Völzke Henry, Grimm Rita, Robinson Daniel M, Wolff Birger, Schwahn Christian, Hertwig Sabine, Motz Wolfgang, Rettig Rainer
Institute of Epidemiology and Social Medicine, Ernst Moritz Arndt University, Walther Rathenau Strasse 48, D-17487 Greifswald, Germany.
Clin Sci (Lond). 2004 Jan;106(1):35-42. doi: 10.1042/CS20030042.
The aim of the present study was to test for possible associations between candidate gene polymorphisms and the risk of restenosis and recurrent restenosis after percutaneous transluminal coronary angioplasty (PTCA) without stenting. We followed up 511 PTCA patients, and restenosis and recurrent restenosis were defined according to angiographical criteria. Genotyping of the beta-fibrinogen -455 G/A, glycoprotein (GP) IIIa PlA1/PlA2, plasminogen activator inhibitor-1 (PAI-1) 4G/5G, factor V Leiden 1691 G/A, tumour necrosis factor alpha (TNFalpha) -238 G/A, TNFalpha -308 G/A, interleukin (IL)-1alpha -889 C/T, IL-1beta -511 C/T, methylenetetrahydrofolate reductase (MTHFR) 677 C/T and endothelial nitric oxide synthase (eNOS) 4 b/a gene polymorphisms was performed by PCR and restriction-fragment-length-polymorphism-based techniques. One hundred and sixty patients (31.3%) developed restenosis and in 130 of these patients, of whom 123 were available for analysis, a second PTCA without stenting was performed. Of these patients, 35 (28.5%) developed recurrent restenosis. None of the investigated genotypes were associated with the risk of restenosis or recurrent restenosis after PTCA. The degree of stenosis before and immediately after PTCA and the severity of the lesion were independent predictors for restenosis after PTCA. In conclusion, there was no association between the beta-fibrinogen -455 G/A, GP IIIa PlA1/A2, PAI-1 4G/5G, factor V Leiden 1691 G/A, TNFalpha -238 G/A, TNFalpha -308 G/A, IL-1alpha -889 C/T, the IL-1beta -511 C/T, MTHFR 677 C/T and eNOS 4 b/a gene polymorphisms and the risk of restenosis after PTCA as well as recurrent restenosis after repeated PTCA.
本研究的目的是检测候选基因多态性与无支架经皮腔内冠状动脉成形术（PTCA）后再狭窄及复发性再狭窄风险之间的可能关联。我们对511例PTCA患者进行了随访，并根据血管造影标准定义再狭窄和复发性再狭窄。采用基于聚合酶链反应（PCR）和限制性片段长度多态性的技术，对β-纤维蛋白原-455 G/A、糖蛋白（GP）IIIa PlA1/PlA2、纤溶酶原激活物抑制剂-1（PAI-1）4G/5G、凝血因子V莱顿1691 G/A、肿瘤坏死因子α（TNFα）-238 G/A、TNFα -308 G/A、白细胞介素（IL）-1α -889 C/T、IL-1β -511 C/T、亚甲基四氢叶酸还原酶（MTHFR）677 C/T和内皮型一氧化氮合酶（eNOS）4 b/a基因多态性进行基因分型。160例患者（31.3%）发生再狭窄，其中130例患者（123例可供分析）接受了第二次无支架PTCA。在这些患者中，35例（28.5%）发生复发性再狭窄。所研究的基因型均与PTCA后再狭窄或复发性再狭窄风险无关。PTCA前后的狭窄程度及病变严重程度是PTCA后再狭窄的独立预测因素。总之，β-纤维蛋白原-455 G/A、GP IIIa PlA1/A2、PAI-1 4G/5G、凝血因子V莱顿1691 G/A、TNFα -238 G/A、TNFα -308 G/A、IL-1α -889 C/T、IL-1β -511 C/T、MTHFR 677 C/T和eNOS 4 b/a基因多态性与PTCA后再狭窄风险以及重复PTCA后复发性再狭窄均无关联。
