Hoppmann Petra, Koch Werner, Schömig Albert, Kastrati Adnan
Deutsches Herzzentrum München and 1. Medizinische Klinik rechts der Isar, Technische Universität München, München, Germany.
Eur Heart J. 2004 Feb;25(4):335-41. doi: 10.1016/j.ehj.2003.12.004.
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).
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.
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.
基质金属蛋白酶-1(stromelysin-1)与冠状动脉初次成功干预后管腔过度再狭窄过程有关。我们研究了基质金属蛋白酶-1基因5A/6A启动子多态性与支架置入术或经皮腔内冠状动脉成形术(PTCA)后再狭窄相关的可能性。
该研究纳入3333例有症状冠状动脉疾病的连续患者,这些患者接受了支架植入术(n = 2857)或PTCA(n = 476)。主要终点是血管造影再狭窄,定义为随访6个月血管造影时直径狭窄≥50%。基质金属蛋白酶-1基因5A5A、5A6A和6A6A基因型携带者的再狭窄率分别为28.1%、27.8%和29.5%(P = 0.71)。1年时,各基因型组之间因缺血症状或体征在血管造影再狭窄情况下发生死亡或心肌梗死的发生率以及干预部位血运重建的需求无显著差异。对接受支架植入术的患者和接受PTCA治疗的患者进行单独分析,未表明5A/6A多态性与再狭窄之间存在与治疗类型相关的关联。
我们的数据强烈表明,基质金属蛋白酶-1基因的5A/6A多态性与冠状动脉干预后的血管造影再狭窄或1年临床结局无关。