男性血脂水平与冠状动脉狭窄程度的相关性研究
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摘要
目的:探讨在男性无糖尿病史、吸烟史、家族史人群中,血脂水平与冠状动脉狭窄程度的相关关系,了解血脂水平在此类患者中的对冠状动脉狭窄程度的预测价值,为冠心病的预防与治疗提供依据。
     方法:采用回顾性病例分析,查阅2007年1月至2007年12月在山东省立医院介入中心行冠状动脉造影检查患者共计842例,选择符合条件的患者96例。取空腹血浆,测定TC、TG、HDL-C、LDL-C、ApoAI、ApoB、Lp(a)、FBG、DB、TB、UA,并记录年龄、血压等临床资料,采用GS计算冠状动脉狭窄程度。依据狭窄程度大于50%的主要血管支数,分为对照组、单支、双支、多支病变组;依据GS值由低到高排序,以四分位数为节点分为0-16、17-40、41-72及74以上组。分析在各分组中血脂各成份与冠状动脉病变程度的相关关系及各血脂间,血脂与其他因素间相互作用对冠状动脉狭窄程度的影响。
     结果:TC、LDL-C、年龄在多支病变组均显著高于其他各组,并与冠状动脉狭窄支数成显著性正相关(P<0.001);DB在多支病变组显著低于其他各组,并与冠状动脉狭窄支数成显著性负相关(P=0.010);ApoB、Lp(a)与冠状动脉狭窄支数成正相关,P值分别为0.014、0.024,但两者在不同冠状动脉狭窄支数间差异均未达到统计学显著性;TG、HDL-C、ApoAI、FBG、TB、UA及血压与冠状动脉狭窄支数间相关性无统计学意义。不同GS组间,TC、LDL-C均存在显著性差异(P<0.05),在偏相关分析中与GS成显著性正相关,P值分别为0.036,0.001;Lp(a)、年龄在不同GS组间差异明显(P<0.05),但随分值的增加表现出先增加后降低趋势,最高值分别位于17-40及41-74组,与GS的偏相关关系未达到统计学意义;TG、HDL-C、ApoAI、ApoB、FBG、DB、TB、UA及血压在不同GS组间差异均无统计学意义,且偏相关关系均未达到统计学显著性。多元线性回归显示:男性GS受年龄、脉压、FBG、HDL-C、LDL-C影响显著,回归方程为:GS=1.061年龄-0.799脉压+9.401 FBG-15.657 HDL-C+18.992 LDL-C-58.466。
     结论:TC、LDL-C、Lp(a)、ApoB与冠状动脉狭窄程度之间存在正相关关系,HDL-C与冠状动脉狭窄程度呈负相关,TG、ApoAI在本研究中未得出与冠状动脉狭窄程度间存在相关性;血脂水平可以预测冠状动脉狭窄的严重程度,尤其是TC及LDL-C。
Objectives Investigating the correlation between serum lipids concentration and existence as well as severity of coronary atherosclerosis in the men with no diabetes mellitus, Cigarette smoking and family history, to help identify the predicting value of serum lipids concentration in these people and provide evidence for the prevention and therapeutics of coronary artery disease.
     Methods A retrospective study was conducted on 96 patients fitting the admission standards from the 842 ones who underwent their first angiography in the Intervention Center of Shandong Provincial Hospital between January and December in 2007. Fasting serum concentrations of TC,TG,HDL-C,LDL-C, Lp(a),ApoAI,ApoB, FBG,DB,TB,UA were measured, also the Age, Blood pressure and other clinical data were collected; the severity of coronary artery stenosis was evaluated by the GS. All patients were classified as control group, single-vessel group, double-vessel group and multiple-vessel group, according to the number of main coronary arteries which stenosis was more than 50% diameter; and were assigned into the following quartiles: 0-16,17-40, 41-72,and above 74, according to the GS. The correlativity between every serum lipids concentration and the extent of coronary artery stenosis were analyzed and the interaction between serum lipids and other factors were also studied to identify the their influence to the severity of coronary artery stenosis.
