RESUMO
AIM: To analyze the influence of pharmacogenetic factors on the risk of clopidogrel resistance and cardiovascular events during 18-months follow-up. SUBJECTS AND METHODS: Two hundred and fifty patients taking clopidogrel were examined. Platelet function was determined by optical aggregometry. Thromboxane A synthase 1 (TBS1) gene polymorphism was investigated in all the patients. The impact of TBS1 gene polymorphism on the risk of clopidogrel resistance and cardiovascular events was analyzed during 18 months of follow-up. RESULTS: The carriage of TBS1 gene polymorphism AA was shown to affect the risk of clopidogrel resistance. Cardiovascular complications significantly less frequently occurred in TBSI gene polymorphism AA carriers during 18 months. CONCLUSION: The carriage of a slow AA allele of the'TBS1 gene is suggested to be a clinically significant protective factor in the secondary prevention of coronary heart disease
Assuntos
Doença das Coronárias/genética , Resistência a Medicamentos/genética , Inibidores da Agregação Plaquetária/uso terapêutico , Tromboxano-A Sintase/genética , Ticlopidina/análogos & derivados , Clopidogrel , Doença das Coronárias/tratamento farmacológico , Doença das Coronárias/metabolismo , Citocromo P-450 CYP2C19/genética , Interpretação Estatística de Dados , Feminino , Frequência do Gene , Humanos , Estimativa de Kaplan-Meier , Masculino , Agregação Plaquetária/efeitos dos fármacos , Inibidores da Agregação Plaquetária/administração & dosagem , Polimorfismo Genético , Prognóstico , Estudos Prospectivos , Risco , Tromboxano-A Sintase/metabolismo , Ticlopidina/administração & dosagem , Ticlopidina/uso terapêuticoRESUMO
AIM: To analyze the influence of clinical and pharmacogenetic factors on the risk of resistance to original or generic clopidogrel and that of cardiovascular events (CVE) during 12 months of follow-up. SUBJECTS AND METHODS: Two hundred and fifty patients admitted to Moscow hospitals in October 2011 to September 2012 were examined. All the patients received clopidogrel. During their stay at hospital, venous blood samples were collected twice (before and 7-10 days after continuous clopidogrel intake). Platelet function was determined by optical aggregometry. A less than 10% reduction in platelet aggregation was taken as a resistance criterion. In addition, CYP2C9 and CYP2C19 gene polymorphisms were investigated. RESULTS: Whether original or generic clopidogrel is used, the level of baseline or post-7-day ADP-induced platelet aggregation (ADP aggregation) fails to affect the risk of its resistance. Evaluation of ADP-induced platelet aggregation in patients with different CYP2C9 and CYP2C19 gene polymorphisms during the administration of original or generic clopidogrel also showed no significant differences in its resistance. During the 12-month follow-up, CVE significantly less frequently occurred as a result of the intake of original versus generic clopidogrel. CONCLUSION: The use of original clopidogrel does not affect the risk of resistance to antiplatelet drugs, but it is associated with the lower incidence of CVE during a year.