期刊论文详细信息
Lipids in Health and Disease
Identification of the HDL-ApoCIII to VLDL-ApoCIII ratio as a predictor of coronary artery disease in the general population: The Chin-Shan Community Cardiovascular Cohort (CCCC) study in Taiwan
Chao-Yuh Yang2  Yuan-Teh Lee1  Chu-Huang Chen2  Ming-Fong Chen3  Kuo-Liong Chien3  Hung-Ju Lin3  Hsiu-Ching Hsu3  Chii-Ming Lee3  Po-Yuan Chang3 
[1] Department of Internal Medicine, China Medical University, Taichung, Taiwan;L5 Research Center, China Medical University Hospital, Taichung, Taiwan;Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, No. 7, Chung-Shan South Road, Taipei, 100, Taiwan
关键词: Apolipoprotein CIII (ApoCIII);    Very-low-density lipoprotein (VLDL);    High-density lipoprotein (HDL);    Chin-Shan Community Cardiovascular Cohort (CCCC) Study;    Cardiovascular risk factors;    Lipoproteins;    Coronary artery disease;    Apolipoproteins;   
Others  :  1160135
DOI  :  10.1186/1476-511X-11-162
 received in 2012-04-21, accepted in 2012-10-30,  发布年份 2012
PDF
【 摘 要 】

Background

Apolipoprotein (Apo) levels are considered more reliable than plasma lipoprotein levels for predicting coronary artery disease (CAD). However, a unanimous Apo marker for CAD has not been identified. In the Chin-Shan Community Cardiovascular Cohort (CCCC), we sought to identify a common Apo marker for predicting CAD in the general population.

Methods

We examined the cross-sectional association between Apo markers and CAD in the CCCC from 1990 to 2001. Among 3,602 subjects, 90 had angiographically proven CAD (>50% stenosis in ≥1 vessel), and 200 did not have CAD. These subjects were divided into the following 4 groups for analysis: normolipidemic (total cholesterol [TC] <200 mg/dL, triglyceride [TG] <150 mg/dL), hypertriglyceridemic (TC <200 mg/dL, TG ≥150 mg/dL), hypercholesterolemic (TC ≥200 mg/dL, TG <150 mg/dL), and hyperlipidemic (TC ≥200 mg/dL, TG ≥150 mg/dL).

Results

Compatible with findings in other populations, our results showed that CAD patients in the CCCC had higher ApoB and lower high-density lipoprotein (HDL) cholesterol and ApoAI concentrations than non-CAD subjects, but the differences were not significant in all groups. Plasma concentrations of ApoE and lipoprotein (a) were not consistently correlated with CAD. In contrast, the ratio of HDL-ApoCIII to very-low-density lipoprotein (VLDL)-ApoCIII was the only universal determinant for CAD in the normolipidemic group (P=0.0018), the hypertriglyceridemic group (P=0.0001), the hypercholesterolemic group (P=0.0001), and the hyperlipidemic group (P=0.0001). Overall, a high HDL-ApoCIII/VLDL-ApoCIII ratio was observed in all CAD patients, including those with a normal lipid profile. In multivariate analyses, the HDL-ApoCIII/VLDL-ApoCIII ratio was the strongest predictor for CAD among all lipid factors investigated (odds ratio, 2.04; 95% confidence interval, 1.46–2.84; P<0.0001).

Conclusions

A high HDL-ApoCIII to VLDL-ApoCIII ratio is a better marker for predicting CAD than are the conventional lipid markers or ApoAI and ApoB. High HDL-ApoCIII and low VLDL-ApoCIII values in CAD, irrespective of lipid variations, suggest that ApoCIII is markedly transported from VLDL to HDL in this disease. Measurement of plasma ApoCIII may improve CAD prediction in the general population.

【 授权许可】

   
2012 Chang et al.; licensee BioMed Central Ltd.

【 预 览 】
附件列表
Files Size Format View
20150410094457715.pdf 495KB PDF download
Figure 2. 58KB Image download
Figure 1. 60KB Image download
【 图 表 】

Figure 1.

Figure 2.

