P2Y12 Inhibitors: Pharmacologic Mechanism and Clinical Relevance

Gioel Gabrio      Secco; Rosario      Parisi; Francesca      Mirabella; Rossella      Fattori; Giulia      Genoni; Pierfrancesco      Agostoni; Giuseppe De      Luca; Paolo Nicola      Marino; Alessandro      Lupi; Andrea      Rognoni

doi:10.2174/1871525711311020005

Abstract

Platelets play a critical role in the pathogenesis of atherothrombotic processes and inhibition of platelet aggregation by antiplatelet therapy is essential and really important in the acute coronary syndromes or in the setting of percutaneous coronary intervention. The first family of adenosine diphosphate P2Y12 receptors inhibiting drug is represented by thienopyridines and among these ticlopidine was the first approved by Food and Drug Administration; actually its use is discouraged because of its potential side effects (neutropenia, anemia, gastrointestinal distress and thrombotic thrombocytopenic purpura). The second generation of thienopyridines is represented by clopidogrel that has replaced ticlopidine in the clinical practice; clopidogrel has the largest clinical experience. Prasugrel represents the third generation. It inhibits platelet aggregation by irreversibly blocking the adenosine diphosphate P2Y12 receptor. Ticagrelor, Cangrelor and Enilogrel represent the last generation of thienopyridines.

This review is focused on the effects of adenosine diphosphate P2Y12 inhibitors.

Keywords: Antithrombotic therapy, coronary thrombosis, acute coronary syndrome, primary PCI, coronary intervention, STEMI, P2Y12 inhibitors, pharmacologic mechanism, bleeding, in stent restenosis.