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.
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.
Gross
C Michael
CM
Franz-Volhard-Klinik, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Perrot
Andreas
A
Geier
Christian
C
Posch
Maximillian G
MG
Hassfeld
Sabine
S
Kramer
Jochen
J
Schmidt
Sibylle
S
Derer
Wolfgang
W
Dietz
Rainer
R
Ozcelik
Cemil
C
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*
D044140:Receptor, Angiotensin, Type 1; D000808:Angiotensinogen; D019382:Human Growth Hormone; D007703:Peptidyl-Dipeptidase A