Impact of the eicosapentaenoic acid to arachidonic acid ratio on plaque characteristics in statin-treated patients with coronary artery disease

Elsevier

Available online 5 December 2022

Journal of Clinical LipidologyAuthor links open overlay panelAbstractBackground

A low eicosapentaenoic acid (EPA)/arachidonic acid (AA) ratio is associated with an increased risk of cardiovascular events in patients with coronary artery disease (CAD).

Objective

To clarify the impact of the EPA/AA ratio on the characteristics of non-culprit coronary plaques in statin-treated patients with CAD.

Methods

A total of 370 consecutive stable coronary disease patients treated with statins, who underwent percutaneous coronary intervention for the culprit lesion and optical coherence tomography (OCT) imaging of the non-culprit plaque in a culprit vessel were included. The characteristics of non-culprit plaques assessed using OCT were compared between the lower EPA/AA group (EPA/AA <0.4, n = 255) and the higher EPA/AA group (EPA/AA ≥0.4, n = 115).

Results

The prevalence of lipid-rich plaque (58.8 vs. 41.7%, p = 0.003) and plaque with macrophages (56.5 vs. 31.3%, p <0.001) was significantly higher in the lower EPA/AA group than in the higher EPA/AA group. This association was observed even if the LDL-C level was <100 mg/dL. The prevalence of thin-cap fibroatheroma was significantly higher in patients with lower EPA/AA and higher LDL-C (≥100 mg/dL) than in those with higher EPA/AA and lower LDL-C (<100 mg/dL) (odds ratio: 2.750, 95% confidence interval: 1.182-6.988, p = 0.024). An EPA/AA <0.4 was independently associated with a higher prevalence of lipid-rich plaque, plaque with macrophages, and cholesterol crystals.

Conclusion

Lower EPA/AA ratio was associated with higher prevalence of vulnerable characteristics in non-culprit plaques. The present results suggest the importance of EPA/AA ratio on the secondary prevention of CAD.

Introduction

A low eicosapentaenoic acid (EPA)/arachidonic acid (AA) ratio is an indicator of increased risk for cardiovascular events 1,2. Preclinical and clinical studies have demonstrated that EPA stabilizes plaques by inducing an anti-inflammatory response and reducing platelet aggregation 3,4,5. In contrast, AA facilitates plaque instability through the activation of inflammatory processes and platelet activation 6,7. Thus, having a low EPA/AA ratio may destabilize and progress the coronary plaques and cause subsequent adverse coronary event 8,9. This association between a low EPA/AA ratio and increased risk for cardiovascular events has also been shown in statin-treated patients with coronary artery disease (CAD). In a substudy of the JELIS (Japan EPA Lipid Intervention Study), which included patients with established CAD and statin treatment, a higher risk of sudden cardiac death or myocardial infarction in patients with a lower on-treatment EPA/AA than in those with a higher EPA/AA was demonstrated 10. Hence, a low EPA/AA ratio in statin-treated patients with CAD is considered a residual risk and a therapeutic target. However, the association between the EPA/AA ratio and the characteristics of coronary plaque in statin-treated patients with established CAD remains to be elucidated. In the present study, we assessed the characteristics of non-culprit plaques in detail by using optical coherence tomography (OCT) and investigated their association with the EPA/AA ratio among statin-treated patients with established CAD.

Section snippetsStudy population

This was a retrospective observational study conducted at a single center. From a total of 1123 consecutive patients with stable CAD who underwent OCT-guided PCI between January 2012 and December 2020 at our institution, we identified 776 statin-treated patients after excluding those with missing data on their EPA/AA ratio (n = 137) and n-3 fatty acid use (n = 72). Of those, a total of 370 patients were included in the present study, who underwent OCT assessment of non-culprit plaques in

Clinical characteristics

The clinical characteristics are shown in Table 1. Those in the lower EPA/AA group was significantly younger than those in the higher EPA/AA group (67.6 ± 1.0 vs. 71.4 ± 8.4, years, p = 0.001). A history of undergoing PCI was significantly higher in the lower EPA/AA group than in the higher EPA/AA group. The lower EPA/AA group had lower high-density lipoprotein cholesterol levels (51.9 ± 13.8 vs. 55.9 ± 15.1, mg/dL, p = 0.014) and higher triglyceride levels (135.5 [95.0-185.8] vs. 120.0

Discussion

The main findings of the present study were as follows: (1) The prevalence of lipid-rich plaques and plaque with macrophages was significantly higher in the lower EPA/AA group than in the higher EPA/AA group even if the LDL-C level was < 100 mg/dL; (2) The prevalence of TCFA was significantly higher in patients with EPA/AA < 0.4 and LDL-C ≥ 100 mg/dL than in those with EPA/AA ≥ 0.4, and LDL-C < 100 mg/dL; (3) The EPA/AA ratio < 0.4 was independently associated with a higher prevalence of

Conclusions

A lower EPA/AA ratio was associated with a higher prevalence of vulnerable characteristics in non-culprit plaques among statin-treated patients with stable CAD. The present results suggest the importance of the EPA/AA ratio in the secondary prevention among patients with established CAD.

CRediT authorship contribution statement

Kiyoshi Asakura: Formal analysis, Investigation, Writing – original draft, Visualization. Yoshiyasu Minami: Conceptualization, Data curation, Methodology, Validation, Formal analysis, Visualization, Project administration. Takako Nagata: Investigation. Masahiro Katamine: Investigation. Aritomo Katsura: Investigation. Takuya Hashimoto: Supervision. Daisuke Kinoshita: Supervision, Investigation. Junya Ako: Supervision, Project administration.

Declaration of Competing Interest

None.

Acknowledgments

We thank Kazuhiro Fujiyoshi, Teruyoshi Nemoto, Ryota Kakizaki, Toshimitsu Sato, and Ayami Kato for their contributions in data collection.

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© 2022 Published by Elsevier Inc. on behalf of National Lipid Association.

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