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 > or =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 (> or =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.
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 > or =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 (> or =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.
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