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.
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.
authors.affiliation: Franz-Volhard-Klinik, Charité-Universitätsmedizin Berlin, Berlin, Germany.
authors.forename: C Michael
authors.initials: CM
authors.lastname: Gross
authors.forename: Andreas
authors.initials: A
authors.lastname: Perrot
authors.forename: Christian
authors.initials: C
authors.lastname: Geier
authors.forename: Maximillian G
authors.initials: MG
authors.lastname: Posch
authors.forename: Sabine
authors.initials: S
authors.lastname: Hassfeld
authors.forename: Jochen
authors.initials: J
authors.lastname: Kramer
authors.forename: Sibylle
authors.initials: S
authors.lastname: Schmidt
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Derer
authors.forename: Rainer
authors.initials: R
authors.lastname: Dietz
authors.forename: Cemil
authors.initials: C
authors.lastname: Ozcelik
mesh_terms: D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000808:Angiotensinogen / Q000235:genetics*; D049109:Cell Proliferation; D017023:Coronary Angiography; D023903:Coronary Restenosis / Q000453:epidemiology / Q000235:genetics* / Q000503:physiopathology; D003920:Diabetes Mellitus / Q000453:epidemiology; D005260:Female; D017353:Gene Deletion; D019382:Human Growth Hormone; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000628:therapy; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics*; D012008:Recurrence; D012084:Renin-Angiotensin System / Q000235:genetics; D015607:Stents / Q000009:adverse effects*
chemical_list: D044140:Receptor, Angiotensin, Type 1; D000808:Angiotensinogen; D019382:Human Growth Hormone; D007703:Peptidyl-Dipeptidase A