Available online 5 December 2022
Author links open overlay panelAbstractBackgroundA low eicosapentaenoic acid (EPA)/arachidonic acid (AA) ratio is associated with an increased risk of cardiovascular events in patients with coronary artery disease (CAD).
ObjectiveTo clarify the impact of the EPA/AA ratio on the characteristics of non-culprit coronary plaques in statin-treated patients with CAD.
MethodsA 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).
ResultsThe 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.
ConclusionLower 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.
IntroductionA 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 populationThis 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 characteristicsThe 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
DiscussionThe 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
ConclusionsA 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 statementKiyoshi 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 InterestNone.
AcknowledgmentsWe thank Kazuhiro Fujiyoshi, Teruyoshi Nemoto, Ryota Kakizaki, Toshimitsu Sato, and Ayami Kato for their contributions in data collection.
View full text© 2022 Published by Elsevier Inc. on behalf of National Lipid Association.
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