Why the study?
To summarize research on the influence of P2Y12 genetic polymorphisms on the pharmacodynamics and efficacy of P2Y12 inhibitors.
Do P2Y12 genetic and epigenetic factors independently predict inadequate response to P2Y12 inhibitors?
Do P2Y12 genetic and epigenetic factors independently predict inadequate response to P2Y12 inhibitors?
Genetic polymorphisms of the P2Y12 receptor are unlikely to be independent predictors of antiplatelet drug efficacy, highlighting the complex interplay of multiple genetic, epigenetic, and clinical factors.
Isolated P2Y12 genotyping should not guide therapy; leaves open multifactorial genetic-clinical interactions in antiplatelet response.
This review summarizes the results of research that focus on the influence of P2Y₁₂ genetic polymorphisms on the pharmacodynamics and the efficacy of P2Y₁₂ inhibitors. We found that the conclusions of the studies are unequivocal, and despite several strong candidates, such as G52T (rs6809699) or T744C (rs2046934), they may not be independent predictors of the inadequate response to the drug. Most probably, P2Y₁₂ genetic polymorphisms contribute to the effect exerted by other gene variants (such as CYP2C19*2/*3/*17), drug interactions, or patient habits, such as smoking. Also, epigenetic modifications, such as methylation or miRNA levels, may play a role in the efficacy of antiplatelet treatment.
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Danielak et al. (2022) studied this question.
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