Anna Remková
Optimal antiplatelet therapy is a result of a delicate balance between its efficacy and safety. Acetylsalicylic acid and clopidogrel therapy is associated with the high degree of variability in response to the drug and some patients are drug-resistant. Clopidogrel is inactivated by polymorphism in the gene encoding CYP2C19. This variant, which occurs in about 30 % of the population, reduces the concentration of the active metabolite and decreases the efficacy of the drug by about 25-30 %. CYP2C19 gene polymorphism relates to increased platelet reactivity and predicts risk of high post-treatment platelet reactivity. Platelet reactivity can be assessed with conventional aggregometry. The patients who could profit from other type of antiplatelet therapy can be selected by this method. New inhibitors of platelet activity such as prasugrel and ticagrelor seem to provide better protection against thrombotic events than clopidogrel or acetylsalicylic acid. However, they are associated with a higher risk for bleeding events.