【 参考文献 】
  • [1]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) final report Circulation 2002, 106(25):3143-3421.
  • [2]Arsenault BJ, Rana JS, Stroes ES, Despres JP, Shah PK, Kastelein JJ, Wareham NJ, Boekholdt SM, Khaw KT: Beyond low-density lipoprotein cholesterol: respective contributions of non-high-density lipoprotein cholesterol levels, triglycerides, and the total cholesterol/high-density lipoprotein cholesterol ratio to coronary heart disease risk in apparently healthy men and women. J Am Coll Cardiol 2009, 55(1):35-41.
  • [3]Di Angelantonio E, Sarwar N, Perry P, Kaptoge S, Ray KK, Thompson A, Wood AM, Lewington S, Sattar N, Packard CJ, et al.: Major lipids, apolipoproteins, and risk of vascular disease. JAMA 2009, 302(18):1993-2000.
  • [4]Parish S, Peto R, Palmer A, Clarke R, Lewington S, Offer A, Whitlock G, Clark S, Youngman L, Sleight P, et al.: The joint effects of apolipoprotein B, apolipoprotein A1, LDL cholesterol, and HDL cholesterol on risk: 3510 cases of acute myocardial infarction and 9805 controls. Eur Heart J 2009, 30(17):2137-2146.
  • [5]Walldius G, Jungner I, Holme I, Aastveit AH, Kolar W, Steiner E: High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study. Lancet 2001, 358(9298):2026-2033.
  • [6]Kawakami A, Aikawa M, Libby P, Alcaide P, Luscinskas FW, Sacks FM: Apolipoprotein CIII in apolipoprotein B lipoproteins enhances the adhesion of human monocytic cells to endothelial cells. Circulation 2006, 113(5):691-700.
  • [7]Kawakami A, Yoshida M: Apolipoprotein CIII links dyslipidemia with atherosclerosis. J Atheroscler Thromb 2009, 16(1):6-11.
  • [8]Shin MJ, Krauss RM: Apolipoprotein CIII bound to apoB-containing lipoproteins is associated with small, dense LDL independent of plasma triglyceride levels in healthy men. Atherosclerosis 2010, 211(1):337-341.
  • [9]Ito Y, Azrolan N, O'Connell A, Walsh A, Breslow JL: Hypertriglyceridemia as a result of human apo CIII gene expression in transgenic mice. Science 1990, 249(4970):790-793.
  • [10]Qu S, Perdomo G, Su D, D'Souza FM, Shachter NS, Dong HH: Effects of apoA-V on HDL and VLDL metabolism in APOC3 transgenic mice. J Lipid Res 2007, 48(7):1476-1487.
  • [11]Marcoux C, Tremblay M, Fredenrich A, Davignon J, Cohn JS: Lipoprotein distribution of apolipoprotein C-III and its relationship to the presence in plasma of triglyceride-rich remnant lipoproteins. Metabolism: clinical and experimental 2001, 50(1):112-119.
  • [12]Eisenberg S, Olivecrona T: Very low density lipoprotein. Fate of phospholipids, cholesterol, and apolipoprotein C during lipolysis in vitro. Lipid Res 1979, 20(5):614-623.
  • [13]Sehayek E, Eisenberg S: Mechanisms of inhibition by apolipoprotein C of apolipoprotein E-dependent cellular metabolism of human triglyceride-rich lipoproteins through the low density lipoprotein receptor pathway. J Biol Chem 1991, 266(27):18259-18267.
  • [14]Le NA, Gibson JC, Ginsberg HN: Independent regulation of plasma apolipoprotein C-II and C-III concentrations in very low density and high density lipoproteins: implications for the regulation of the catabolism of these lipoproteins. J Lipid Res 1988, 29(5):669-677.
  • [15]Lee Y, Lin RS, Sung FC, Yang C, Chien K, Chen W, Su T, Hsu H, Huang Y: Chin-Shan Community Cardiovascular Cohort in Taiwan-baseline data and five-year follow-up morbidity and mortality. J Clin Epidemiol 2000, 53(8):838-846.
