Platelet represents the cornerstone of both physiologic hemostasis and
thrombosis acting via different pathways. Adenosine diphosphate (ADP) plays a crucial
role in platelet activation and thrombus formation through its interaction with platelet
P2Y12 receptor, making therefore this receptor an interesting therapeutic target for
anti-thrombotic agents.
Around the world, millions of people affected by coronary artery disease are treated
with anti-platelet agents. Indeed, dual anti-platelet therapy, consisting of a combination
of aspirin and a P2Y12 receptor antagonist, is the recommended strategy in patients
with acute coronary syndrome and those who underwent percutaneous coronary
intervention with stent implantation. Furthermore, the introduction of different
generations of P2Y12 receptor antagonists has immensely improved the clinical
outcome, as well established through literature.
Although the concept to replace “one size fits all” paradigm to a more individualized
approach in anti-platelet therapy seems to be rational, in the area of based evidence
medicine, a clear prognostic impact of such a strategy is not yet clearly demonstrated.
In the current chapter, we tried to summarize the mechanisms of P2Y12 receptor
antagonists anti-platelet action, to report clinical proofs regarding the efficacy/safety of new generations of this class of drugs, and to discuss the place of a tailored strategy
and its impact on improving clinical outcome.
Keywords: Anti-aggregation therapy, Bleeding, Cangrelor, Clinical outcome,
Clopidogrel, Coronary artery disease, Dual anti-platelet therapy, Elinogrel,
Genetic testing, High on-treatment platelet reactivity, Ischemic event, Low ontreatment
platelet reactivity, Percutaneous coronary intervention, Platelet
aggregation, Platelet reactivity, Prasugrel, P2Y12 receptor, P2Y12 receptor
inhibitors, Stent implantation, Ticagrelor.