     Results TC, LDL-C and Age were significantly higher in the multiple-vessel group than in the other group, and were demonstrated to be highly significantly (P<0.001) associated with the number of stenotic coronary arteries; DB was significantly lower in the multiple-vessel group than in the other group and had a significant negative correlation with the number of stenotic coronary arteries (P=0.010); ApoB, Lp(a) had positive correlation with the number of stenotic coronary arteries(P=0.014 and 0.024, respectively), but the differences between the groups had no significance; There were no relationship between the number of stenotic coronary arteries and TG,HDL-C, ApoAI, FBG,TB,UA, Blood Pressure. TC and LDL-C had no significant difference between different GS groups, but significant positive correlation with the GS in the partial correlation analysis (P=0.036 and 0.001, respectively); The partial correlativity between Lp(a),Age and the GS had no significance, but the differences between distinct GS groups were significant, and highest value were located in 17-40 and 41-74 group respectively; Other observed factors had no significance not only in the comparison between different GS groups, but also in the partial correlation analysis with the GS. By multiple linear regression, there were significant relationships between Age, pulse pressure, FBG, HDL-C, LDL-C and GS in men. The regression equation was: GS=1.061age-0.799pulse pressure+9.401FBG-15.657HDL-C+18.992LDL-C-58.466.
     Conclusions There was a negative correlation for HDL-C, and positive correlations for TC, LDL-C, Lp(a), ApoB, and no significant correlation for TG, ApoAI, with the severity of coronary stenosis; The serum lipids concentration can predict the severity of coronary, especially the TC and LDL-C.
引文
[1]He J,Gu D,Wu X,et al.Major causes of death among men and women in China.N Engl J Med,2005;353(11):1124-1134.
    [2]Sidney C,Smith JR,Greenland P.et al.Prevention Conference V:Beyond Secondary Prevention:Identifying the high-risk patient for primary prevention:executive summary.Circulation.2000;101:111-116.
    [3]Goraya TY,Leibson CL,Palumbo PJ,et al.Coronary atherosclerosis in diabetes mellitus:a population-based autopsy study.J Am Coll Cardiol.2002;40:946-953.
    [4]Rachel H,Federica B,Mark W.Excess risk of fatal coronary heart in men and women:meta-analysis disease associated with diabetes of 37 prospective cohort studies.BMJ.2006;332:73-78.
    [5]Guthikonda S,Sinkey C,Barenz T,et al.Xanthine oxidase inhibition reverses endothelial dysfunction in heavy smokers.Circulation.2003;107(3):416-421.
    [6]DeVon HA,Zerwic JJ.The symptoms of unstable angina:do women and men differ? Nurs Res.2003;52:108-118.
    [7]Expert Committee on the Diagnosis and Classification of Diabetes Mellitus.Report of the expert committee on the diagnosis and classification of diabetes mellitus.Diabetes Care.2003;26(suppl 1):S5-S20.
    [8]翁新植译.WHO关于吸烟情况调查方法标准化的建议(节译).心肺血管学报.1984;3(1):21.
    [9]Castelnuovo DA,Rotondo S,Iacoviello L.et al.Meta-analysis of wine and beer consumption in relation to vascular risk.Circulation.2002;105(24):2836-2844.
    [10]Gensini GG.A more meaningful scoring system for determining the severity of coronary of coronary heart disease(letter).Am J Cardiol.1983;51:606.
    [11]Casscells W,Naghavi M,Willerson JT.Vulnerable Atherosclerotic Plaque:A Multifocal Disease.Circulation.2003;107(16):2072-2075.
    [12]Parathasarathy S,Steinbery D,Joeeph L.et al.The role of oxidized low density lipoproteins in the pathogenesis of atherosclerosis.Ann Rev Med.1992;43:219.
    [13]Shepherd J,Blauw GJ,Murphy MB,et al.PROSPER study group.Pravastatin in elderly individuals at risk of vascular disease(PROSPER):a randomized controlled trial.PROspective Study of Pravastatin in the Elderly at Risk.Lancet.2002;360:1623-1630.
    [14]Sever PS,Dahlof B,Poulter NR,et al.ASCOT investigators.Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations,in the Anglo-Scandinavian Cardiac Outcomes Trial Lipid Lowering Ann(ASCOT-LLA):a multicentre randomized controlled trial.Lancet.2003;361:1149-1158.
    [15]Grundy SM.Role of low-density lipoproteins in atherogenesis and development of coronary heart disease.Clin Chem.1995;41(1):139-146.
    [16]Expert Panel on Detection,Evaluation,and Treatment of High Blood Cholesterol in Adults(Adult Treatment Panel Ⅲ).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.
    [17]中国成人血脂异常防治指南制订联合委员会.中国成人血脂异常防治指南.2007;35(5):390-419.
