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山东大学学报 (医学版) ›› 2019, Vol. 57 ›› Issue (8): 110-116.doi: 10.6040/j.issn.1671-7554.0.2019.287

• • 上一篇    

血脂正常人群HDL-C纵向变化与冠心病的关联性分析:一项回顾性队列研究

李明卓1,2,孙秀彬1,2,王春霞3,杨洋4,刘新辉1,2,刘言训1,2,薛付忠1,2,袁中尚1,2   

  1. 1. 山东大学公共卫生学院生物统计学系, 山东 济南 250012;2. 山东大学健康医疗大数据研究院, 山东 济南 250012;3. 济宁医学院附属医院健康管理中心, 山东 济宁 272000;4. 山东省立医院神经内科, 山东 济南 250021
  • 发布日期:2022-09-27
  • 通讯作者: 袁中尚. E-mail:yuanzhongshang@sdu.edu.cn

Association between longitudinal changes of HDL-C and coronary heart disease in a population with normal serum lipids: a retrospective cohort study

LI Mingzhuo1,2, SUN Xiubin1,2, WANG Chunxia3, YANG Yang4, LIU Xinhui1,2, LIU Yanxun1,2, XUE Fuzhong1,2, YUAN Zhongshang1,2   

  1. 1. Department of Biostatistics, School of Public Health, Shandong University, Jinan 250012, Shandong, China;
    2. Healthcare Big Data Institute of Shandong University, Jinan 250012, Shandong, China;
    3. Health Management Center, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong, China;
    4. Department of Neurology, Shandong Provincial Hospital, Jinan 250021, Shandong, China
  • Published:2022-09-27

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摘要： 目的 探讨血脂正常人群的高密度脂蛋白胆固醇(HDL-C)纵向变化与冠心病(CHD)的关联性。 方法 基于大规模健康管理队列,选取基线年龄20岁至70岁、CHD诊断前或截尾事件出现时至少有2次体检记录、随访过程中血脂正常、重要指标无缺失的人群建立回顾性研究队列。HDL-C的纵向变化定义为末次随访的HDL-C水平减去基线HDL-C水平;按照其四分位数将研究对象分为4组:HDL-C下降组(Q1组),HDL-C稳定组(Q2组),HDL-C平缓升高组(Q3组),HDL-C升高组(Q4组)。随后,HDL-C的变化被作为连续型变量和分组变量分别放入Cox回归模型,分步调整各类混杂因素,评价HDL-C纵向变化与CHD发生的关联性。 结果 共计8 958例参与者入选了研究队列,总计随访时间43 527.26人年,新发CHD124例,发病密度为2.85/1 000人年。将HDL-C纵向变化看作连续型变量时,分步调整潜在的混杂因素(年龄、性别、高血压、吸烟、饮酒、体质量指数、空腹血糖、基线HDL-C、体质量指数的改变、低密度脂蛋白胆固醇的改变等)后,HDL-C升高始终是CHD发病的保护因素,发病风险(HR)及其95%置信区间(CI)为0.38(0.16~0.87);将HDL-C纵向变化看作分组变量时,与Q1组比较,Q4组始终具有较低的CHD发病风险,最终Cox模型的HR(95%CI)为0.43(0.24~0.78)。 结论 在血脂正常人群中,HDL-C的纵向升高是CHD的独立保护因素。

关键词: 高密度脂蛋白胆固醇的纵向变化, 冠心病, 血脂正常的队列人群, Cox回归模型

Abstract: Objective To investigate the relationship between the longitudinal changes of high-density lipoprotein cholesterol(HDL-C)and coronary heart disease(CHD)in people with normal blood lipids. Methods Based on the large-scale health management cohort, a retrospective study cohort was constructed in the population aged 20 to 70 years at baseline, with at least two physical examination records before the diagnosis of CHD or when the cut-off events occurred, maintaining normal blood lipids during the follow-up, and having no important variables missing. Change in HDL-C was calculated by subtracting the baseline value from the level at the end of follow-up, and the subjects were 山 东 大 学 学 报 (医 学 版)57卷8期 -李明卓,等.血脂正常人群HDL-C纵向变化与冠心病的关联性分析:一项回顾性队列研究 \=-divided into 4 groups according to the quartiles of HDL-C change: Q1 is the HDL-C descending group, Q2 is the HDL-C stable group, Q3 is the HDL-C gently increasing group, while Q4 is the HDL-C increasing group. After that, Cox regression models were used to evaluate the correlation between the longitudinal changes of HDL-C and CHD by defining HDL-C change as a continuous variable or a categorical variable. Confounding factors were adjusted stepwisely. Results A total of 8 958 participants were enrolled in the study cohort. Total follow-up time was 43 527.26 person-years, with 124 new CHD cases. Incidence density was 2.85/1 000 person-years. When HDL-C change was considered as a continuous variable, HDL-C change was always a protective factor for CHD morbidity with adjustment for potential confounding factors(age, gender, hypertension, smoking, drinking, body mass index, fasting plasma glucose, baseline HDL-C, body mass index change, low density lipoprotein cholesterol change, etc.)step by step, and the hazard ratio(HR)and 95% confidence interval(CI)was 0.38(0.16-0.87); when HDL-C change was considered as a categorical variable, compared with Q1 group, Q4 group always had a lower risk of developing CHD, the HR(95% CI)of Q4 group in the all-adjusted Cox model was 0.43(0.24-0.78). Conclusion Longitudinal elevated HDL-C is an independent protective factor for CHD in people with normal blood lipids.

