Clinical Chemistry Link to Randox Laboratories Web Site
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Clinical Chemistry 51: 1661-1665, 2005. First published July 14, 2005; 10.1373/clinchem.2005.051581
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
clinchem.2005.051581v1
51/9/1661    most recent
Right arrow Submit an electronic Letter to
the Editor about this paper
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (7)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gulesserian, T.
Right arrow Articles by Huber, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gulesserian, T.
Right arrow Articles by Huber, K.
Related Collections
Right arrow Molecular Diagnostics and Genetics
Right arrow Lipids, Lipoproteins, and Cardiovascular Risk Factors
(Clinical Chemistry. 2005;51:1661-1665.)
© 2005 American Association for Clinical Chemistry, Inc.


Lipids, Lipoproteins, and Cardiovascular Risk Factors

Clinical Restenosis after Coronary Stent Implantation Is Associated with the Heme Oxygenase-1 Gene Promoter Polymorphism and the Heme Oxygenase-1 +99G/C Variant

Talin Gulesserian1,2,2, Catharina Wenzel4,2, Georg Endler1, Raute Sunder-Plassmann1, Claudia Marsik1, Christine Mannhalter1, Nelly Iordanova4, Mariann Gyöngyösi3, Johann Wojta3, Stefan Mustafa1, Oswald Wagner1,a and Kurt Huber4

1 Clinical Institute of Medical and Chemical Laboratory Diagnostics, 2 Division of Pediatric Cardiology, Department of Pediatric and Adolescent Medicine, and 3 Department of Cardiology, Medical University of Vienna, Vienna, Austria.
4 3rd Department of Medicine (Cardiology and Emergency Medicine), Wilhelminenhospital, Vienna, Austria.

aAddress correspondence to this author at: Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Vienna, Austria. Fax 43-1-40400-5389; e-mail Oswald.Wagner{at}meduniwien.ac.at.

Background: Vascular remodeling after percutaneous coronary stent implantation frequently leads to restenosis. Heme oxygenase 1 (HO-1) is involved in the generation of the endogenous antioxidant bilirubin and carbon monoxide, both of which exert antiinflammatory and antiproliferative effects. The aim of the present study was to evaluate the influence of genetic risk factors combined with the conventional risk factors on the development of coronary restenosis after percutaneous coronary intervention (PCI) with stent implantation.

Methods: The HO-1 gene GT dinucleotide repeat promoter polymorphism and HO-1 +99G/C variant were evaluated in 199 patients with coronary artery disease after coronary stent implantation and control angiography at 6 months after the intervention. Coronary restenosis was confirmed by quantitative angiography.

Results: Carriers of the long allele of the HO-1 gene promoter (>29 repeats) had a significantly higher risk of developing restenosis after PCI than noncarriers [odds ratio (OR) = 1.9; 95% confidence interval (95% CI), 1.0–3.4; P = 0.04]. Interestingly, the allele longer than 29 repeats conferred a significantly higher risk of developing restenosis (OR = 3.4; 95% CI, 1.2–9.1; P = 0.017) in nonsmokers than in smokers (OR = 2.0; 95% CI, 0.7–5.2; P = 0.18).

Conclusions: The long allele of the HO-1 gene promoter (>29 repeats) polymorphism, which leads to low HO-1 inducibility, may represent an independent prognostic marker for restenosis after PCI and stent implantation. The effect of the >29 repeat allele is attenuated in smokers, who have chronic exogenous CO exposure.




The following articles in journals at HighWire Press have cited this article:


Home page
Am. J. Respir. Cell Mol. Bio.Home page
L. E. Fredenburgh, M. A. Perrella, and S. A. Mitsialis
The Role of Heme Oxygenase-1 in Pulmonary Disease
Am. J. Respir. Cell Mol. Biol., February 1, 2007; 36(2): 158 - 165.
[Abstract] [Full Text] [PDF]


Home page
JAMAHome page
T. W. Sedlak and S. H. Snyder
Messenger Molecules and Cell Death: Therapeutic Implications
JAMA, January 4, 2006; 295(1): 81 - 89.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2005 by the American Association for Clinical Chemistry.