期刊论文详细信息
P1(A) polymorphism of platelet glycoprotein IIIa and risk of restenosis after coronary stent placement
Article
关键词: ANGIOGRAPHIC FOLLOW-UP;    MYOCARDIAL-INFARCTION;    MEMBRANE-GLYCOPROTEINS;    ANTICOAGULANT-THERAPY;    RANDOMIZED TRIAL;    ARTERY DISEASE;    SMOOTH-MUSCLE;    ANGIOPLASTY;    INTEGRIN;    THROMBOSIS;   
DOI  :  10.1161/01.CIR.99.8.1005
来源: SCIE
【 摘 要 】

Background-Platelets play a central role in the process of restenosis after percutaneous coronary interventions. A polymorphism of platelet glycoprotein IIIa (Pl(A)) has been associated with a higher risk of coronary thrombosis. We designed this prospective study to test the hypothesis that Pl(A) polymorphism of glycoprotein IIIa is associated with an increased risk for restenosis after coronary stent placement. Methods and Results-The study included 1150 consecutive patients with successful coronary stent placement and 6-month follow-up with coronary angiography. The end point of the study was the incidence of angiographic restenosis (greater than or equal to 50% diameter stenosis) at follow-up. Of the 1150 patients, 72.5% were homozygous for Pl(A1), 24.7% were heterozygous (Pl(A1/A2)), and 2.8% were homozygous for Pl(A2). Patients with the Pl(A2) allele demonstrated a significantly higher restenosis rate than did those without (47% versus 38%; OR, 1.42; 95% CI, 1.09 to 1.84). The risk was highest in homozygous carriers of Pl(A2) (53.1% restenosis rate). After adjustment for several clinical and angiographic characteristics, the presence of the Pl(A2) allele remained a significantly independent risk factor for restenosis (adjusted OR, 1.35; 95% CI, 1.07 to 1.70). The influence of the Pl(A2) allele on restenosis was stronger in women. Women with Pl(A2) had a restenosis rate of 52% compared with the 33% incidence among women homozygous for Pl(A1) (OR, 2.21; 95% CI, 1.27 to 3.85). Conclusions-This study showed a significant association between the Pl(A) polymorphism of glycoprotein IIIa and the risk of restenosis after coronary stent placement. The risk was more pronounced in patients homozygous for Pl(A2) allele and in female patients.

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