Thienopyridine-derived clopidogrel, prasugrel, cyclopentyltriazole pyrimidine-derived ticagrelor, and non-thienopyridine-derived ATP analogue cangrelor block the P2Y12 component of ADP receptors on the platelet surface. This prevents activation of the GPIIb/IIIa receptor complex, thereby reduces platelet aggregation. The platelet activation pathway caused by ADP is blocked by P2Y12, and therefore, these drugs have a crucial role in preventing ischemic complications in patients undergoing acute coronary syndrome, including unstable angina, myocardial infarction, and percutaneous coronary intervention. In addition, the use of P2Y12 inhibitors for secondary prevention has also been focused on in clinical studies. The results of recent studies show a lot of variances in terms of duration of use, dosage, and individualized treatment management.
The main concern in the clinical use of P2Y12 is dual antiplatelet therapy (with aspirin and a P2Y12 receptor blocker) following intracoronary stenting to prevent stent thrombosis. However, there are also other multifactorial variables in terms of P2Y12 inhibitor use. In this chapter, current and precise medicines regarding P2Y12 inhibitor use are evaluated, from gene testing to escalation and de-escalation strategies. Taking all these into account, providing appropriate drugs selection considering treatment time, onset time, duration of use, side effect profile, treatment limitations, and evaluating and interpreting differences in clinical use based on randomized trials will shed light on coronary heart disease treatment choice.
Keywords: Acute coronary syndromes, Clopidogrel resistance, CYP2C19 gene testing, De-escalation, Dual antiplatelet treatment, Escalation, Gene polymorphisms, Ischemic stroke, P2Y12 inhibitors, Precision medicine, Triple antithrombotic therapy, Vascular heart disease.