Koroner arter hastalarında insan trombosit antijen-1 gen polimorfizmi ile klopidogrel direnci ilişkisi
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Tarih
2013
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Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Amaç: İnsan trombosit antijeni-1 (İTA-1) gen polimorfizminin koroner arter hastalığı (KAH) ile ilişkili olduğu ve trombosit fonksiyonlarını etkilediği öne sürülmüştür. Bu çalışmada KAH olan ve olmayan bireylerde İTA-1 gen polimorfizminin dağılımını ve KAH olan bireylerde İTA-1 gen polimorfizminin trombosit kümelenmesiyle ilişkisini incelemeyi amaçladık. Çalışma planı: Çalışmaya perkütan koroner girişim (PKG) uygulanan 94 hasta ve kontrol grubu olarak koroner anjiyografisi normal olan 115 birey alındı. KAH grubunda PKG sonrası beşinci gün impedans agregometre ile trombosit kümelenmesi (KB) ölçüldü. Trombosit kümelenmesinin >490 KB/dakika olması klopidogrel direnci olarak tanımlandı. Tüm katılımcılardan İTA-1 gen polimorfizmini araştırmak için kan örnekleri alındı. Bulgular: Hasta ve kontrol grubu arasında İTA-1 gen polimorfizmi yönünden fark yoktu (A aleli için %78.7 ve %78.1, p=AD; B aleli için %21.3 ve %21.9, p=AD). Klopidogrel direnci olan ve olmayan gruplar arasındaki analizde İTA-1A ve İTA-1B alleleri sıklığı açısından fark tespit edilmedi (Her iki grupta, A aleline sahip hasta oranları %78.7 ve %78.9, p=AD; B aleli için %21.3 ve %21.1, p=AD). Ayrıca, KAH’da İTA-1A ve İTA-1B alellerine sahip hastalarda trombosit kümelenmesi açısından fark yoktu (294±240 ve 259±261 KB/dakika, p=AD). Sonuç: İnsan trombosit antijeni-1 gen polimorfizmi dağılımı KAH olan ve olmayan bireylerde benzerdir. KAH’da, impedans agregometre ile değerlendirilen trombosit kümelenmesi ve klopidogrel direnci, İTA-1 gen polimorfizmi ile ilişkili değildir.
Objectives: It has been proposed that human platelet anti- gen-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 be- tween 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 ag- gregometry on the fifth day of percutaneous coronary inter- vention (PCI). Platelet aggregation >480 AU*min was defined as the clopidogrel resistance group. Blood samples were ob- tained 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 with- out 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 anti- gen-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 be- tween 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 ag- gregometry on the fifth day of percutaneous coronary inter- vention (PCI). Platelet aggregation >480 AU*min was defined as the clopidogrel resistance group. Blood samples were ob- tained 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 with- out 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.
Açıklama
Anahtar Kelimeler
Kalp ve Kalp Damar Sistemi
Kaynak
Türk Kardiyoloji Derneği Arşivi
WoS Q Değeri
Scopus Q Değeri
Cilt
41
Sayı
5
