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This editorial refers to ‘A head-to-head pharmacodynamic comparison of prasugrel vs. ticagrelor after switching from clopidogrel in patients with coronary artery disease: results of a prospective randomized study’†, by F. Rollini et al. on page 2722.

Clopidogrel is a thienopyridine prodrug, the active metabolite of which (CAM) inhibits the interaction of ADP with its platelet P2Y12 receptor, which plays a central role in platelet activation and thrombus formation.1 In combination with aspirin, it is recommended for patients with acute coronary syndromes (ACS) and for those undergoing percutaneous coronary interventions (PCIs) to reduce the risk of subsequent cardiovascular events such as stent thrombosis or other major adverse cardiovascular events (MACE).1 Its clinical utility is hampered by the wide interindividual variability of pharmacological response, with a significant proportion of subjects (∼30%) who are poor responders, displaying high on-treatment platelet reactivity (HPR).2,3 Impaired transformation of the prodrug to CAM by hepatic cytochrome P450 (CYP) is among the most important causes of HPR. Because patients with HPR are at increased risk of MACE,2,3 alternative P2Y12 antagonists displaying a lower degree of interindividual variability of platelet inhibition are necessary in order to protect the large majority of patients from stent thrombosis and MACE.

Issue Section:
Clinical Research > Editorial
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