Heme oxygenase-1 gene promoter polymorphism and restenosis following coronary stenting.

Abstract

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. 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). This study does not support a clinically relevant association of the HO-1 promoter polymorphism with restenosis and ischaemic events after coronary stenting.