Abstract
AimTo prospectively determine the role of platelet glycoprotein IIIa (GP IIIa) gene PlA1/PlA2 polymorphism on the long-term clinical outcome in patients with coronary artery disease undergoing coronary stenting.Design and settingProspective observational study in the University Hospital of Caen (France).Patients and methods1 111 symptomatic consecutive Caucasian patients treated with percutaneous coronary intervention including stent implantation underwent genotyping for GP IIIa PlA1/A2.Main outcome measuresLong-term clinical outcome in terms of the rate of major adverse cardiac events (MACE, ie death from any cause, non-fatal Q wave or non Q wave myocardial infarction, and need for coronary revascularisation) was obtained and subsequently stratified according to the GP IIIa PlA1/A2 polymorphism.ResultsThree groups of patients were determined according to the GP IIIa PlA1/A2 polymorphism (71.6% had the A1/A1, 25.8% had the A1/A2 and 2.6% had the A2/A2 genotype). These three groups were comparable for all clinical characteristics including sex ratio, mean age, vascular risk factors, previous coronary events, baseline angiographic exam, indication for the percutaneous coronary intervention and drug therapy). The incidence of MACE was similar in these 3 groups of patients during a mean follow-up period of 654+/-152 days. Independent risk factors for MACE were a left ventricular ejection fraction < 40%, absence of treatment with a beta-blocker and absence of treatment with an angiotensin converting enzyme inhibitor during follow-up.ConclusionThe GP IIIa PlA1/A2 polymorphism does not influence the clinical long-term outcome in patients with symptomatic coronary disease undergoing percutaneous coronary intervention with stent implantation.
Highlights
Many previous studies have shown evidence for a genetic predisposition in coronary artery disease (CAD) and some of the several tested single polymorphisms seem to be implicated [1]
The A1/A2 Glycoprotein IIIa (GPIIIa) polymorphism [4] can influence both platelet activation and aggregation [5,6,7] and affects post occupancy signalling by the platelet fibrinogen receptor IIb/IIIa [8]
We report here our findings on the role of glycoprotein IIIa (GP IIIa) PlA1/A2 polymorphism based on long-term clinical outcome (> 18 months) of a large observational study of patients undergoing percutaneous coronary intervention (PCI) with successful coronary stenting
Summary
Many previous studies have shown evidence for a genetic predisposition in coronary artery disease (CAD) and some of the several tested single polymorphisms seem to be implicated [1]. The glycoprotein IIb/IIIa (GPIIb/IIIa) is a platelet membrane receptor for fibrinogen and von Willebrand factor. The A1/A2 GPIIIa polymorphism [4] can influence both platelet activation and aggregation [5,6,7] and affects post occupancy signalling by the platelet fibrinogen receptor IIb/IIIa [8]. In vitro antiaggregation by abciximab was reduced in platelets with the PlA2 polymorphism [9]. The Framingham Offspring Study showed heightened platelet aggregability among patients with PlA2 allele [5], the clinical impact of this polymorphism remains unclear despite many casecontrol studies [10,11,12,13,14,15], many observational studies [1622] and 3 meta-analyses [23,24,25]
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