Takada Kaoru, Ishikawa Shuichi, Yokoyama Naoyuki, Hosogoe Naoyoshi, Isshiki Takaaki
Division of Cardiology, Department of Internal Medicine, Teikyo University School of Medicine.
Int Heart J. 2014;55(3):228-33. doi: 10.1536/ihj.13-295. Epub 2014 May 7.
Eicosapentaenoic acid (EPA) has been widely accepted to have antiatherosclerotic effects. The aim of this study was to investigate the antiplatelet effect of EPA combined with acetylsalicylic acid (ASA) following stent implantation. Eighteen patients who had undergone coronary stent implantation at least 8 months previously were included. All patients were given EPA ethyl ester (EPA-E) 1.8 g/day in addition to ASA 100 mg/day for 12 weeks. After the treatment, the plasma EPA/arachidonic acid (AA) ratio increased significantly from 0.40 ± 0.2 to 1.08 ± 0.39 (P < 0.001). There were no changes in the maximum platelet aggregation (MPA) induced by adenosine diphosphate (5 and 20 µmol/L), AA (0.3 and 0.5 mg/mL), or collagen (2 and 4 µg/mL). Furthermore, no significant differences were observed in the expression of PAC-1 and CD62P on the platelet surface membranes or in the soluble P-selectin concentration. With further analysis, a significant negative correlation was found between collagen (2 µg/mL)-induced MPA and plasma EPA/AA ratio (r = -0.507, P = 0.032). The patients were then divided into 2 groups according to the median EPA/AA ratio value of 0.92. In the high EPA/AA ratio group (n = 10), collagen-induced MPA was significantly suppressed after EPA-E administration (45.3 ± 15.9 versus 39.0 ± 16.3, P = 0.033). In contrast, there were no significant changes in platelet aggregation (56.0 ± 9.8 versus 57.1 ± 11.4, P = 0.745) in the low EPA/AA ratio group (n = 8). EPA treatment had a potential to suppress collagen-induced platelet aggregation in patients with a high plasma EPA/AA ratio.
二十碳五烯酸（EPA）具有抗动脉粥样硬化作用已被广泛认可。本研究旨在探讨支架植入后EPA联合乙酰水杨酸（ASA）的抗血小板作用。纳入18例至少在8个月前接受过冠状动脉支架植入术的患者。所有患者在服用100mg/天ASA的基础上，加用1.8g/天的EPA乙酯（EPA-E），持续12周。治疗后，血浆EPA/花生四烯酸（AA）比值从0.40±0.2显著升高至1.08±0.39（P<0.001）。由二磷酸腺苷（5和20μmol/L）、AA（0.3和0.5mg/mL）或胶原（2和4μg/mL）诱导的最大血小板聚集（MPA）无变化。此外，在血小板表面膜上PAC-1和CD62P的表达或可溶性P-选择素浓度方面未观察到显著差异。进一步分析发现，胶原（2μg/mL）诱导的MPA与血浆EPA/AA比值之间存在显著负相关（r=-0.507，P=0.032）。然后根据EPA/AA比值中位数0.92将患者分为2组。在高EPA/AA比值组（n=10）中，服用EPA-E后胶原诱导的MPA显著受到抑制（45.3±15.9对39.0±16.3，P=0.033）。相比之下，低EPA/AA比值组（n=8）的血小板聚集无显著变化（56.0±9.8对57.1±11.4，P=0.745）。EPA治疗有可能抑制血浆EPA/AA比值高的患者中胶原诱导血小板聚集。
