Bregar Urska, Jug Borut, Keber Irena, Cevc Matija, Sebestjen Miran
Department of Angiology, University of Ljubljana Medical Centre, Zaloška 7, 1000, Ljubljana, Slovenia,
Heart Vessels. 2014 May;29(3):313-9. doi: 10.1007/s00380-013-0367-5. Epub 2013 May 28.
Raising high-density lipoprotein cholesterol (HDL-C) is an important strategy for reducing residual cardiovascular risk. In the present study, we sought to assess the effect of extended-release niacin/laropiprant on endothelial function in patients after a myocardial infarction with target low-density lipoprotein cholesterol (LDL-C). In this double-blind, placebo-controlled trial, 63 men (35-60 years of age) after a myocardial infarction were randomized to either niacin/laropiprant (1000/20 mg daily for 4 weeks and 2000/40 mg daily thereafter) or placebo. Flow-mediated dilation (FMD) and nitroglycerin-induced (GTN) dilation of the brachial artery, total cholesterol (TC), LDL-C, HDL-C, triglycerides (TG), lipoprotein(a) [Lp(a)], and apolipoprotein (Apo) A1/B were measured at baseline and after 12 weeks of intervention. FMD significantly increased (from 3.9 ± 5.1 to 9.8 ± 4.4%, p < 0.001) in the niacin/laropiprant group, but not in the placebo group (4.6 ± 4.4 to 6.1 ± 4.4%, p = 0.16) (p = 0.02 for comparison of interventions). GTN dilation also increased in the niacin/laropiprant group (from 12.5 ± 6.1 to 16.7 ± 4.8%, p = 0.02), but not in the placebo group (13.4 ± 5.0 to 15.1 ± 5.2%, p = 0.18), (p = 0.60 for comparison of interventions). Niacin/laropiprant reduced TC and LDL-C (p = 0.05 for both) and increased HDL-C (p < 0.001) without influencing TG, with no changes in the placebo group. Lp(a) (p = 0.026) and ApoB (p = 0.014) were significantly lower in the niacin/laropiprant group, with no difference in the placebo group. ApoA1 did not change in either of the groups (p = 0.13; p = 0.26). FMD and GTN dilation improvements did not correlate with changes in the lipid profile. Niacin/laropiprant improves endothelium-dependent and endothelium-independent dilation of the brachial artery. This improvement does not correlate with changes in lipid parameters.
提高高密度脂蛋白胆固醇（HDL-C）是降低心血管残余风险的重要策略。在本研究中，我们旨在评估缓释烟酸/拉罗匹仑对心肌梗死后低密度脂蛋白胆固醇（LDL-C）达标的患者内皮功能的影响。在这项双盲、安慰剂对照试验中，63名心肌梗死后的男性（35 - 60岁）被随机分为烟酸/拉罗匹仑组（每日1000/20毫克，持续4周，此后每日2000/40毫克）或安慰剂组。在基线和干预12周后测量肱动脉的血流介导的血管舒张（FMD）和硝酸甘油诱导的（GTN）血管舒张、总胆固醇（TC）、LDL-C、HDL-C、甘油三酯（TG）、脂蛋白(a) [Lp(a)]和载脂蛋白（Apo）A1/B。烟酸/拉罗匹仑组的FMD显著增加（从3.9±5.1%增至9.8±4.4%，p<0.001），而安慰剂组未增加（从4.6±4.4%增至6.1±4.4%，p = 0.16）（干预组比较p = 0.02）。烟酸/拉罗匹仑组的GTN血管舒张也增加（从12.5±6.1%增至16.7±4.8%，p = 0.0)，但安慰剂组未增加（从13.4±5.0%增至15.1±5.2%，p = 0.18）（干预组比较p = 0.60）。烟酸/拉罗匹仑降低了TC和LDL-C（两者p = 0.05）并增加了HDL-C（p<0.001），而未影响TG，安慰剂组无变化。烟酸/拉罗匹仑组的Lp(a)（p = 0.026）和ApoB（p = 0.014）显著降低，安慰剂组无差异。两组的ApoA1均未改变（p = 0.13；p = 0.26）。FMD和GTN血管舒张的改善与血脂谱变化无关。烟酸/拉罗匹仑改善了肱动脉的内皮依赖性和非内皮依赖性血管舒张。这种改善与血脂参数的变化无关。
