Effects of extended-release niacin on lipoprotein particle size, distribution, and inflammatory markers in patients with coronary artery disease

Effects of extended-release niacin on lipoprotein particle size, distribution, and inflammatory markers in patients with coronary artery disease
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DOI:
10.1016/j.amjcard.2006.04.011
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发表时间:
2006-09-15
影响因子:
2.8
通讯作者:
Karas, Richard H.
Karas, Richard H.
中科院分区:
医学3区
文献类型:
--
作者:
Kuvin, Jeffrey T.;Dave, Devang M.;Karas, Richard H.

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在这项研究中,54 名患有稳定性冠状动脉疾病的受试者在现有疗法中添加了烟酸,为期 3 个月。各组之间的平均总胆固醇、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)和甘油三酯水平相似。与基线值相比,三个月的烟酸治疗使总 HDL 增加了 7.5%,甘油三酯降低了 15%(p < 0.005),而总胆固醇和 LDL 水平保持不变。添加烟酸导致大颗粒 HDL 增加 32%(p < 0.001),小颗粒 HDL 减少 8%(p = 0.0032),大颗粒 LDL 增加 82%(p = 0.09),小颗粒 LDL 减少 12%(p = 0.008)。烟酸降低了脂蛋白相关磷脂酶 A2 和 C 反应蛋白水平(分别为 20% 和 15%,两次比较的 p < 0.05)。接受安慰剂的受试者的任何测试参数与基线相比没有显着变化。总之,在针对冠状动脉疾病且 LDL 水平已得到良好控制的患者的现有医疗方案中添加烟酸,可以有利地改善脂蛋白颗粒大小和炎症标志物的分布,从而有望提供动脉粥样硬化保护。改变脂蛋白颗粒分布和炎症标志物对该人群中动脉粥样硬化和临床心血管事件的替代标志物的影响尚不清楚。 (c) 2006 Elsevier Inc. 保留所有权利。
In this study, niacin was added to existing therapy for 3 months in 54 subjects with stable coronary artery disease. Average total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglyceride levels were similar between groups. Three months of niacin treatment increased total HDL by 7.5% and decreased triglycerides by 15 % compared with baseline values (p < 0.005 for each), whereas total cholesterol and LDL levels remained unchanged. Addition of niacin resulted in a 32% increase in large-particle HDL (p < 0.001), an 8% decrease in small-particle HDL (p = 0.0032), an 82% increase in large-particle LDL (p = 0.09), and a 12% decrease in small-particle LDL (p = 0.008). Niacin decreased lipoprotein-associated phospholipase A2 and C-reactive protein levels (20% and 15%, respectively, p < 0.05 for the 2 comparisons). No significant changes from baseline were seen in any tested parameter in subjects who received placebo. In conclusion, addition of niacin to existing medical regimens for patients with coronary artery disease and already well-controlled LDL levels favorably improves the distribution of lipoprotein particle sizes and inflammatory markers in a manner that would be expected to confer atheroprotection. The effect of altering lipoprotein particle distribution and inflammatory markers on surrogate markers of atherosclerosis and clinical cardiovascular events in this population remains unclear. (c) 2006 Elsevier Inc. All rights reserved.