期刊文献+

不稳定型心绞痛病人血清载脂蛋白A、B与冠状动脉造影血管病变的关系 被引量:4

CORRELATION BETWEEN SERUM APOLIPOPROTEIN A and B AND THE SEVERITY OF CORONARY ARTERIOPATHY
下载PDF
导出
摘要 ①目的探讨不稳定型心绞痛病人血清载脂蛋白A、B(apoA、apoB)及相关脂类,抗凝、纤溶指标与冠状动脉病变的关系.②方法选择行冠状动脉造影病人173例,其中不稳定型心绞痛病人136例,均经冠状动脉造影证实至少一支冠状动脉狭窄>70%,其中单支病变65例,双支或多支病变71例,冠状动脉造影正常者(对照组)37例.采空腹静脉血2 mL检测生化全套.③结果对照组、单支病变组、多支病变组apoB、三酰甘油(TG)、总胆固醇(TC)、抗凝血酶Ⅲ、纤维结合蛋白水平及apoB/apoA比较有显著统计学意义(F=3.70~6.08,P<0.05);而apoA1、纤溶酶原各组间差异无显著性(F=0.09、2.78,P>0.05).apoB、TG、纤溶酶原、纤维结合蛋白含量及apoB/apoA与冠状动脉积分呈正相关(r=0.502~0.605,P<0.05),apoA1与冠状动脉积分呈负相关(r=-0.601,P<0.01).④结论apoB、apoB/apoA的升高是冠心病的危险因素,并与冠状动脉病变的严重程度有关. Objective To investigate the relationship between coronary arteriopathy and serum relative markers including apoA, apoB, other related lipids, antithrombin Ⅲ, profibrinolysin and fibronectin in unstable angina patients. Methods One hundred and seventy-three patients were divided into unstable angina group (n=136) and control group (n=37) by coronary arteriography. The unstable angina patients who had one or more coronary obstructions greater than 70% were sub-divided into a singlevascular lesion group (n=65) and a multiple vascular lesion group (n=71). All blood samples were taken after fasting and then serum relative markers were determined. Results There were significant differences in apoB,TG, TC, AntithrombinⅢ, fibronectin and apoB/apoA among the three groups (F=3.70-6.08,P〈0.05) but not in apoA1 and profibrinolysin (F=0.09, 2.78;P〉0.05). ApoB, apoB/apoA, TG, profibrinolysin and fibronectin were positively correlated with coronary artery stenosis scores(r=0. 502-0.605, P〈0.05) while apoA1 was negatively correlated (r=-0.601, P〈0.01). Conclusion The increase of apoB and apoB/apoA is one of the risk factors of CHD, and is related to the severity of CHD.
出处 《青岛大学医学院学报》 CAS 2005年第2期121-122,124,共3页 Acta Academiae Medicinae Qingdao Universitatis
关键词 心绞痛 不稳定型 载脂蛋白类 冠状动脉造影术 angina,unstable apolipoprotein coronary angiography
  • 相关文献

参考文献7

  • 1Austin MA,Breslon JL,Hennekens CH,et al. Low dencity lipoprotein subclass parttens and risk of myocardial infarction[J].JAMA, 1988,82:495. 被引量:1
  • 2赵水平主编..临床血脂学[M].长沙:湖南科学技术出版社,1997:446.
  • 3Banka CL, Black AS, Curtiss LK. Localization of an apolipoprotein A-1 epitope critical for lipoprotein-mediated cholesterol efflux from monocytic cells [J]. J Biol Chem, 1994,269:10288. 被引量:1
  • 4Minnich A, Collet X, Toghami A, et al. Sitedirected mutagenesis and structure-function analysis of human apolipoprotein A-1: relationship between LCAT activation and lipid binding[J]. JBiolChem, 1992, 267:16553. 被引量:1
  • 5武晓静.不稳定斑块的基因治疗[J].心血管病学进展,2002,23(3):177-179. 被引量:5
  • 6徐燕华,傅明德.载脂蛋白与细胞胆固醇移出[J].心血管病学进展,2001,22(2):82-84. 被引量:2
  • 7Hara H, Yokoyama S. interaction of free apolipoprotein with macrophages: formation of high density lipoprotein-like lipoproteins and reduction of cellular cholesterol[J]. Biol Chem,1991,266: 3080. 被引量:1

二级参考文献19

  • 1[1]Conti CR. Updated pathophysiologic concepts in unstable coronary artery disease [J]. Am Heart J,2001 ,141(2 suppl) :S12-S14.JJ, Yang H, et al. Monoclonal T-cell proliferation and zzo G, Goronzy 被引量:1
  • 2[2]Liuplaque instability in acute coronary syndromes[J]. Circulation, 2000, 101:2883-2888. 被引量:1
  • 3[3]Stulc T, Ceska R. Cholesterol lowering and the vessel wall: new insights and future perspectives[J]. Physiol Res,2001,50:461-471 被引量:1
  • 4[4]Wilson JM, Chowdhury NR, Grossman M, et al. Temporary amelioration of hyperlipidemia in low density lipoprotein receptor-deficient rabbita transplanted with genetically modified hepatocytes[J]. Proc Natl Acad Sci lISA,1990,87: 8437-8441. 被引量:1
  • 5[5]Wilson JM. Clinical protocol. Ex vivo gene therapy of familial hypercholesterolemia[J]. Hum Gene Ther, 1992,3:179-222. 被引量:1
  • 6[6]Kohayashi K, Oka K. Reversal of hypercholesterolemia in low denaity lipoprotein receptor knockout mice by adenovirus-mediated gene transfer of the very low density lipoprotein receptor[J]. J Biol Chem ,1996,271:6852-6860. 被引量:1
  • 7[7]Benoit P, Emmanuel F, Caillaud JM, et a1. Somatic gene transfer of human ApoA-1 inhibits atherosclerosis progression in mouse models[J]. Circulation, 1999,99:105-110. 被引量:1
  • 8[8]Hughes SD, Verstuyft J, Rubin EM, et al. HDL deficiency in genetically engineered mice requires elevated LDL to accelerate atherogenesis[J]. Arterioscler Thromb Vasc Biol, 1997,17 : 1725-1729. 被引量:1
  • 9[9]George SJ. Therapeutic potential of matrix metalloproteinase inhibitors in atherosclerosis[J]. Expert Opin Investig Drugs, 2000, 9:993-1007. 被引量:1
  • 10[10]Ricote M, Li A, Wilson T, et al. The peroxisome proliferater-activated receptor- is a negative regulator of macrophage activation [J]. Nature,1998,391 : 79-82. 被引量:1

共引文献5

同被引文献18

引证文献4

二级引证文献15

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部