title: Comparison of on-treatment platelet reactivity between triple antiplatelet therapy with cilostazol and standard dual antiplatelet therapy in patients undergoing coronary interventions: a meta-analysis.
abstract: BACKGROUND
  The recent literature has shown that triple antiplatelet therapy with cilostazol in addition to the standard dual antiplatelet therapy with aspirin and clopidogrel may reduce platelet reactivity and improve clinical outcomes following percutaneous coronary intervention. The purpose of this meta-analysis is to compare the efficacy of triple antiplatelet therapy and dual antiplatelet therapy in regard to on-treatment platelet reactivity.
  
  
  METHODS
  Nine studies (n = 2179) comparing on-treatment platelet reactivity between dual antiplatelet therapy (n = 1193) and triple antiplatelet therapy (n = 986) in patients undergoing percutaneous coronary intervention were included. Primary end points were P2Y12 reaction unit (PRU) and platelet reactivity index (PRI). Secondary end points were platelet aggregation with adenosine diphosphate (ADP) 5 and 20 µmol/L and P2Y12% inhibition. Mean difference (MD) and 95% confidence intervals (CI) were computed and 2-sided α error <.05 was considered as a level of significance.
  
  
  RESULTS
  Compared to dual antiplatelet therapy, triple antiplatelet therapy had significantly lower maximum platelet aggregation with ADP 5 µmol/L (MD: -14.4, CI: -21.6 to -7.2, P < .001) and 20 µmol/L (MD: -14.9, CI: -22.9 to -6.8, P < .001), significantly lower PRUs (MD: -45, CI: -59.4 to -30.6, P < .001) and PRI (MD: -26, CI: -36.8 to -15.2, P < .001), and significantly higher P2Y12% inhibition (MD: 18.5, CI: 2.3 to 34.6, P = .025).
  
  
  CONCLUSIONS
  Addition of cilostazol to conventional dual antiplatelet therapy significantly lowers platelet reactivity and may explain a decrease in thromboembolic events following coronary intervention; however, additional studies evaluating clinical outcomes will be helpful to determine the benefit of triple antiplatelet therapy.
authors.affiliation: 1Department of Internal Medicine, East Tennessee State University, Johnson City, TN, USA.
authors.forename: Hemang B
authors.initials: HB
authors.lastname: Panchal
authors.forename: Tejaskumar
authors.initials: T
authors.lastname: Shah
authors.forename: Parthavkumar
authors.initials: P
authors.lastname: Patel
authors.forename: Kais
authors.initials: K
authors.lastname: Albalbissi
authors.forename: Janos
authors.initials: J
authors.lastname: Molnar
authors.forename: Brandon
authors.initials: B
authors.lastname: Coffey
authors.forename: Sandeep
authors.initials: S
authors.lastname: Khosla
authors.forename: Vijay
authors.initials: V
authors.lastname: Ramu
mesh_terms: D001241:Aspirin / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D001792:Blood Platelets / Q000187:drug effects; D000077407:Cilostazol; D000077144:Clopidogrel; D003324:Coronary Artery Disease / Q000628:therapy; D004359:Drug Therapy, Combination; D006801:Humans; D062645:Percutaneous Coronary Intervention / Q000379:methods*; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D013777:Tetrazoles / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D013923:Thromboembolism / Q000453:epidemiology / Q000517:prevention & control; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D010975:Platelet Aggregation Inhibitors; D013777:Tetrazoles; D000077144:Clopidogrel; D000077407:Cilostazol; D013988:Ticlopidine; D001241:Aspirin
keywords: antiplatelet therapy; cilostazol; percutaneous coronary intervention; platelet reactivity