证据表明冠状动脉疾病回归的新病理生理机制:肝脏脂酶介导的LDL密度变化
A Zambon1, J E Hokanson, B G Brown
1Department of Medicine, Division of Metabolism, Endocrinology and Nutrition, University of Washington, Seattle, Wash. 98195-6426, USA.
Circulation
|April 20, 1999
概括
降脂疗法通过改变低密度脂蛋白 (LDL) 颗粒密度来改善冠状动脉疾病 (CAD). 这项研究表明,肝脂酶 (HL) 活性的变化是对CAD进展的这些有利影响的关键.
科学领域:
- 心血管医学 心血管医学
- 脂质代谢 脂质代谢是什么
- 动脉样硬化研究 动脉样硬化研究
背景情况:
- 小而密集的LDL颗粒与冠状动脉疾病 (CAD) 有关,并在降脂治疗期间预测疾病的进展.
- 在家族动脉样硬化治疗研究 (FATS) 中,强化降脂治疗显示出显著的CAD改善.
- 这项研究研究了LDL密度,肝脂酶 (HL) 和CAD进展之间的相互作用.
研究的目的:
- 检查LDL颗粒密度,肝脂酶 (HL) 活性和冠状动脉疾病 (CAD) 进展之间的关系.
- 确定一种新的生物学机制,可以证明脂质改变疗法对CAD的有益作用.
- 评估不同的降脂疗法如何影响LDL密度和HL活性.
主要方法:
- 88名FATS参与者有记录的冠状动脉疾病被随机分配给洛瓦斯塔丁-科莱斯蒂波尔,尼亚-科莱斯蒂波尔或常规疗法.
- 测量了肝脂酶 (HL) 和脂蛋白脂酶的血水平,以及LDL密度.
- 在LDL浮力和HL活动的变化与冠状动脉狭窄严重程度的变化相关.
主要成果:
- 洛瓦斯-可莱斯蒂波尔和尼亚-可莱斯蒂波尔疗法显著增加了LDL浮力 (分别为7.7%和10.3%) 并降低了HL活性 (分别为-14%和-17%).
- LDL浮力和HL活性的变化与CAD严重程度的变化密切相关 (P<0.001).
- 增加的LDL浮力是CAD回归最强的预测因素,解释了冠状动脉狭窄变化的37%.
结论:
- 治疗引起的肝脂酶 (HL) 活性变化改变了LDL粒子密度,有利地影响了CAD的进展.
- 这代表了一种新的,具有临床意义的机制,将脂质改变疗法与冠状动脉疾病的改善联系起来.
- 这些发现支持这样的假设,即调节HL活动是管理CAD的可行策略.
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