急性冠状动脉综合症患者血清肿瘤坏死因子-α变化的临床意义被引量：8

Clinical Value of the Changing TNF-α in the Serum of ACS Patients

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摘要目的探讨肿瘤坏死因子-α(TNF-α)在急性冠状动脉综合征(ACS)患者血清中浓度变化及其意义。方法选取40例ACS患者,其中不稳定型心绞痛(UAP)患者19例,急性心肌梗死(AMI)患者21例。60例非ACS患者,其中稳定型心绞痛(SAP)患者21例,陈旧性心肌梗死(OMI)患者19例。冠状动脉造影正常者20例为正常对照组,采用放射免疫法测定上述病例的血清TNF-α浓度。结果SAP、UAP、AMI、OMI患者血清TNF-α浓度均显著高于正常对照组。ACS组血清TNF-α水平显著高于非ACS组;AMI组血清TNF-α水平显著高于UAP组;SAP组与OMI组血清TNF-α水平无显著性差异;SAP与UAP患者冠状动脉狭窄程度比较无显著性差异。结论TNF-α参与冠心病的形成,并且在ACS的发病中起重要作用。检测血清TNF-α浓度将有助于诊断和预测ACS的发生、发展和预后。

作者许英淑崔惠润

机构地区吉林市医院心血管内科

出处《中国心血管杂志》 2006年第3期208-209,共2页 Chinese Journal of Cardiovascular Medicine

关键词急性冠状动脉综合征肿瘤坏死因子-Α

分类号 R541.4 [医药卫生—心血管疾病]

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参考文献7

1Ridker PM, Rifai N, Pfeffer M, et al. Elevatoin of tamomecrosis facto-alpha and increased risk of recurrent coronary events after myocardial infarction[J]. Circulation, 2000,101 : 2149-2153.
2Isner JM, Keamey M, Bortman S, et al. Apoptosis in human atherosclerosis and restenosis [ J ]. Circulation, 1995, 91 : 2703-2711.
3Brown DI, Hibbs MS, Kearney M, et al. Identification of 92-KD gelatinase in human coronary atheroscierotic lesions[J]. Circulatoin, 1995,91:2125-2131.
4Cedis ZS, Sukhoua GK, Lark MW, et al. Increased expression of matrix metal-loproreinases and matrix degrading activity. In vulnerable regions of human atherosclerotic plaques[J]. J Clin Ivest, 1994,94 : 2493-2503.
5杨中苏,刘以林,王士雯.冠状动脉粥样硬化斑块的稳定性研究进展[J].国外医学（老年医学分册）,2001,22(3):97-99. 被引量：13
6Entman ML, Smith WC. Postreper fusion inflammation a model for reaction to injury in cardiovascular disease [J]. Cardiovasc Res, 1994,28:1301-1311.
7刘丁,赵丽.急性心肌梗死患者肿瘤坏死因子的动态变化[J].中华内科杂志,2000,39(7):499-499. 被引量：12

二级参考文献15

1[1]Zaman AG, Helft G, Worthley SG et al. The role of plaqe rupture and thrombosis in coronary artery disease. Atherosclerosis, 2000;149(2)∶251～266
2[2]Abedi H, Zachary J. Signalling mechanisms in the regulation of vascular cell migration. Cardiovase Res, 1995;30∶544～556
3[3]Bennett MR, Maedonald K, Chan SW et al. Cooperative interactions between RB and p53 regulate cell proliferation, cell senecence and apoptosis in human vascular smooth muscle cells from atherosclerotic plaques. Circ Res, 1998;82∶704～712
4[4]Yonemitsu Y, Kaneda Y, Tanaka S et al. Transfer of wild-type p53 gene effectively inhibits vascular smooth muscle cell proliferation in vitro and in vivo. Circ Res, 1998;82∶147～156
5[5]Libby P. Molecular basis of the acute coronary syndromes. Circulation, 1995;91∶2844～2850
6[6]Isner JM, Kearney M, Bortman S et al. Apoptosis in human atherosclerosis and restenosis. Circulation, 1995;91∶2703～2711
7[7]Vander Wal AC, Becker AE. Clinically stable angina is not necessarily associated with histologically stable atherosclerotic plaques. Heart, 1996;76∶112～117
8[8]Aikawa M, Rabkin E, Okada Y et al. Lipid lowering by diet reduces matrix metalloproteinase activity and increases collagen content of rabbit atheroma: A potential mechanism of lesion stabilization. Circulation, 1998;97∶2433～2444
9[9]Treasure CB, Klein JL, Wintraub WS et al. Beneficial effects of cholesterol-lowering therapy on the coronary endothelium in patients with coronary artery disease. N Engl J Med, 1995;332∶481～487
10[10]Vanden Heuvel JP. Peroxisome Proliferator activeted receptors: a critical link among fatty acids, gene expression and carcinogenosis. J Nutr, 1999;129∶575～580