Tani Shigemasa, Nagao Ken, Yagi Tsukasa, Atsumi Wataru, Hirayama Atsushi
Department of Health Planning Center, Nihon University Hospital, 1-6 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8309, Japan.
Department of Cardiology, Nihon University Hospital, Tokyo, Japan.
Am J Cardiovasc Drugs. 2017 Feb;17(1):49-59. doi: 10.1007/s40256-016-0195-y.
We hypothesized that the additional administration of eicosapentaenoic acid (EPA) in patients with stable coronary artery disease (CAD) receiving statin has the potential to lower the serum pentraxin 3 (PTX3) level, an indicator of plaque stabilization.
We randomly assigned CAD patients already receiving statin therapy to an EPA group (1800 mg/day, n = 53) or control group (n = 53).
No significant difference was found in the change in the plasma PTX3 level between the groups. However, in a subgroup analysis, a significant percentage reduction in the plasma PTX3 level was observed in patients receiving strong statin compared with the patients receiving moderate statin in the EPA group (-5.6 vs. 14.7 %, p = 0.0082), while no such difference in the percentage change in the plasma PTX3 level was noted between the two same statin subgroups in the control group. A multiple logistic regression analysis identified the addition of EPA to ongoing strong statin treatment as an independent predictor of PTX3 level reduction. Furthermore, even in patients with relatively well-controlled serum lipid levels, pretreatment with EPA added to ongoing statin therapy reduced serum non-high-density lipoprotein cholesterol and triglyceride-rich lipoproteins as residual risk factors.
Through this study design, the results could not support the hypothesis that adding EPA in patients with stable CAD receiving varying degrees of statin treatment reduces the plasma PTX3 level comprehensively. However, addition of EPA to ongoing strong statin treatment, but not ongoing moderate statin treatment, may reduce the plasma PTX3 level, possibly leading to coronary plaque stabilization.
UMIN ( http://www.umin.ac.jp/ ), Study ID: UMIN000010452.
我们假设,在接受他汀类药物治疗的稳定型冠状动脉疾病(CAD)患者中额外给予二十碳五烯酸(EPA),有可能降低血清五聚素3(PTX3)水平,PTX3是斑块稳定性的一个指标。
我们将已接受他汀类药物治疗的CAD患者随机分为EPA组(1800毫克/天,n = 53)或对照组(n = 53)。
两组间血浆PTX3水平的变化无显著差异。然而,在亚组分析中,与EPA组中接受中等强度他汀类药物治疗的患者相比,接受高强度他汀类药物治疗的患者血浆PTX3水平有显著百分比降低(-5.6%对14.7%,p = 0.0082),而对照组中两个相同他汀类药物亚组间血浆PTX3水平的百分比变化无此差异。多因素逻辑回归分析确定,在正在进行的高强度他汀类药物治疗中添加EPA是PTX3水平降低的独立预测因素。此外,即使在血清脂质水平控制相对良好的患者中,在正在进行的他汀类药物治疗基础上加用EPA预处理也可降低血清非高密度脂蛋白胆固醇和富含甘油三酯的脂蛋白作为残余危险因素。
通过本研究设计,结果不支持在接受不同程度他汀类药物治疗的稳定型CAD患者中添加EPA可全面降低血浆PTX3水平这一假设。然而,在正在进行的高强度他汀类药物治疗中添加EPA,而非中等强度他汀类药物治疗,可能会降低血浆PTX3水平,可能导致冠状动脉斑块稳定。