This review summarizes the prevalence, mechanisms, and potential clinical implications of inadequate platelet inhibition or resistance to prasugrel.
What are the prevalence, mechanisms, and potential clinical implications of prasugrel resistance?
While prasugrel is generally more potent than clopidogrel, this review highlights that inadequate platelet inhibition or 'resistance' can occasionally occur, warranting further understanding of its mechanisms and clinical implications.
Prasugrel is a third-generation thienopyridine that inhibits ADP-induced platelet activation by irreversibly blocking the P2Y12 receptor. Given in healthy volunteers in dosages used clinically, it invariably inhibits platelet aggregation. When administered in patients, it has been shown to result in a faster, more consistent and stronger inhibition of platelet aggregation compared with the most widely used clopidogrel. However, cases of inadequate platelet inhibition or of the so-called 'resistance' to prasugrel have been occasionally reported. The focus of this review is prasugrel resistance prevalence, mechanisms and potential clinical implications.
Dimitrios Alexopoulos (2011) conducted a review in Prasugrel resistance. Prasugrel vs. Clopidogrel was evaluated on Prasugrel resistance prevalence, mechanisms, and clinical implications. This review summarizes the prevalence, mechanisms, and potential clinical implications of inadequate platelet inhibition or resistance to prasugrel.
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