Ballantyne Christie M, Shah Sukrut, Sapre Aditi, Ashraf Tanya B, Tobias Sandra C, Sahin Tayfun, Ye Ping, Dong Yugang, Sheu Wayne Huey-Heng, Kang Duk-Hyun, Ferreira Rossi Paulo Roberto, Moiseeva Yulia, Briones Ignacio Rodriguez, Johnson-Levonas Amy O, Mitchel Yale B
Baylor College of Medicine, Houston, Texas.
Merck & Co., Inc., Kenilworth, New Jersey.
Am J Cardiol. 2017 Aug 15;120(4):569-576. doi: 10.1016/j.amjcard.2017.03.255. Epub 2017 Apr 12.
This phase 3, multiregional, randomized, double-blind, placebo-controlled study assessed the efficacy/safety profile of anacetrapib added to ongoing therapy with statin ± other lipid-modifying therapies in patients with hypercholesterolemia who were not at their low-density lipoprotein (LDL-C) goal (as per the National Cholesterol Education Program Adult Treatment Panel III guidelines) and in those with low high-density lipoprotein cholesterol (HDL-C). Patients on a stable dose of statin ± other lipid-modifying therapies and with LDL-C ≥70 to <115, ≥100 to <145, ≥130, or ≥160 mg/dl for very high, high, moderate, or low CHD risk or at LDL-C goal (per CHD risk category) with HDL-C ≤40 mg/dl were randomized in a ratio of 1:1 to anacetrapib 100 mg (n = 290) or placebo (n = 293) for 24 weeks, followed by a 12-week off-drug phase. The co-primary end points were % change from baseline in LDL-C and HDL-C and the safety profile of anacetrapib. Treatment with anacetrapib reduced LDL-C (BQ) by 37% (95% confidence interval -42.5, -31.0) and increased HDL-C by 118% (95% confidence interval 110.6, 125.7) relative to placebo (p <0.001 for both). Anacetrapib also reduced non-HDL-C, apolipoprotein B, and lipoprotein a and increased apolipoprotein AI versus placebo (p <0.001 for all). There were no clinically meaningful differences between the anacetrapib and placebo groups in the % patients who discontinued drug due to an adverse event or in abnormalities in liver enzymes, creatine kinase, blood pressure, electrolytes, or adjudicated cardiovascular events. Treatment with anacetrapib substantially reduced LDL-C and also increased HDL-C and was well tolerated over 24 weeks in statin-treated patients with hypercholesterolemia or low HDL-C.
这项3期、多区域、随机、双盲、安慰剂对照研究评估了在接受他汀类药物±其他调脂治疗的高胆固醇血症患者中(这些患者未达到低密度脂蛋白胆固醇[LDL-C]目标,依据美国国家胆固醇教育计划成人治疗小组III指南)以及高密度脂蛋白胆固醇[HDL-C]水平低的患者中,在现有治疗基础上加用阿那曲泊帕的疗效/安全性。接受稳定剂量他汀类药物±其他调脂治疗且LDL-C水平为≥70至<115、≥100至<145、≥130或≥160mg/dl(分别对应极高、高、中或低冠心病风险)或达到LDL-C目标(根据冠心病风险类别)且HDL-C≤40mg/dl的患者,按1:1比例随机分为阿那曲泊帕100mg组(n = 290)或安慰剂组(n = 293),治疗24周,随后为12周的停药期。共同主要终点为LDL-C和HDL-C相对于基线的百分比变化以及阿那曲泊帕的安全性。与安慰剂相比,阿那曲泊帕治疗使LDL-C降低了37%(95%置信区间-42.5,-31.0),HDL-C升高了118%(95%置信区间110.6,125.7)(两者p均<0.001)。与安慰剂相比,阿那曲泊帕还降低了非HDL-C、载脂蛋白B和脂蛋白a,并升高了载脂蛋白AI(所有p均<0.001)。在因不良事件停药的患者百分比或肝酶、肌酸激酶、血压、电解质异常或判定的心血管事件方面,阿那曲泊帕组和安慰剂组之间无临床意义上的差异。在接受他汀类药物治疗的高胆固醇血症或HDL-C水平低的患者中,阿那曲泊帕治疗在24周内显著降低了LDL-C,同时升高了HDL-C,且耐受性良好。