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 and Andrea Rognoni
Affiliation: Coronary Care Unit and Catheterization Laboratory, Hospital “Maggiore della Carita”, Corso Mazzini 18, 28100 Novara, Italy.
Keywords: Antithrombotic therapy, coronary thrombosis, acute coronary syndrome, primary PCI, coronary intervention,
STEMI, P2Y12 inhibitors, pharmacologic mechanism, bleeding, in stent restenosis.
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.
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