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七种肾素血管紧张素系统基因多态性与冠状动脉支架置入术后患者再狭窄的相关性

Association of seven renin angiotensin system gene polymorphisms with restenosis in patients following coronary stenting.

作者信息

Zhu Min, Yang Minjun, Lin Jiangbo, Zhu Huanhuan, Lu Yifei, Wang Bing, Xue Yinshen, Fang Congfeng, Tang Lijiang, Xu Baohui, Jiang Jianjun, Chen Xiaofeng

机构信息

1 Laboratory of Cardiovascular Disease, Taizhou Hospital, Wenzhou Medical University, China.

2 Enze Medical Research Center, Taizhou Hospital, Wenzhou Medical University, China.

出版信息

J Renin Angiotensin Aldosterone Syst. 2017 Jan;18(1):1470320316688774. doi: 10.1177/1470320316688774.

Abstract

BACKGROUND AND OBJECTIVE

Percutaneous coronary intervention, despite being effective for coronary revascularization, causes in-stent restenosis due to neointimal hyperplasia in a large number of patients. The renin-angiotensin system is involved in neointimal hyperplasia. This study sought to evaluate seven gene polymorphisms of key renin-angiotensin system components, including angiotensinogen, angiotensin-converting enzyme and angiotensin II type 1a receptors, and their associations with in-stent restenosis in patients with coronary artery disease following coronary stenting.

METHODS AND RESULTS

Three hundred and fifty-two patients undergoing coronary drug-eluting stent implantation were recruited. Seventy-five patients (21.3%) were diagnosed as restenosis by angiography. Genotyping for angiotensin-converting enzyme insertion/deletion demonstrated a significant association of angiotensin-converting enzyme DD genotype with the occurrence of restenosis. Direct DNA sequencing revealed no association of angiotensinogen (M235T, G217A, G152A, G-6A, and A-20C) or angiotensin II type I receptor A1166C polymorphisms with in-stent restenosis. However, angiotensin II type 1a A1166C polymorphism was significantly associated with increased susceptibility to restenosis in a subgroup of patients aged more than 60 years.

CONCLUSION

Thus, our study suggests that genetic polymorphisms of angiotensin-converting enzyme insertion/deletion are associated with in-stent restenosis in coronary artery disease patients following coronary stenting.

摘要

背景与目的

经皮冠状动脉介入治疗尽管对冠状动脉血运重建有效,但在大量患者中会因新生内膜增生导致支架内再狭窄。肾素 - 血管紧张素系统参与新生内膜增生过程。本研究旨在评估肾素 - 血管紧张素系统关键成分的七个基因多态性,包括血管紧张素原、血管紧张素转换酶和血管紧张素II 1a型受体,以及它们与冠状动脉疾病患者冠状动脉支架置入术后支架内再狭窄的相关性。

方法与结果

招募了352例行冠状动脉药物洗脱支架植入术的患者。75例患者(21.3%)经血管造影诊断为再狭窄。血管紧张素转换酶插入/缺失基因分型显示血管紧张素转换酶DD基因型与再狭窄的发生显著相关。直接DNA测序显示血管紧张素原(M235T、G217A、G152A、G - 6A和A - 20C)或血管紧张素II 1型受体A1166C多态性与支架内再狭窄无相关性。然而,血管紧张素II 1a型A1166C多态性在年龄大于60岁的患者亚组中与再狭窄易感性增加显著相关。

结论

因此,我们的研究表明血管紧张素转换酶插入/缺失的基因多态性与冠状动脉疾病患者冠状动脉支架置入术后的支架内再狭窄相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d73/5843879/c07f0b0652f6/10.1177_1470320316688774-fig1.jpg

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