The platelet reactivity after percutaneous coronary intervention in patients with double antiplatelet therapy: impact of genetic polymorphisms
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For citation: Golukhova EZ, Ryabinina MN, Bulaeva NI, at al. The platelet reactivity after percutaneous coronary intervention in patients with double antiplatelet therapy: impact of genetic polymorphisms. Kreativnaya kardiologiya. 2013; 2: 15-27 (in Russian).
Keywords: ischemic heart disease genetic polymorphism antiplatelet therapy platelet aggregation
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Material and methods. 55 SCAD-patients aged 36 to 75 years (mean age 59±9.68 years) were studied pre- and postoperatively, mean follow-up was 2 years. Beside conventional investigations, antiplatelet therapy efficacy was assessed by Thromboelastogrphy (TEG) and panel Рlаtеlеt Мaррing with arachidonic acid and ADP-induced platelet aggregation and light transmission aggregometry. Detecting a genetic polymorphism in CYP2C19*2 and CYP2C19*3 were held using allele-specific polymerase chain reaction at the end of follow-up period.
Results. Among study group – 11 patients had MACE (major adverse cardiac events). According to the study, high levels of ADPinduced platelet aggregation (more than 48%, p=0,027) and PRU (more than 225, p=0,00046) influenced on the development of complications. Our analysis revealed a normal genotype (GG) in 39 patients, heterozygous polymorphisms CYP2C19 (GA) G681A allele were detected in 14 patients, and 2 patients has homozygous polymorphisms CYP2C19 (AA) G681A allele. All 55 patients in our study had normal CYP2C19*3 (Trp212Ter) genotype of CYP2C19 gene. We revealed a statistically significant influence of various genotypes of CYP2C19*2 (GG, GA, AA) on the average values of platelet aggregation (F (1,51)=5,75, p=0,02). Also a reliable relationship between MACE and the platelet aggregation according to the LTA (F (1,51)=10,52, p=0,002) was obtained. The interaction of these two factors was significant (F (1,51)=5,57, p=0,022). In our study there was no significant relationship between the different genotypes CYP2C19*2 and the average values of PRU (p=0,057), however, their joint impact on MACE was statistically significant (p=0,041).
Conclusion. Patients with high on-treatment platelet reactivity had a significantly increased risk of having MACE. The platelet reactivity was higher in patients with heterozygous and homozygous carriers of CYP2C19*2 versus normal genotype.
Abstract
Objective. To assess antiplatelet therapy efficacy considering the CYP2C19*2 and CYP2C19*3 genetic testing before percutaneous coronary intervention (PCI) in patients with stable coronary artery disease (SCAD).Material and methods. 55 SCAD-patients aged 36 to 75 years (mean age 59±9.68 years) were studied pre- and postoperatively, mean follow-up was 2 years. Beside conventional investigations, antiplatelet therapy efficacy was assessed by Thromboelastogrphy (TEG) and panel Рlаtеlеt Мaррing with arachidonic acid and ADP-induced platelet aggregation and light transmission aggregometry. Detecting a genetic polymorphism in CYP2C19*2 and CYP2C19*3 were held using allele-specific polymerase chain reaction at the end of follow-up period.
Results. Among study group – 11 patients had MACE (major adverse cardiac events). According to the study, high levels of ADPinduced platelet aggregation (more than 48%, p=0,027) and PRU (more than 225, p=0,00046) influenced on the development of complications. Our analysis revealed a normal genotype (GG) in 39 patients, heterozygous polymorphisms CYP2C19 (GA) G681A allele were detected in 14 patients, and 2 patients has homozygous polymorphisms CYP2C19 (AA) G681A allele. All 55 patients in our study had normal CYP2C19*3 (Trp212Ter) genotype of CYP2C19 gene. We revealed a statistically significant influence of various genotypes of CYP2C19*2 (GG, GA, AA) on the average values of platelet aggregation (F (1,51)=5,75, p=0,02). Also a reliable relationship between MACE and the platelet aggregation according to the LTA (F (1,51)=10,52, p=0,002) was obtained. The interaction of these two factors was significant (F (1,51)=5,57, p=0,022). In our study there was no significant relationship between the different genotypes CYP2C19*2 and the average values of PRU (p=0,057), however, their joint impact on MACE was statistically significant (p=0,041).
Conclusion. Patients with high on-treatment platelet reactivity had a significantly increased risk of having MACE. The platelet reactivity was higher in patients with heterozygous and homozygous carriers of CYP2C19*2 versus normal genotype.
