defined.
Case-Control (n=102)
No
Absolute Event Rate: 2.23% vs 2.7%
p-value: p=0.0068
Plasma omega-3 fatty acid profiling combined with predictive modeling reliably estimates the erythrocyte omega-3 index and correlates with carotid plaque instability, offering a potential tool for diagnostic and therapeutic monitoring.
Lower EPA+DHA levels were associated with carotid atherosclerosis; hypothesis-generating for omega-3 profiling in plaque assessment, pending prospective validation.
Background/Objectives: Omega-3 highly unsaturated fatty acids (HUFAs), particularly EPA and DHA, have anti-inflammatory and lipid-modulating properties for treating atherosclerosis. However, the relationship between plasma fatty acid profiles, omega-3 status, and statin efficacy in carotid atherosclerosis remains poorly defined. Objectives: This study evaluates plasma and plaque fatty acid (FA) composition, explores their associations with plaque stability, and examines the relationship of omega-3 levels, lipid biomarkers (VLDL-C, LDL-C, HDL-C, total cholesterol, and triglycerides) with statin and β-blocker treatment. A mathematical model was developed to predict the erythrocyte omega-3 index from plasma. Methods: In this case–control study, plasma and carotid plaques of 52 patients undergoing carotid endarterectomy were analyzed. Plasma was compared with that of 50 healthy controls. FAs were quantified by LC-MS/MS. Plaques were histologically classified as stable or unstable. Results: Atherosclerotic patients showed disturbed FA metabolism, including decreased plasma omega-3 EPA + DHA, SFAs and HUFAs, increased MUFAs, and impaired desaturase and elongase activity. Unstable plaques had higher MUFA and lower HUFA content compared with stable plaques. Significant correlations between plasma EPA + DHA and HDL-C and triglycerides were observed in statin-naïve patients, whereas statins appeared to attenuate these associations. Co-treatment with β-blockers had no significant effect. A validated logit-based model accurately predicted the erythrocyte omega-3 index from plasma (R2 = 0.782). Conclusions: Altered plasma and plaque FA profiles correlate with atherosclerosis’s plaque instability and inflammatory lipid profiles. Statins significantly influence these associations, suggesting their complex interaction with lipid metabolism. Plasma measurements of omega-3 fatty acids in combination with predictive modelling may be beneficial for diagnostic and therapeutic monitoring in carotid atherosclerosis.
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Eroshchenko et al. (2025) conducted a case-control in Carotid atherosclerosis (n=102). Carotid atherosclerosis vs. Healthy controls was evaluated on Plasma omega-3 EPA + DHA levels (%) (p=0.0068). Patients with carotid atherosclerosis had significantly lower plasma omega-3 EPA + DHA levels (2.23%) compared to healthy controls (2.70%), reflecting disturbed systemic fatty acid metabolism.
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