Sandra L Close

TL;DR: Carriers of a reduced-function CYP2C19 allele had significantly lower levels of the active metabolite of clopidogrel, diminished platelet inhibition, and a higher rate of major adverse cardiovascular events, including stent thrombosis, than did noncarriers.

TL;DR: The current findings do not support the need to avoid concomitant use of PPIs, when clinically indicated, in patients receiving clopidogrel or prasugrel.

TL;DR: Thienopyridines are metabolized to active metabolites that irreversibly inhibit the platelet P2Y12 adenosine diphosphate receptor, and the pharmacodynamic response to clopidogrel is more variable than the response to prasugrel.

TL;DR: Common functional CYP genetic variants do not affect active drug metabolite levels, inhibition of platelet aggregation, or clinical cardiovascular event rates in persons treated with prasugrel, and these pharmacogenetic findings are in contrast to observations with clopidogrel.

TL;DR: Individuals with the ABCB1 3435C→T genotype have reduced platelet inhibition and are at increased risk of recurrent ischaemic events during clopidogrel treatment, and in patients with acute coronary syndromes who have undergone percutaneous intervention, this polymorphism is significantly associated with the risk of cardiovascular death, myocardial infarction, or stroke.