Shim Chi Young, Park Sungha, Yoon Se-Jung, Park Hyun-Young, Kim Hung Tae, Oh Bermseok, Park Chanmi, Ko Young-Guk, Choi Donghoon, Jang Yangsoo, Chung Namsik
Division of Cardiology, Cardiovascular Research Institute, Yonsei University College of Medicine, Seoul, South Korea.
Cardiology. 2007;107(4):261-8. doi: 10.1159/000095516. Epub 2006 Sep 4.
Interaction between advanced glycosylation end products (AGEs) and receptor for AGEs (RAGE) in vessel wall may lead to inflammation, smooth muscle cell proliferation, and extracellular matrix production, culminating in exaggerated intimal hyperplasia and restenosis. We investigated the possibility that single nucleotide polymorphisms of the genes encoding RAGE are associated with in-stent restenosis after coronary stenting.
Our study included 334 consecutive non-diabetic male patients with symptomatic coronary artery disease who underwent bare metal stent implantation. Follow-up angiography was performed in 297 patients (88.9%), 6 months after intervention. We screened -1106T-->C, -443T-->C, -388T-->A, -257G-->A, +557G-->A and +1704G-->T RAGE polymorphisms in these patients. Genotyping was performed by single base extension with amplifying primers and probes for TaqMan.
A total of 355 target lesions were evaluated, in 297 patients. There was no significant association of the -1106T-->C, -443T-->C, -388T-->A, -257G-->A, +557G-->A or +1704G-->T polymorphisms with in-stent restenosis after coronary artery stenting. We did not observe a significant difference between the genotype distributions and the rates of angiographic restenosis between the polymorphisms. In a multivariate analysis of angiographic restenosis, we examined the possible influence of the baseline, lesion-related, and procedural variables. After adjustment for these potentially confounding factors, the multivariate analysis did not reveal an association of polymorphism with angiographic restenosis.
Our observation suggests that the RAGE gene polymorphism is not associated with in-stent restenosis after coronary artery stenting in non-diabetic patients in the Korean population.
血管壁中晚期糖基化终末产物（AGEs）与AGEs受体（RAGE）之间的相互作用可能导致炎症、平滑肌细胞增殖和细胞外基质生成，最终导致内膜增生过度和再狭窄。我们研究了编码RAGE的基因单核苷酸多态性与冠状动脉支架置入术后支架内再狭窄相关的可能性。
我们的研究纳入了334例连续的有症状冠心病非糖尿病男性患者，这些患者接受了裸金属支架植入术。297例患者（88.9%）在干预6个月后进行了随访血管造影。我们在这些患者中筛查了RAGE基因的-1106T→C、-443T→C、-388T→A、-257G→A、+557G→A和+1704G→T多态性。通过使用TaqMan的扩增引物和探针进行单碱基延伸来进行基因分型。
共评估了297例患者的355个靶病变。-1106T→C、-443T→C、-388T→A、-257G→A、+557G→A或+1704G→T多态性与冠状动脉支架置入术后支架内再狭窄之间无显著关联。我们未观察到多态性之间的基因型分布和血管造影再狭窄率有显著差异。在血管造影再狭窄的多因素分析中，我们检查了基线、病变相关和手术变量的可能影响。在对这些潜在混杂因素进行调整后，多因素分析未显示多态性与血管造影再狭窄有关联。
我们的观察结果表明，在韩国人群的非糖尿病患者中，RAGE基因多态性与冠状动脉支架置入术后支架内再狭窄无关。
