Why the study?
What is the genetic basis for inter-patient variability in response to newer antiplatelets and anticoagulants compared to traditional therapies?
What is the genetic basis for inter-patient variability in response to newer antiplatelets and anticoagulants compared to traditional therapies?
This review highlights the pharmacogenetic factors contributing to inter-patient variability in response to newer antiplatelet and anticoagulant therapies, emphasizing the potential for individualized drug optimization.
May guide individualized antiplatelet and anticoagulant dosing; leaves open need for prospective trials before clinical adoption.
INTRODUCTION: The study of pharmacogenomics presents the possibility of individualised optimisation of drug therapy tailored to each patients' unique physiological traits. Both antiplatelet and anticoagulant drugs play a key role in the management of cardiovascular disease. Despite their importance, there is a substantial volume of literature to suggest marked person-to-person variability in their effect. Areas covered: This article reviews the data available for the genetic cause for this inter-patient variability of antiplatelet and anticoagulant drugs. The genetic basis for traditional antiplatelets (i.e. aspirin) is compared with the newly available antiplatelet medicines (clopidogrel, prasugrel and ticagrelor). Similarly, the pharmacogenetics of warfarin is compared with the newer direct oral anticoagulants (DOACs) in detail. Expert Opinion: We identify strengths and weaknesses in the research thus far; including shortcomings in trial design and a review of newer analytical techniques. The direction of this research and its real-world implications are discussed.
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O’Connor et al. (2017) studied this question.
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