Key words: Longitudinal change of high-density lipoprotein cholesterol, Coronary heart disease, Cohort with normal blood lipids, Cox regression model

中图分类号: 

  • R541
[1] Lozano R, Naghavi M, Foreman K, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010[J]. Lancet, 2012, 380(9859): 2095-2128.
[2] 陈伟伟, 高润霖, 刘力生, 等.《中国心血管病报告2017》概要[J]. 中国循环杂志, 2018, 33(1): 1-8.
[3] 血脂康调整血脂对冠心病二级预防研究协作组. 中国冠心病二级预防研究[J]. 中华心血管病杂志, 2005, 33(2): 109-115. Collaborative Group for China Coronary Secondary Preventioni Using Xuezhikang. China coronary secondary prevention study(CCSPS)[J]. Chinese Journal of Cardiology, 2005, 33(2): 109-115.
[4] 王彦琦, 张培影. 冠心病与血脂异常的认识进展[J]. 中西医结合心脑血管病杂志, 2015, 13(11): 1287-1289.
[5] Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the third report of the national cholesterol education program(NCEP)expert panel on detection, evaluation, and treatment of high blood cholesterol in adults(adult treatment panel III)[J]. JAMA, 2001, 285(19): 2486-2497.
[6] Carey VJ, Bishop L, Laranjo N, et al. Contribution of high plasma triglycerides and low high-density lipoprotein cholesterol to residual risk of coronary heart disease after establishment of low-density lipoprotein cholesterol control[J]. Am J Cardiol, 2010, 106(6): 757-763.
[7] Ling Y, Jiang J, Wu B, et al. Serum triglyceride, high-density lipoprotein cholesterol, apolipoprotein B, and coronary heart disease in a Chinese population undergoing coronary angiography[J]. J Clin Lipidol, 2017, 11(3): 646-656.
[8] Colantonio LD, Bittner V, Reynolds K, et al. Association of serum lipids and coronary heart disease in contemporary observational studies[J]. Circulation, 2016, 133(3): 256-264.
[9] Yuan Z, Yang Y, Wang C, et al. Trajectories of long-term normal fasting plasma glucose and risk of coronary heart disease: a prospective cohort study[J]. J Am Heart Assoc, 2018, 7(4): e007607. doi:10.1161/JAHA.117.007607.
[10] Jun JE, Jee JH, Bae JC, et al. Association between changes in thyroid hormones and incident type 2 diabetes: a seven-year longitudinal study[J]. Thyroid, 2017, 27(1): 29-38.
[11] Lee G, Choi S, Kim K, et al. Association of hemoglobin concentration and its change with cardiovascular and all-cause mortality[J]. J Am Heart Assoc, 2018, 7(3): e007723. doi:10.1161/JAHA.117.007723.
[12] Carroll MD, Lacher DA, Sorlie PD, et al. Trends in serum lipids and lipoproteins of adults, 1960-2002[J]. JAMA, 2005, 294(14): 1773-1781.
[13] Rahilly-Tierney C, Bowman TS, Djoussé L, et al. Change in high-density lipoprotein cholesterol and incident coronary heart disease in apparently healthy male physicians[J]. Am J Cardiol, 2008, 102(12): 1663-1667.
[14] 刘娅飞, 邢娉, 徐秀琴, 等. 山东多中心健康管理纵向观察队列[J]. 山东大学学报(医学版), 2017, 55(6): 30-36. LIU Yafei, XING Ping, XU Xiuqin, et al. Shandong multi-center longitudinal cohort for health management: a brief introduction[J]. Journal of Shandong University(Health Science), 2017, 55(6): 30-36.
[15] Joint Committee for Guideline Revision. 2018 Chinese Guidelines for Prevention and Treatment of Hypertension—A report of the Revision Committee of Chinese Guidelines for Prevention and Treatment of Hypertension [J]. J Geriatr Cardiol, 2019, 16(3): 182-241.