    [18]赵水平.降胆固醇防治心脑血管疾病的现状.中华内科杂志.2005;2:168-170.
    [19]von Fckardstein A,Hersberger M,Rohrer L.Current understanding of the metabolism and biological actions of HDL.Curr Opin Clin Nutr Metab Care.2005;8:147- 152.
    [20]Marrugat J,Aoalnas PD,Agostino R,et al.Coronary risk estimation in spaivusinga calibrated Framingham function.Rev Esp Cardiol.2003;56:253-261.
    [21]Gorro AM Jr.High-density lipoprotein cholesterol and triglycerides as therapeutic targets for preventing and treating coronary artery disease.Am Heart J.2002;144(6suppl):S33-S42.
    [22]Cestelli WP,Garrison RJ,Wilson PW,et al.Ineidenee of coronary heart disease and lipoprotein cholesterol levels. The Framingham Study. JAMA.1986;256:2835-2838.
    [23] Nissen SE, Tuzeu EM, Schoenhagen P, et al. Effect of intensive compared moderate lipid-lowering therapy on progression of coronary atherosclerosis.JAMA.2004;291 (9): 1071 -1080.
    [24] Duffy D, Rader DJ. Emerging therapies targeting high-density lipoprotein metabolism and reverse cholesterol transport.Circulation.2006;l 13:1140- 1150.
    [25] Spieker LE , Sudano I, Hurlimann D , et al. High-density lipoprotein restores endothelial function in hypercholesterolemia men. Circulation.2002;105: 1399-1402.
    [26] Barter PJ, Caulfield M, Eriksson M, et al. Effects of torcetrapib in patients at high risk for coronary events. N Engl J Med. 2007; 357: 2109-2122.
    [27] Kastelein JJ, van Leuven SI, Burgess L, et al. Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia. N Engl J Med. 2007; 356:1620-1630.
    [28] Austin MA. Plasma triglyceride and coronary heart disease. Arterioscler Thromb. 1991;11:2-14.
    [29] Jepensen J, Hein H, Suadicani P, et al. Triglyceride concentration and ischemic heart disease: an eight-year follow-up in the Copenhagen male study. Circulation.1998;97(11):1029-1036.
    [30] Shahar E, Chambless LE, Rosamond WD, et al. Plasma lipid profile and incident ischemic stroke; the atherosclerosis risk in communities(ARIC) study. Stroke.2003;34(5):623-631.
    [31] Lamarche B, Despres JP, Moorjam S, et al. Triglycerides and HDL-C as risk factors for ischemic heart disease. Results from the Quebec cardiovascular study.Atherosclerosis. 1996; 119:235-243.
    [32] Patsch JR, Miesenbock G, Hopferwieser T, et al. Relation of triglyceride metabolism and coronary artery disease: studies in the postprandial state.Arterioscler Thromb. 1992;12:1336-1345.
    
    [33] Verschuren WM, Jacobs DR, Bloemberg BP, et al. Serum total cholesterol and Long-term coronary heart disease mortality in different cultures. Twenty-five-year fallow-up of the seven countries srudy.JAMA.1995;274(2):131-136.
    [34] Yazici M, Demircan S, Ibrahimili F, et al. The importance of lipoprotein(a) in pathogenesis of the high risk unstable angina. Anadolu Kardiyol Derg. 2006; 6:13-17.
    [35] Rader DJ, Brewer HB. Lipoprotein(a). Clinical approach to a unique atherogenic lipoprotein. JAMA. 1992;267(8): 1109-1112.
    [36] Lundstam U, Eva HC, Olssonq, et al. Proteoglycans contribution to association of Lp(a) and LDL with smooth muscle cell extracellular matrix. Arterioscler Thromb Vasc Biol.1999;19:1162-1167.
    [37] Galle J, Bengen J, Schollmeyer P, et al. Impairment of endothelium-dependent dilation in rabbit renal arteries by oxidized lipoprotein(a).Circulation.1995;92(6):1582-1589.
    [38] Galle J, Heermeier K, Wanner C. Atherogenic lipoproteins,oxidative stress, and cell death. Kidney Int Suppl.1999;71:S62.
    [39] Kennedy M, Barrera G, Nakamura K, et al. ABCG1 has a critical role in mediating cholesterol efflux to HDL and preventing cellular lipid accumulation.Cell Metab.2005;1(2): 121-131.
