Oral anti-platelet agents targeting the platelet P2Y12 receptor are an integral component of treating patients undergoing
percutaneous coronary interventions. Advancements in the design of stents and catheters are pushing the technique
towards treatment of high risk lesions whose failure would expose patients to catastrophic events. Success of these
complex procedures largely lays on efficacy of anti-platelet drugs and the limitation of stent restenosis and/or thrombosis.
Clopidogrel has been the most commonly used agent in this respect worldwide. However, there are certain shortcomings
of clopidogrel, the most important of which is the wide response variability of platelet inhibition. Thus, clinicians are facing
challenges in treating patients where high inhibition of platelets is necessary and the response to clopidogrel may be
insufficient. In the last few years, cilostazol, a phosphodiesterase (PDE) 3 inhibitor, has been tested in the setting of acute
coronary syndromes: it exerts not only anti-platelet actions, but also pleiotropic effects, including inhibition on neointimal
hyperplasia, therefore preventing both stent restenosis and thrombosis. Therefore, cilostazol may be considered, on top of
our current anti-platelet therapy, as a potential candidate to achieve optimal platelet inhibition especially in patients undergoing
primary-PCI (p-PCI) or high risk procedures. This review will focus on the pharmacological characteristics of
cilostazol and the initial evidences that support the use of this drug in the setting of p-PCI.
Keywords: Cilostazol, antiplatelet therapy, primary-PCI, P2Y12 receptor, clopidogrel, stent restenosis, thrombosis, phosphodiesterase (PDE) 3 inhibitor, neointimal hyperplasia, acute coronary syndromes
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