OBJECTIVES: The purpose of this study was to determine the impact of adjunctive cilostazol in patients with high post-treatment platelet reactivity (HPPR) undergoing coronary stenting. BACKGROUND: Although addition of cilostazol to dual antiplatelet therapy enhances adenosine diphosphate (ADP)-induced platelet inhibition, it is unknown whether adjunctive cilostazol can reduce HPPR. METHODS:Sixty patients with HPPR after a 300-mg loading dose of clopidogrel were enrolled. HPPR was defined as maximal platelet aggregation (Agg(max)) >50% with 5 micromol/l ADP. Patients were randomly assigned to receive either adjunctive cilostazol (triple group; n = 30) or high maintenance dose (MD) clopidogrel (high-MD group; n = 30). Platelet function was assessed at baseline and after 30 days with conventional aggregometry and the VerifyNow assay. RESULTS:Baseline platelet function measurements were similar in both groups. After 30 days, significantly fewer patients in the triple versus high-MD group had HPPR (3.3% vs. 26.7%, p = 0.012). Percent inhibitions of 5 micromol/l ADP-induced Agg(max) and late platelet aggregation (Agg(late)) were significantly greater in the triple versus high-MD group (51.1 +/- 22.5% vs. 28.0 +/- 18.5%, p < 0.001, and 70.9 +/- 27.3% vs. 45.3 +/- 23.4%, p < 0.001, respectively). Percent inhibitions of 20 micromol/l ADP-induced Agg(max) and Agg(late) were consistently greater in the triple versus high-MD group. Percent change of P2Y12 reaction units demonstrated a higher antiplatelet effect in the triple versus high-MD group (39.6 +/- 24.1% vs. 23.1 +/- 29.9%, p = 0.022). CONCLUSIONS:Adjunctive cilostazol reduces the rate of HPPR and intensifies platelet inhibition as compared with a high-MD clopidogrel of 150 mg/day.
RCT Entities:
OBJECTIVES: The purpose of this study was to determine the impact of adjunctive cilostazol in patients with high post-treatment platelet reactivity (HPPR) undergoing coronary stenting. BACKGROUND: Although addition of cilostazol to dual antiplatelet therapy enhances adenosine diphosphate (ADP)-induced platelet inhibition, it is unknown whether adjunctive cilostazol can reduce HPPR. METHODS: Sixty patients with HPPR after a 300-mg loading dose of clopidogrel were enrolled. HPPR was defined as maximal platelet aggregation (Agg(max)) >50% with 5 micromol/l ADP. Patients were randomly assigned to receive either adjunctive cilostazol (triple group; n = 30) or high maintenance dose (MD) clopidogrel (high-MD group; n = 30). Platelet function was assessed at baseline and after 30 days with conventional aggregometry and the VerifyNow assay. RESULTS: Baseline platelet function measurements were similar in both groups. After 30 days, significantly fewer patients in the triple versus high-MD group had HPPR (3.3% vs. 26.7%, p = 0.012). Percent inhibitions of 5 micromol/l ADP-induced Agg(max) and late platelet aggregation (Agg(late)) were significantly greater in the triple versus high-MD group (51.1 +/- 22.5% vs. 28.0 +/- 18.5%, p < 0.001, and 70.9 +/- 27.3% vs. 45.3 +/- 23.4%, p < 0.001, respectively). Percent inhibitions of 20 micromol/l ADP-induced Agg(max) and Agg(late) were consistently greater in the triple versus high-MD group. Percent change of P2Y12 reaction units demonstrated a higher antiplatelet effect in the triple versus high-MD group (39.6 +/- 24.1% vs. 23.1 +/- 29.9%, p = 0.022). CONCLUSIONS: Adjunctive cilostazol reduces the rate of HPPR and intensifies platelet inhibition as compared with a high-MD clopidogrel of 150 mg/day.