Background: Coronary artery disease remains the leading cause of death globally. Dual antiplatelet
treatment with aspirin and aP2Y12 receptor significantly reduces thrombotic events. However, antiplatelet drug
response displays considerable interindividual variability.
Methods: Genetic factors account for up to 70% of impaired drug response. A number of genes encoding proteins
involved in the pharmacokinetic pathway have been found to alter drug response.
Results: According to most studies, CYP2C19 gene is the strongest genetic determinant. The novel antiplatelet
agents prasugrel and ticagrelor, seem to overcome genetic restrictions but in expense of increased bleeding rates.
Achieving a balance between adequate platelet inhibition and bleeding complications is challenging.
Conclusion: Genetic screening may provide valuable guidance towards an efficient antiplatelet treatment. However,
the lack of randomized controls trials testing the effect of a genotype-guided therapy, forbids the implementation
of genetic testing into clinical practice.