[16] 中华医学会糖尿病学分会.中国2型糖尿病防治指南(2017年版)[J]. 中国实用内科杂志, 2018, 38(4): 292-344. Chinese Diabetes Society. Guidelines for the prevention and control of type 2 diabetes in China(2017 Edition)[J]. Chinese Journal of Practical Internal Medicine, 2018, 38(4): 292-344.
[17] 中国成人血脂异常防治指南修订联合委员会. 中国成人血脂异常防治指南(2016年修订版)[J]. 中国循环杂志, 2016, 31(10): 937-953.
[18] Nakanishi N, Nakamura K, Ichikawa S, et al. Relationship between lifestyle and serum lipid and lipoprotein levels in middle-aged Japanese men[J]. Eur J Epidemiol, 1999, 15(4): 341-348.
[19] 余红梅. Cox比例风险回归模型诊断及预测有关问题的研究[D]. 西安: 第四军医大学, 2001.
[20] 王春霞, 许艺博, 杨宁, 等. 基于健康管理队列的冠心病风险预测模型[J]. 山东大学学报(医学版), 2017, 55(6): 66-71. WANG Chunxia, XU Yibo, YANG Ning, et al. A prediction model for coronary heart disease risks based on health management cohort[J]. Journal of Shandong University(Health Science), 2017, 55(6): 66-71.
[21] Hadaegh F, Khalili D, Ghasemi A, et al. Triglyceride/HDL-cholesterol ratio is an independent predictor for coronary heart disease in a population of Iranian men[J]. Nutr Metab Cardiovasc Dis, 2009, 19(6): 401-408.
[22] Ling Y, Jiang J, Wu B, et al. Serum triglyceride, high-density lipoprotein cholesterol, apolipoprotein B, and coronary heart disease in a Chinese population undergoing coronary angiography[J]. J Clin Lipidol, 2017, 11(3): 646-656. doi:10.1016/j.jacl.2017.02.017.
[23] Hata Y, Nakajima K. Life-style and serum lipids and lipoproteins[J]. J Atheroscler Thromb, 2000, 7(4): 177-197.
[24] Singh IM, Shishehbor MH, Ansell BJ. High-density lipoprotein as a therapeutic target: a systematic review[J]. JAMA, 2007, 298(7): 786-798.
[25] Briel M, Ferreira-Gonzalez I, You JJ, et al. Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis[J]. BMJ, 2009, 338: b92. doi:10.1136/bmj.b92.
[26] Holmes MV, Asselbergs FW, Palmer TM, et al. Mendelian randomization of blood lipids for coronary heart disease[J]. Eur Heart J, 2015, 36(9): 539-550.
[27] Mahdy Ali K, Wonnerth A, Huber K, et al. Cardiovascular disease risk reduction by raising HDL cholesterol: current therapies and future opportunities[J]. Br J Pharmacol, 2012, 167(6): 1177-1194.
[28] Howard BV. Insulin resistance and lipid metabolism[J]. Am J Cardiol, 1999, 84(1A): 28J-32J.
[29] Karabacak M, Varol E, Kahraman F, et al. Low high-density lipoprotein cholesterol is characterized by elevated oxidative stress[J]. Angiology, 2014, 65(10): 927-931.
[30] Hegarty KM, Turgiss LE, Mulligan JJ, et al. Effect of cigarette smoking on high density lipoprotein phospholipids[J]. Biochem Biophys Res Commun, 1982, 104(1): 212-219.
[31] Jan CF, Chang HC, Tantoh DM, et al. Duration-response association between exercise and HDL in both male and female Taiwanese adults aged 40 years and above[J]. Oncotarget, 2018, 9(2): 2120-2127.
[32] Brinkley TE, Halverstadt A, Phares DA, et al. Hepatic lipase gene -514C>T variant is associated with exercise training-induced changes in VLDL and HDL by lipoprotein lipase[J]. J Appl Physiol, 2011, 111(6): 1871-1876.
[33] Kobayashi J, Mabuchi H. Lipoprotein lipase and atherosclerosis[J]. Ann Clin Biochem, 2015, 52(Pt 6): 632-637.
[34] Mensink RP, Katan MB. Effect of dietary trans fatty acids on high-density and low-density lipoprotein cholesterol levels in healthy subjects[J]. N Engl J Med, 1990, 323(7): 439-445.
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