European Heart Journal Advance Access published online on March 30, 2007
European Heart Journal, doi:10.1093/eurheartj/ehm036
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Heme oxygenase-1 gene promoter polymorphism and restenosis following coronary stenting
Deutsches Herzzentrum München, 1. Medizinische Klinik Rechts der Isar, Technische Universität München, Lazarettstrasse 36, München D-80636, Germany
Received 30 July 2006; revised 13 December 2006; accepted 1 February 2007.
* Corresponding author. Tel: +49 89 1218 4073; fax: +49 89 1218 4013. E-mail address: klaustiroch{at}hotmail.com
Aims: Gene expression analyses, cell culture experiments, animal models, and association studies suggest a protective role of the heme oxygenase-1 (HO-1) protein against restenosis. The length of a polymorphic (GT)n dinucleotid repeats sequence in the HO-1 gene promoter influences the transcriptional activity. We evaluated, whether an association existed between this polymorphism and the incidence of restenosis after coronary stenting.
Methods and results: Of the 1807 consecutive patients included in this study, 1357 (75%) patients had 6 months follow-up angiography. Restenosis, the primary endpoint, was defined as angiographic restenosis, diameter stenosis of 
50%, and clinical restenosis, target vessel revascularization during the first year. The combined 1 year incidence of death and myocardial infarction (MI) was evaluated as secondary endpoint. We divided the alleles similar to previous studies: class S less repeats (<25), and class L more repeats (25), leading to SS, SL, and LL genotypes. Angiographic restenosis rate showed no significant difference for the studied genotypes—SS 29.2%, SL 29.5%, and LL genotype 29.6% (P = 0.99). There was no significant difference regarding clinical restenosis (P = 0.28) and combined incidence of death or MI (P = 0.98).
Conclusion: This study does not support a clinically relevant association of the HO-1 promoter polymorphism with restenosis and ischaemic events after coronary stenting.
Key Words: Heme oxygenase • Restenosis • Stent • Polymorphism • Genetics
All authors have reviewed the manuscript and are supporting its submission to the European Heart Journal. Tables, illustrations or figures are original and not duplicated from previously published work so no further written permission is necessary.
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