RESUMO
BACKGROUND: Intimal hyperplasia and vascular remodeling are major mechanisms of restenosis after coronary artery angioplasty. Angiotensin II causes restenosis by stimulating cell proliferation and vascular constriction and nitric oxide prevents restenosis by inhibiting cell proliferation and stimulating vascular dilatation. Angiotensin converting enzyme (ACE) and nitric oxide synthase (NOS) are the main determinants of the activity of the angiotensin II and the nitric oxide. In this study, we tested whether the genetic polymorphisms of the ACE and the NOS gene are the risk factors of restenosis and whether the effect of the genetic polymorphisms in stent group is different from that in balloon angioplasty group. We also tested whether there are interactions among the polymorphisms. METHODS: We determined ACE I/D polymorphism and NOS A/B and G/T polymorphism in 219patients (77 patients (81 lesions) in stent group and 142 patients (181 lesions) in balloon angioplasty group) who underwent PTCA and follow up coronary angiography in Seoul national university hospital from January 1996 to May 1999. RESULTS: Restenosis (50% of reference diameter) was observed in 78/262(30%) lesions (18/81(22%) lesions in stent group, 60/181(33%) lesions in balloon angioplasty group). ACE DD genotype is the significant risk factor for increment of late luminal loss and loss index in stent group. In stent group, means of the late luminal loss and loss index of the lesions of the DD genotype are 1.12+/-0.61mm and 74.7+/-38.3% and those of the non-DD genotype are 0.72+/-0.77mm and 44.9+/-67.5% but DD genotype is not the risk factor for restenosis after balloon angioplasty. The restenosis rate, late luminal loss and loss index are not significantly different according to NOS polymorphisms. No significant interaction among the polymorphisms is observed. CONCLUSION: ACE DD genotype is a significant risk factor for restenosis after stent insertion but is not a risk factor for restenosis after balloon angioplasty in Korean. This result reflects the different mechanism of restenosis after stent insertion and balloon angioplasty. NOS polymorphisms are not associated with restenosis and no interaction between the polymorphisms is observed.