Recurrent in-stent restenosis is not associated with the angiotensin-converting enzyme D/I, angiotensinogen Thr174Met and Met235Thr, and the angiotensin-II receptor 1 A1166C polymorphism

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Title:	Recurrent in-stent restenosis is not associated with the angiotensin-converting enzyme D/I, angiotensinogen Thr174Met and Met235Thr, and the angiotensin-II receptor 1 A1166C polymorphism
Creators Name:	Gross, C.M., Perrot, A., Geier, C., Posch, M.G., Hassfeld, S., Kramer, J., Schmidt, S., Derer, W., Dietz, R. and Oezcelik, C.
Abstract:	Although great progress has been made in reducing renarrowing of the lumen after stenting of coronary arteries, a considerable number of patients develop recurrent in-stent stenosis. Several studies suggest that neointimal proliferation is the crucial pathophysiological process underlying restenosis after stenting. The renin-angiotensin-aldosterone system (RAS) has been implicated in the development of neointimal hyperplasia. We tested the hypothesis that polymorphisms of the RAS genes are associated with recurrent in-stent restenosis (ISR). Coronary stent implantation was performed in 272 patients with clinical symptoms or objective signs of ischemia. At follow-up angiography 6 months after stenting, 81 patients (29.8%) revealed in-stent restenosis. These patients underwent balloon angioplasty and were scheduled for a further 6 months of follow up. One year after initial stenting of the coronary artery, 39 patients displayed no significant angiographic ISR, whereas 42 patients developed recurrent in-stent restenosis (RISR). The survey of specific functional polymorphisms of the RAS, namely the angiotensin-I converting enzyme (ACE) D/I, the angiotensinogen (AGT) T174M and M235T, and A1166C of the angiotensin-II receptor 1 (AGTR1), revealed that the incidence RISR in the high-risk cohort was not associated with any of the polymorphisms examined in this study.
Keywords:	Angiotensinogen, Cell Proliferation, Coronary Angiography, Coronary Balloon Angioplasty, Coronary Restenosis, Diabetes Mellitus, Gene Deletion, Genetic Polymorphism, Human Growth Hormone, Myocardial Ischemia, Peptidyl-Dipeptidase A, Recurrence, Renin-Angiotensin System, Stents, Type 1 Angiotensin Receptor
Source:	Journal of Invasive Cardiology
ISSN:	1042-3931
Publisher:	Health Management Publications
Volume:	19
Number:	6
Page Range:	261-264
Date:	1 June 2007
Official Publication:	http://www.invasivecardiology.com/article/7304
PubMed:	View item in PubMed

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