Platelet glycoprotein IIIa (platelet antigen 1/platelet antigen 2) polymorphism and 1-year outcome in patients with stable coronary artery disease

被引:21
作者
Addad, Faouzi [2 ]
Elalamy, Ismail [3 ]
Chakroun, Tahar [1 ]
Abderrazek, Fatma [4 ]
Dridi, Zohra [2 ]
Hamdi, Sonia [2 ]
Hassine, Mohssen [4 ,5 ]
Ben-Farhat, Mohamed [2 ]
Gerotziafas, Grigoris [3 ]
Hatmi, Mohamed [3 ]
Gamra, Habib [2 ]
机构
[1] Hop Farhat Hached, Ctr Reg Transfus Sanguine, Unite Rech Etud Fonct Plaquettaires UR 06SP05, Sousse 4000, Tunisia
[2] Fattouma Bourguiba Univ Hosp, Dept Cardiol A, Cardiac Thrombosis Res Unit, Monastir, Tunisia
[3] Tenon Hosp ER2 UPMC, Dept Hematol, Paris, France
[4] Fattouma Bourguiba Univ Hosp, Haematol Lab, Monastir, Tunisia
[5] Inst Pasteur, Dept Infect & Epidemiol, Paris, France
关键词
cardiac events; coronary artery disease; platelet glycoprotein IIIa; platelet PLA1/PLA2 polymorphism; MYOCARDIAL-INFARCTION; RISK; RECEPTOR; PL(A2); PIA2; ASSOCIATION; ACTIVATION; MECHANISMS; ASPIRIN; EVENTS;
D O I
10.1097/MBC.0b013e32833e47c1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Platelet glycoprotein IIb/IIIa is a membrane receptor which plays a key role in coronary artery disease and thrombotic events. However, there is a considerable controversy regarding the clinical impact of glycoprotein IIIa platelet antigen 1 (PlA1)/platelet antigen 2 (PlA2) polymorphism as a risk factor for myocardial infarction. To evaluate the association between glycoprotein IIIa PlA1/PlA2 polymorphism and 1-year cardiovascular events occurrence in aspirin-treated patients with stable coronary artery disease. We prospectively included 188 postacute coronary syndrome patients (183 men) aged 59 +/- 10 years and receiving aspirin (250 mg/day). The clinical outcome at 1 year was the composite end point of nonfatal myocardial infarction, stroke, recurrent unstable angina or cardiac death. Genotyping for PlA1/PlA2 polymorphism was conducted using PCR and restriction fragment length polymorphism analysis. The genotype distribution of glycoprotein IIIa PlA1/PlA2 polymorphism was PlA1/PlA1, 55.3%; PlA1/PlA2, 39.3% and PlA2/PlA2, 4%. Incidence of composite end point in homozygous PlA1/PlA1 carriers was significantly higher than in PlA2/PlA2 and PlA1/PlA2 patients [14.4 vs. 3.6% odds ratio 4.5 (1.2-16.6, 95% confidence interval); P=0.012]. Multivariate analysis identified three strong predictive factors of cardiac death: age more than 65 years [odds ratio=6.8, (1.4-34, 95% confidence interval); P=0.018], ventricular ejection fraction less than 50% [odds ratio=8.6, (1.7-42.6, 95% confidence interval); P=0.008] and homozygous PlA1/PlA1 genotype [odds ratio=8.8, (1.0-78.6, 95% confidence interval); P=0.014]. Our results demonstrated that glycoprotein IIIa PlA1/PlA1 genotype carriers have a significantly increased risks of acute vascular ischemic events associated with a poor prognosis at 1 year. These postacute coronary syndrome patients might require an optimized secondary antithrombotic prophylaxis strategy. Blood Coagul Fibrinolysis 21: 674-678 (c) 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.
引用
收藏
页码:674 / 678
页数:5
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