Background Vascular smooth muscle cells (VSMCs) can express heme-oxygenase (HO), a rate-limiting enzyme in the degradation of heme to bilirubin, ferritin and carbon monoxide (CO). VSMC-derived CO can suppress VSMC proliferation and may serve as an antiproliferation factor. The promoter region of HO-1 shows a polymorphism with different (GT)_n repeats that has been reported to differently induce gene expression. The objective of this study was to examine the effect of this variation on the occurrence of restenosis after in-stent treatment in patients with coronary artery disease. Methods Candidates who underwent coronary stent implantation were genotyped for the HO-1 promoter polymorphism using polymerase chain reaction (PCR) and automated DNA capillary sequencer. Serum levels of IL-6 and C-reactive protein (CRP) were obtained at baseline, 24 hours and 48 hours after stenting. The primary end point for the study was angiographic evidence of in-stent restenosis at 6 months. All parameters for evaluation of restenosis were analysed by quantitatve computer-assisted angiographic analysis (QCA). Results One hundred and eighty-seven patients who underwent coronary stent implantation were studied of whom 27.8% showed ≥50% restenosis after 6 months. The distribution of (GT)_n repeats of all patients in the promoter region of HO-1 genotype ranged from 22 to 42, with (GT)_ 25 and (GT)_ 32 being the two most common alleles. The allelic repeats were divided into the short class (S) with 29 (GT)_n, the middle class (M) with 30-37 (GT)_n and the long class (L) with 38 (GT)_n. There was no significant difference in the restenosis between the genotype groups or between post operation levels of inflammation markers, but carriers of the S allele (n=120) had 33.3% lower baseline IL-6 compared with non-S carriers (n=67, P=0.0008). Conclusions Although no association was observed between the HO-1 promoter polymorphism aod coronary in-stent restenosis following the stent procedure, the association with plasma IL-6 levels suggests that HO-1 S allele might protect from the atherosclerotic inflammatory process. Background Vascular smooth muscle cells (VSMCs) can express heme-oxygenase (HO), a rate-limiting enzyme in the degradation of heme to bilirubin, ferritin and carbon monoxide (CO). VSMC-derived CO can suppress VSMC proliferation and may serve as an antiproliferation factor. The promoter of HO-1 shows a polymorphism with different (GT) _n repeats that has been reported to induce induce gene expression. The objective of this study was to examine the effect of this variation on the occurrence of restenosis after in-stent treatment in patients with coronary artery disease. Methods Candidates who underwent coronary stent implantation were genotyped for the HO-1 promoter polymorphism using polymerase chain reaction (PCR) and automated DNA capillary sequencer. Serum levels of IL-6 and C-reactive The primary end point for the study was angiographic evidence of in-stent restenosis at 6 months. All parameter (CRP) was obtained at baseline for 24 hours and 48 hours after stenting. s for evaluation of restenosis were analysed by quantitatve computer-assisted angiographic analysis (QCA). Results One hundred and eighty-seven patients who underwent coronary stent implantation were studied of whom 27.8% showed ≥50% restenosis after 6 months. The distribution of ( GT) _n repeats of all patients in the promoter region of HO-1 genotype ranged from 22 to 42, with (GT) _25 and (GT) _ 32 being the two most common alleles. The allelic repeats were divided into the short class (S) with 29 (GT) _n, the middle class (M) with 30-37 (GT) _n and the long class (L) with 38 (GT) _n. There was no significant difference in the restenosis between the genotype groups or between post operation levels of inflammation markers, but carriers of the S allele (n = 120) had 33.3% lower baseline IL-6 compared with non-S carriers (n = 67, P = 0.0008) between the HO-1 promoter polymorphism aod coronary in-stent restenosis following the stent procedure, the association with plasma IL-6 levels suggests that HO-1 S allele might protect from the atherosclerotic inflammatory process.