Department of Medicine, Duke University Medical Center, Durham, North Carolina.
J Am Coll Cardiol. 2013 Oct 22;62(17):1580-4. doi: 10.1016/j.jacc.2013.07.023. Epub 2013 Jul 31.
This study sought to examine the relationship between niacin treatment, lipoproteins, and cardiovascular (CV) outcomes in this secondary analysis of the AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome With Low HDL/High Triglycerides and Impact on Global Health Outcomes) trial.
During a 3-year follow-up in 3,414 patients with established CV disease and low high-density lipoprotein cholesterol (HDL-C) levels, combined niacin + low-density lipoprotein cholesterol (LDL-C)-lowering therapy did not reduce CV events compared with LDL-C-lowering therapy alone.
Subjects taking simvastatin and/or ezetimibe were randomized to receive extended-release (ER) niacin 1,500 to 2,000 mg or minimal immediate-release niacin (≤ 150 mg) as placebo at bedtime. LDL-C levels in both groups were maintained from 40 to 80 mg/dl. Hazard ratios were estimated by using Cox proportional hazards models for relationships between lipoproteins and the composite endpoint of CV death, myocardial infarction, acute coronary syndrome, ischemic stroke, or symptom-driven revascularization.
CV outcomes were not associated with ER niacin in any baseline lipoprotein tertile. In a subset of patients in both the highest triglyceride (≥ 198 mg/dl) and lowest HDL-C (<33 mg/dl) tertiles, ER niacin showed a trend toward benefit (hazard ratio: 0.74, p = 0.073). In-trial LDL-C levels, non-HDL-C levels, and the total cholesterol/HDL-C ratio were positively associated with CV events in the control group, but these relationships were absent in the ER niacin group.
Baseline lipoprotein tertiles did not predict differential benefit or harm with ER niacin added to LDL-C-lowering therapy, but a small dyslipidemic subgroup may benefit. ER niacin attenuated expected relationships of lipoprotein risk factors with CV events, raising the possibility that nonlipoprotein actions of niacin could affect risk. (Niacin Plus Statin to Prevent Vascular Events [AIM-HIGH]; NCT00120289).
本研究旨在通过 AIM-HIGH（代谢综合征伴低 HDL/高甘油三酯患者的动脉粥样硬化血栓形成干预及对全球健康结局的影响）试验的二次分析，探讨烟酸治疗、脂蛋白与心血管（CV）结局之间的关系。
在 3414 例有明确 CV 疾病且 HDL-C 水平较低的患者中，经过 3 年的随访，联合应用烟酸+降低 LDL-C 治疗与单独降低 LDL-C 治疗相比，并未降低 CV 事件发生率。
服用辛伐他汀和/或依折麦布的受试者被随机分为接受缓释烟酸 1500 至 2000mg 或最低剂量即时释放烟酸（≤150mg）作为安慰剂，睡前服用。两组 LDL-C 水平均维持在 40 至 80mg/dl。采用 Cox 比例风险模型估计风险比，用于分析脂蛋白与 CV 死亡、心肌梗死、急性冠脉综合征、缺血性卒中和症状驱动的血运重建的复合终点之间的关系。
在任何基线脂蛋白三分位数中，CV 结局均与缓释烟酸无关。在最高甘油三酯（≥198mg/dl）和最低 HDL-C（<33mg/dl）三分位数的患者亚组中，缓释烟酸有获益趋势（风险比：0.74，p=0.073）。试验中的 LDL-C 水平、非 HDL-C 水平和总胆固醇/HDL-C 比值与对照组的 CV 事件呈正相关，但在缓释烟酸组中不存在这种关系。
基线脂蛋白三分位数不能预测添加 LDL-C 降低治疗后缓释烟酸的获益或危害，但一个较小的血脂异常亚组可能获益。缓释烟酸减弱了脂蛋白危险因素与 CV 事件的预期关系，这提示烟酸的非脂蛋白作用可能会影响风险。（烟酸联合他汀预防血管事件[AIM-HIGH]；NCT00120289）。
