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By definition, precision medicine aims to prevent, diagnose, and optimize individualized treatments on the basis of each patient's individual genetic makeup. While the broad clinical application of such efforts remains somewhat limited, this is not true regarding antiplatelet and anticoagulation therapeutics. Given the central role that these medications play in primary and secondary prevention of numerous cardiovascular disorders, considerable efforts to understand the genetic drivers influencing their effectiveness and adverse outcomes, primarily bleeding risk, have been performed successfully over the last decade. Specific to clopidogrel, and despite its proven benefits, it has been shown that ∼4%–30% of patients do not respond adequately to this drug, resulting in high on-treatment platelet reactivity and increased rates of cardiovascular events.1–3 Clopidogrel, being a prodrug, requires several hepatic enzymes to metabolize it into both biologically active and inactive derivatives. Numerous prior investigations have shown that the CYP2C19 enzyme is the major contributor regarding generation of the bioactive metabolite.1,2,4 Consistent with this observation, both loss of function (LOF) and gain of function genetic variants in CYP2C19 have been consistently associated with clopidogrel efficacy.
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