Adding cilostazol to aspirin and clopidogrel significantly increased the inhibition of ADP-induced platelet aggregation (40.5% vs 23.8%, p=0.004) in patients undergoing primary percutaneous coronary intervention.
RCT (n=60)
1:1
No
Does the addition of cilostazol to aspirin and clopidogrel improve platelet responsiveness and reduce platelet activation in STEMI patients undergoing primary PCI?
Adding cilostazol to standard dual antiplatelet therapy significantly increases the inhibition of ADP-induced platelet aggregation in STEMI patients undergoing primary PCI, potentially mitigating clopidogrel low-responsiveness.
Absolute Event Rate: 40.5% vs 23.8%
p-value: p=0.004
BACKGROUND: Cilostazol increases the cyclic adenosine monophosphate levels in platelets and might ameliorate the antiplatelet activity of clopidogrel. This study investigated the additional effect of cilostazol on platelet aggregation measured by a VerifyNow analyzer and soluble CD40 ligand (sCD40L) as a marker of activated platelet in patients undergoing primary percutaneous coronary intervention (PCI). METHODS AND RESULTS: Sixty cases of primary PCI were randomly assigned to dual (aspirin and clopidogrel) or triple (dual plus cilostazol) therapy. The antiplatelet effects of aspirin and clopidogrel were evaluated by VerifyNow tests. The plasma sCD40L levels at admission, 24 h and 21 days were measured by the ELISA method. The arachidonic acid induced platelet aggregation was similar in both groups. However, the triple group had a significantly lower P2Y12 reaction unit (dual 208.8+/-69.0 vs triple 168.2+/-79.2, p=0.041) and higher % inhibition of adenosine diphosphate (ADP)-induced platelet aggregation (dual 23.8+/-21.4% vs triple 40.5+/-21.0%, p=0.004). In the multivariate analysis, cilostazol was a negative predictor for low responders to clopidogrel (95% confidence interval 0.067-0.711). The plasma sCD40L levels were not significantly different between the 2 groups at the same point of time. CONCLUSIONS: The addition of cilostazol to the combination of aspirin plus clopidogrel significantly increases the inhibition of ADP-induced platelet aggregation. However, there was no additive effect on aspirin-induced antiplatelet activity or lowering of sCD40L.
Kim et al. (2007) conducted an RCT in ST elevation myocardial infarction (STEMI) undergoing primary PCI (n=60). Cilostazol (added to aspirin and clopidogrel) vs. Standard dual regimen (aspirin and clopidogrel) was evaluated on % inhibition of ADP-induced platelet aggregation (p=0.004). Adding cilostazol to aspirin and clopidogrel significantly increased the inhibition of ADP-induced platelet aggregation (40.5% vs 23.8%, p=0.004) in patients undergoing primary percutaneous coronary intervention.