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.
Association of seven renin angiotensin system gene polymorphisms with restenosis in patients following coronary stenting
Min Zhu,Minjun Yang,Jiangbo Lin,Huanhuan Zhu,Yifei Lu,Bing Wang,Yinshen Xue,Cong-feng Fang,Li-jiang Tang,Baohui Xu,Jianjun Jiang,Xiaofeng Chen
Published 2017 in Journal of the Renin-Angiotensin-Aldosterone System
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- Publication year
2017
- Venue
Journal of the Renin-Angiotensin-Aldosterone System
- Publication date
2017-01-01
- Fields of study
Medicine
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- Source metadata
Semantic Scholar, PubMed
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