    [40] Nissen SE, Tsunoda T, Tuzcu EM, et al. Effect of recombinant apoAI milano on coronary atherosclerosis in patients with acute coronary syndromes:a randomized controlled trial. JAMA.2003;290(11):2292-2300.
    [41] Walldius G, Jungner I. ApolipoproteinB and apolipoproteinAI: risk indicators of coronary heart disease and targets for lipid-modifying therapy. Intern Med.2004;255(2):188-205.
    [42] Corsetti JP, Zareba W, Moss AJ,et al. Apolipoprotein B determines risk for recurrent coronary events in post-infarction patients with metabolic syndrome.Atherosclerosis.2004; 177(2):367-373.
    [43] Luz PL, Cesena F, Favarato DF, et al. Comparison of serum lipid values in patients with coronary artery disease at < 50, 50 to 59,60 to 69, and > 70 years of age. Am J Cardiol.2005;96:1640 - 1643.
    [44]刘浩,余金明,陈芳.冠心病患者血脂代谢异常的流行病学研究.中国实用内科杂志.2007;27.
    [45]Assmann G,Cullen P,Evers T,et al.Importance of arterial pulse pressure as a predictor of coronary heart disease risk in PROCAM.Eur Heart J.2005;26(20):2120-2126.
    [46]Zakopoulos NA,Lekakis JP,Papamichael CM,et al.Pulse pressure in normotensives:a marker of cardiovascular disease.Am J Hypertens.2001;14:195-199.
    [47]Ross R.The Pathogenesis of atherosclerosis:a perspective for the 1990s.Nature.1993;362(6423):801-809.
    [48]苏海军,张鹏飞,张梅等.动脉粥样硬化斑块失稳破裂简化模型的高阶动力学研究.中国生物医学工程学报.2006;25(3):322-327.
    [49]Franklin S,Khan S,Wong N,et al.Is pulse pressure useful in predicting risk for coronary heart disease? The Framingham Heart Study.Circulation.1999;100:354-360.
    [50]祖秀光,武宇洲,崔炜等.脉压水平与冠状动脉病变程度的相关性研究.中国循环杂志.2003;18(3):206-208.
    [51]张戈,楚天舒,阮志敏.冠状动脉病变积分与血压特征的相关性研究.中华心血管病杂志.2004;32(9):802-804.
    [52]Zhao R,Shen GX.Functional modulation of antioxidant enzymes in vascular endothelial cells by glycated LDL.Atherosclerosis.2005;179(2):277-284.
    [53]王亮,吕吉元,范春雨.糖耐量减低合并冠状动脉粥样硬化性心脏病患者冠状动脉病变特点.军医进修学院学报.2007;28(5):360-363.
    [54]Kataoka Y,Yasuda S,morii I,et al.Quantitative coronary angiographic studies of patients with angina pectoris and impaired glucose tolerance.Diabetes Care.2005;28(9):2217-2222.
    [55]Short RA,Johnson RJ,Tuttle KR.Uric acid,microalbuminuria and cardiovascular events in high-risk patients.Am J Nephrol.2005;25:36-44.
    [56]Khosla U,Zhariko V,Finch J,et al.Hyperuricemia induces endothelial dysfunction.Kidney Int.2005;67(5):1739-1742.
    [57]Yu WH,Zhou XM,Wen WC,et al.Gender differences in serum uric acid level and risk factors for coronary artery disease.China Journal of Modem Medicine.2004;14(200):119-122.
    [58]Moriarity JT,Folsom AR,Iribarren C,et al.Serum uric acid and risk of coronary heart disease:atherosclerosis risk in communities(ARIC) study.Ann Epidemiol.2000;10(3):136-143.
    [59]Nieto FJ,Iribarren C,Gross MD,et al.Uric acid and serum antioxidant capacity:a reaction to atherosclerosis.Atherosclerosis.2000;148(1):131-139.
    [60]Schwertner HA,Jackson WG,Tolan G.Association of low serum concentration of bilirubin with increased risk of coronary artery disease.Clin Chem.1994;40(1):18-23.
    [61]Puddu PE,Lanti M,Menotti A,et al.Serum uric acid for short-term prediction of cardiovascular disease incidence in the Gubbio population study.Acta Cardiol.2001;56:243- 251.
    [62]杜戎,梁国芬,杨钧国.血清胆红素与冠心病关系的研究进展.心血管病学进展.2004;25(3):232-234.

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