Association of small low-density lipoprotein particles with the incidence of coronary artery disease in men and women.
Association of small low-density lipoprotein particles with the incidence of coronary artery disease in men and women.
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DOI：
10.1001/jama.1996.03540110029028
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发表时间：
1996-09
期刊：
影响因子：
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通讯作者：
C. Gardner;S. Fortmann;R. Krauss
中科院分区：
文献类型：
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作者：
C. Gardner;S. Fortmann;R. Krauss
目的探讨低密度脂蛋白(LDL)颗粒直径与致死性和非致命性冠状动脉疾病(CAD)的关系。设计嵌套式病例对照研究。背景病例和对照是从以人口为基础的男性和女性样本中确定的，结合1979年至1990年斯坦福五城项目(FCP)进行的所有5项横断面调查。参与者事件CAD病例是通过1979年至1992年的FCP监测确定的。对照组按性别、5岁年龄组、调查时间点、种族和FCP治疗条件进行匹配。样本包括124对配对：90对男性和34对女性。主要观察指标用梯度凝胶电泳法测定横断面调查期间采集的血浆样本(70℃保存5~15年)的低密度脂蛋白峰值颗粒直径(LDL大小)。已建立的冠心病危险因素数据来自FCP基线测量。结果冠心病组的低密度脂蛋白直径小于对照组(平均+/-SD)(26.17+/-1.00 nm vs 26.68+/-0.90 nm；P<；.001)。这种关联是在对照低密度脂蛋白大小的五分之一范围内进行分级的。低密度脂蛋白大小的显著病例对照差异与高密度脂蛋白胆固醇(高密度脂蛋白胆固醇)、非高密度脂蛋白胆固醇(非高密度脂蛋白胆固醇)、甘油三酯、吸烟、收缩压和体重指数无关，但调整总胆固醇(TC)与高密度脂蛋白胆固醇(TC：高密度脂蛋白-C)的比率后，差异不显著。在所有的生理危险因素中，在条件Logistic回归分析中，低密度脂蛋白的大小是区分冠心病状态的最好因素。然而，当添加上述生理参数时，TC：HDL-C比率被发现是更强的独立预测冠心病状态的指标。结论：在一项基于人群的前瞻性研究中，冠心病患者的低密度脂蛋白明显小于对照组。这些发现支持了小而致密的低密度脂蛋白颗粒在动脉粥样硬化病因中所起作用的其他证据。
OBJECTIVE To investigate the prospective association of low-density lipoprotein (LDL) particle diameter with the incidence of fatal and nonfatal coronary artery disease (CAD). DESIGN A nested case-control study. SETTING Cases and controls were identified from a population-based sample of men and women combining all of the 5 cross-sectional surveys conducted from 1979 to 1990 of the Stanford Five-City Project (FCP). PARTICIPANTS Incident CAD cases were identified through FCP surveillance between 1979 and 1992. Controls were matched by sex, 5-year age groups, survey time point, ethnicity, and FCP treatment condition. The sample included 124 matched pairs: 90 pairs of men and 34 pairs of women. MAIN OUTCOME MEASURES LDL peak particle diameter (LDL size) was determined by gradient gel electrophoresis on plasma samples collected during the cross-sectional surveys (stored at 70 degrees C for 5-15 years). Established CAD risk-factor data were available from FCP baseline measurements. RESULTS LDL size was smaller among CAD cases than controls (mean +/- SD) (26.17 +/- 1.00 nm vs 26.68 +/- 0.90 nm; P<.001). The association was graded across control quintiles of LDL size. The significant case-control difference in LDL size was independent of levels of high-density lipoprotein cholesterol (HDL-C), non-HDL cholesterol (non-HDL-C), triglyceride, smoking, systolic blood pressure, and body mass index, but was not significant after adjusting for the ratio of total cholesterol (TC) to HDL-C (TC:HDL-C). Among all the physiological risk factors, LDL size was the best differentiator of CAD status in conditional logistic regression. However, when added to the physiological parameters above, the TC:HDL-C ratio was found to be a stronger independent predictor of CAD status. CONCLUSION LDL size was significantly smaller in CAD cases than in controls in a prospective, population-based study. These findings support other evidence of a role for small, dense LDL particles in the etiology of atherosclerosis.