OBJECTIVES: It has been proposed that human platelet antigen-1 (HPA-1) gene polymorphism is associated with coronary artery disease (CAD) and affects platelet function. We aimed to investigate the distribution of HPA gene polymorphism between angiographic CAD and a control group and the relation between HPA gene polymorphism and platelet aggregation. STUDY DESIGN: The study population consisted of 94 patients with angiographic CAD and 115 patients without angiographic CAD. Platelet aggregation was measured with impedance aggregometry on the fifth day of percutaneous coronary intervention (PCI). Platelet aggregation >480 AU*min was defined as the clopidogrel resistance group. Blood samples were obtained from all participants at discharge for investigating HPA-1 gene polymorphism. RESULTS: There was no significant difference in the distribution of HPA-1 gene polymorphism between the control and CAD groups (78.7% vs. 78.1% for A allele and 21.3% vs. 21.9% for B allele, p=NS). The analysis between groups with and without clopidogrel resistance revealed no significant difference in the distribution of HPA-1A and HPA-1B alleles between the groups (A allele 78.7% vs. 78.9% and B allele 21.3% vs. 21.1%, p=NS). In the CAD group, there were no significant differences in platelet aggregation between HPA-1A and HPA-1B alleles (294±240 vs. 259±261 AU*min, p=NS). CONCLUSION: The distribution of HPA-1 gene polymorphism was not different in CAD patients compared to the control group. HPA-1 gene polymorphism was not associated with platelet aggregation or clopidogrel resistance assessed by impedance aggregometry in the CAD group.
OBJECTIVES: It has been proposed that human platelet antigen-1 (HPA-1) gene polymorphism is associated with coronary artery disease (CAD) and affects platelet function. We aimed to investigate the distribution of HPA gene polymorphism between angiographic CAD and a control group and the relation between HPA gene polymorphism and platelet aggregation. STUDY DESIGN: The study population consisted of 94 patients with angiographic CAD and 115 patients without angiographic CAD. Platelet aggregation was measured with impedance aggregometry on the fifth day of percutaneous coronary intervention (PCI). Platelet aggregation >480 AU*min was defined as the clopidogrel resistance group. Blood samples were obtained from all participants at discharge for investigating HPA-1 gene polymorphism. RESULTS: There was no significant difference in the distribution of HPA-1 gene polymorphism between the control and CAD groups (78.7% vs. 78.1% for A allele and 21.3% vs. 21.9% for B allele, p=NS). The analysis between groups with and without clopidogrel resistance revealed no significant difference in the distribution of HPA-1A and HPA-1B alleles between the groups (A allele 78.7% vs. 78.9% and B allele 21.3% vs. 21.1%, p=NS). In the CAD group, there were no significant differences in platelet aggregation between HPA-1A and HPA-1B alleles (294±240 vs. 259±261 AU*min, p=NS). CONCLUSION: The distribution of HPA-1 gene polymorphism was not different in CAD patients compared to the control group. HPA-1 gene polymorphism was not associated with platelet aggregation or clopidogrel resistance assessed by impedance aggregometry in the CAD group.
Authors: Mehmet Balli; Hakan Taşolar; Mustafa Çetin; Caglar Emre Cagliyan; Mehmet Yavuz Gözükara; Mahmut Yilmaz; Zafer Elbasan; Murat Cayli Journal: Postepy Kardiol Interwencyjnej Date: 2015-09-28 Impact factor: 1.426