AIMS: Matrix metalloproteinase stromelysin-1 has been implicated in the process of exaggerated lumen re-narrowing after primarily successful interventions in coronary arteries. We examined the possibility that the 5A/6A promoter polymorphism of the stromelysin-1 gene is associated with restenosis after stenting or percutaneous transluminal coronary angioplasty (PTCA). METHODS AND RESULTS: The study included 3333 consecutive patients with symptomatic coronary artery disease who were treated with stent implantation (n=2857) or PTCA (n=476). Primary end-point was angiographic restenosis, defined as >/=50% diameter stenosis at 6-month follow-up angiography. Restenosis rates were 28.1%, 27.8%, and 29.5% in carriers of the stromelysin-1 genotypes 5A5A, 5A6A, and 6A6A, respectively (P=0.71). The incidence of death or myocardial infarction and the need for revascularization at the site of the intervention due to symptoms or signs of ischaemia in the presence of angiographic restenosis were not significantly different between the genotype groups at 1 year. Separate analysis of the patients who underwent stenting and the patients who were treated with PTCA did not indicate the existence of a treatment type-related association between the 5A/6A polymorphism and restenosis. CONCLUSION: Our data strongly suggest that the 5A/6A polymorphism of the stromelysin-1 gene is not related to angiographic restenosis or the 1-year clinical outcome after interventions in coronary arteries.
AIMS: Matrix metalloproteinase stromelysin-1 has been implicated in the process of exaggerated lumen re-narrowing after primarily successful interventions in coronary arteries. We examined the possibility that the 5A/6A promoter polymorphism of the stromelysin-1 gene is associated with restenosis after stenting or percutaneous transluminal coronary angioplasty (PTCA). METHODS AND RESULTS: The study included 3333 consecutive patients with symptomatic coronary artery disease who were treated with stent implantation (n=2857) or PTCA (n=476). Primary end-point was angiographic restenosis, defined as >/=50% diameter stenosis at 6-month follow-up angiography. Restenosis rates were 28.1%, 27.8%, and 29.5% in carriers of the stromelysin-1 genotypes 5A5A, 5A6A, and 6A6A, respectively (P=0.71). The incidence of death or myocardial infarction and the need for revascularization at the site of the intervention due to symptoms or signs of ischaemia in the presence of angiographic restenosis were not significantly different between the genotype groups at 1 year. Separate analysis of the patients who underwent stenting and the patients who were treated with PTCA did not indicate the existence of a treatment type-related association between the 5A/6A polymorphism and restenosis. CONCLUSION: Our data strongly suggest that the 5A/6A polymorphism of the stromelysin-1 gene is not related to angiographic restenosis or the 1-year clinical outcome after interventions in coronary arteries.
Authors: Veronika Souslova; Paul A Townsend; Jelena Mann; Chris M van der Loos; Anna Motterle; Fulvio D'Acquisto; Derek A Mann; Shu Ye Journal: PLoS One Date: 2010-03-25 Impact factor: 3.240