EFFECTS OF CHD PREVENTION ON LIPOPROTEIN SUBCLASSES

斯坦福大学的冠状动脉风险干预项目为期四年 随机临床试验表明，通过 生活方式的改变和降脂药物的使用显著减少 冠状动脉最小内径狭窄率 119名患者的血管造影可见病变节段与127名患者 对照谁接受了通常的医生护理。与此合作 在试验中，罗纳德·克劳斯博士测量了高密度脂蛋白(HDL) 用梯度凝胶电泳法进行亚类划分。硬件描述语言可以分为两部分 HDL2和三个HDL3子类，由其估计的 颗粒直径：HDL3c(7.2-7.8 nm)、HDL3b(7.8-8.2 nm)、HDL3a(8.2- HDL2a(8.8-9.7 nm)和HDL2b(9.7-12.9 nm)。高密度脂蛋白- 分布的特征也可以由 主峰，可能位于HDL3b或HDL3a区间。 病例对照和血管造影研究表明，冠状动脉 当HDL2b相对于HDL3c和HDL3b降低时，疾病风险增加 我们的目标是评估高密度脂蛋白亚类对冠状动脉病变的影响。 疾病进展，并确定影响高密度脂蛋白亚类的因素 在基线和一段时间内。拟考查的具体问题包括： 1.降低风险计划是否将特定的HDL子类更改为 与对照组相比呢？ 2.高密度脂蛋白梯度凝胶图谱是否描述了男性最有可能 从多因素风险降低中获益？ 3.在降低的患者中，高密度脂蛋白亚类是否有显著变化 摄取脂肪，减轻体重，或服用一种或多种 以下药物：Colestiol，烟酸，氯贝特， 普罗布考、吉非罗齐、非诺贝特、洛伐他汀、瓜尔豆胶或鱼 油吗？ 4.高密度脂蛋白亚类与 肥胖、空腹和负荷后胰岛素和葡萄糖、饮食和 基线用药情况如何？ 初步分析表明：1)在试验期间，试验中的男性 治疗组HDL2b升高；2)特殊干预最多 有效减少冠心病患者的病情进展 基线占优势的高密度脂蛋白-峰值直径低于中位数；3)高密度脂蛋白- 亚类受饮食和肥胖的影响比受 4)碳水化合物、酒精和咖啡因 与基线上的特定子类相关联。数据存储在 计算机文件，除了本文件中包含的分析 应用程序，未进行分析。这些数据是作为NIH的一部分收集的 授予冠心病患者血浆脂蛋白，HL-33577。

The Stanford Coronary Risk Intervention Project was a four-year randomized clinical trial that showed that risk reduction through lifestyle change and lipid-lowering medications significantly reduced the rate of narrowing of the minimum diameter of coronary artery segments with angiographically visible lesions in 119 patients vs. 127 controls who received usual physician care. In collaboration with this trial, Dr. Ronald Krauss measured high-density lipoprotein (HDL) subclasses by gradient gel electrophoresis. HDL may be divided into two HDL2 and three HDL3 subclasses that are approximated by their estimated particle diameters: HDL3c (7.2-7.8 nm), HDL3b (7.8-8.2 nm), HDL3a (8.2- 8.8 nm), HDL2a (8.8-9.7 nm) and HDL2b (9.7-12.9 nm). The HDL- distribution can also be characterized by the diameter of the predominant peak, which may lie in either the HDL3b or HDL3a interval. Case control and angiographic studies suggest that coronary heart disease risk is increased when HDL2b is reduced relative to HDL3c and HDL3b Our objective is to assess the influence of HDL-subclasses with coronary disease progression, and to identify factors influencing HDL subclasses at baseline and over time. The specific questions to be examined are: 1. Did the risk reduction program change specific HDL subclasses as compared to controls? 2. Did the HDL gradient gel profile characterize men most likely to benefit from multifactor risk reduction? 3. Did HDL-subclasses change significantly in patients that reduced fat intake, reduce body weight, or who took one or more of the following medications: colestipol, nicotinic acid, clofibrate, probucol, gemfibrozil, fenofibrate, lovastatin, guar gum or fish oils? 4. What are the cross-sectional associations of HDL-subclasses with adiposity, fasting and post-load insulin and glucose, diet and medications at baseline? Preliminary analyses suggest that: 1) During the trial, men in the treatment group increased HDL2b; 2) the special intervention was most effective in reducing coronary disease progression in subjects with a baseline predominant HDL-peak diameter below the median; 3) HDL- subclasses were more strongly influenced by diet and adiposity than by drugs during the trial; 4) carbohydrates, alcohol and caffeine were associated with specific subclasses at baseline. The data are stored in computer files, and except for the analyses contained in this application, are unanalyzed. These data were collected as part of NIH grant Plasma lipoproteins in coronary artery disease, HL-33577.