  • [16]Lai CL, Chien KL, Hsu HC, Su TC, Chen MF, Lee YT: Left ventricular mass and risk of cardiovascular events and all-cause death among ethnic Chinese–the Chin-Shan Community Cardiovascular Cohort study. Int J Cardiol 2011, 149(3):347-352.
  • [17]Redgrave TG, Carlson LA: Changes in plasma very low density and low density lipoprotein content, composition, and size after a fatty meal in normo- and hypertriglyceridemic man. J Lipid Res 1979, 20(2):217-229.
  • [18]Yang CY, Xie YH, Yang M, Quion JA, Gotto AM Jr: ELISA quantitation of apolipoproteins in plasma lipoprotein fractions: ApoE in ApoB-containing lipoproteins (Lp B:E) and ApoB in ApoE-containing lipoproteins (Lp E:B). J Protein Chem 1995, 14(7):503-509.
  • [19]Green PH, Glickman RM, Saudek CD, Blum CB, Tall AR: Human intestinal lipoproteins. Studies in chyluric subjects. J Clin Invest 1979, 64(1):233-242.
  • [20]Sacks FM, Alaupovic P, Moye LA, Cole TG, Sussex B, Stampfer MJ, Pfeffer MA, Braunwald E: VLDL, apolipoproteins B, CIII, and E, and risk of recurrent coronary events in the Cholesterol and Recurrent Events (CARE) trial. Circulation 2000, 102(16):1886-1892.
  • [21]Lee SJ, Campos H, Moye LA, Sacks FM: LDL containing apolipoprotein CIII is an independent risk factor for coronary events in diabetic patients. Arterioscler Thromb Vasc Biol 2003, 23(5):853-858.
  • [22]Khoo C, Campos H, Judge H, Sacks FM: Effects of estrogenic oral contraceptives on the lipoprotein B particle system defined by apolipoproteins E and C-III content. J Lipid Res 1999, 40(2):202-212.
  • [23]Ebara T, Ramakrishnan R, Steiner G, Shachter NS: Chylomicronemia due to apolipoprotein CIII overexpression in apolipoprotein E-null mice. Apolipoprotein CIII-induced hypertriglyceridemia is not mediated by effects on apolipoprotein E. J Clin Invest 1997, 99(11):2672-2681.
  • [24]Luc G, Fievet C, Arveiler D, Evans AE, Bard JM, Cambien F, Fruchart JC, Ducimetiere P: Apolipoproteins C-III and E in apoB- and non-apoB-containing lipoproteins in two populations at contrasting risk for myocardial infarction: the ECTIM study. Etude Cas Temoins sur 'Infarctus du Myocarde. J Lipid Res 1996, 37(3):508-517.
  • [25]Jong MC, Rensen PC, Dahlmans VE, van der Boom H, van Berkel TJ, Havekes LM: Apolipoprotein C-III deficiency accelerates triglyceride hydrolysis by lipoprotein lipase in wild-type and apoE knockout mice. J Lipid Res 2001, 42(10):1578-1585.
  • [26]Krauss RM: Atherogenicity of triglyceride-rich lipoproteins. Am J Cardiol 1998, 81(4A):13B-17B.
  • [27]Chien KL, Hsu HC, Sung FC, Su TC, Chen MF, Lee YT: Hyperuricemia as a risk factor on cardiovascular events in Taiwan: The Chin-Shan Community Cardiovascular Cohort Study. Atherosclerosis 2005, 183(1):147-155.
  • [28]Jungner I, Marcovina SM, Walldius G, Holme I, Kolar W, Steiner E: Apolipoprotein B and A-I values in 147576 Swedish males and females, standardized according to the World Health Organization-International Federation of Clinical Chemistry First International Reference Materials. Clin Chem 1998, 44(8 Pt 1):1641-1649.
  • [29]Navab M, Reddy ST, Van Lenten BJ, Anantharamaiah GM, Fogelman AM: The role of dysfunctional HDL in atherosclerosis. J Lipid Res 2009, 50(Suppl):S145-S149.
  • [30]Zheng L, Nukuna B, Brennan ML, Sun M, Goormastic M, Settle M, Schmitt D, Fu X, Thomson L, Fox PL, et al.: Apolipoprotein A-I is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease. J Clin Invest 2004, 114(4):529-541.
  文献评价指标  
  下载次数:22次 浏览次数:19次