title: Cilostazol and primary-PCI: mirage or good alternative?
abstract: 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.
authors.affiliation: Department of Cardiovascular Medicine, Catholic University of the Sacred Heart, Rome, Italy. italo.porto@gmail.com
authors.forename: Italo
authors.initials: I
authors.lastname: Porto
authors.forename: Domenico
authors.initials: D
authors.lastname: D'Amario
authors.forename: Filippo
authors.initials: F
authors.lastname: Crea
mesh_terms: D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000503:physiopathology / Q000601:surgery*; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D001145:Arrhythmias, Cardiac / Q000188:drug therapy / Q000503:physiopathology / Q000601:surgery; D001241:Aspirin / Q000009:adverse effects / Q000627:therapeutic use; D000077407:Cilostazol; D000077144:Clopidogrel; D003131:Combined Modality Therapy; D023903:Coronary Restenosis / Q000517:prevention & control; D004359:Drug Therapy, Combination / Q000009:adverse effects; D006333:Heart Failure / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control; D006801:Humans; D058987:Phosphodiesterase 3 Inhibitors / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D011355:Prodrugs / Q000009:adverse effects / Q000627:therapeutic use; D012306:Risk; D015607:Stents / Q000009:adverse effects; D013777:Tetrazoles / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D013927:Thrombosis / Q000209:etiology / Q000517:prevention & control*; D013988:Ticlopidine / Q000009:adverse effects / Q000031:analogs & derivatives / Q000627:therapeutic use
chemical_list: D058987:Phosphodiesterase 3 Inhibitors; D010975:Platelet Aggregation Inhibitors; D011355:Prodrugs; D013777:Tetrazoles; D000077144:Clopidogrel; D000077407:Cilostazol; D013988:Ticlopidine; D001241:Aspirin