Cilostazol could ameliorate platelet responsiveness to clopidogrel in patients undergoing primary percutaneous coronary intervention

Jang Young Kim, Kyounghoon Lee, Myungsang Shin, Minsoo Ahn, Hyunmin Choe, Byung Su Yoo, Junghan Yoon, Kyung Hoon Choe, Seung Hwan Lee

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

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, 24h 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.

Original languageEnglish
Pages (from-to)1867-1872
Number of pages6
JournalCirculation Journal
Volume71
Issue number12
DOIs
Publication statusPublished - 2007 Dec 20

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clopidogrel
Percutaneous Coronary Intervention
CD40 Ligand
Platelet Aggregation
Blood Platelets
Aspirin
Adenosine Diphosphate
Arachidonic Acid
Cyclic AMP
Multivariate Analysis
Enzyme-Linked Immunosorbent Assay
cilostazol
Confidence Intervals

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Cilostazol could ameliorate platelet responsiveness to clopidogrel in patients undergoing primary percutaneous coronary intervention",
abstract = "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, 24h 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.",
author = "Kim, {Jang Young} and Kyounghoon Lee and Myungsang Shin and Minsoo Ahn and Hyunmin Choe and Yoo, {Byung Su} and Junghan Yoon and Choe, {Kyung Hoon} and Lee, {Seung Hwan}",
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Cilostazol could ameliorate platelet responsiveness to clopidogrel in patients undergoing primary percutaneous coronary intervention. / Kim, Jang Young; Lee, Kyounghoon; Shin, Myungsang; Ahn, Minsoo; Choe, Hyunmin; Yoo, Byung Su; Yoon, Junghan; Choe, Kyung Hoon; Lee, Seung Hwan.

In: Circulation Journal, Vol. 71, No. 12, 20.12.2007, p. 1867-1872.

Research output: Contribution to journalArticle

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T1 - Cilostazol could ameliorate platelet responsiveness to clopidogrel in patients undergoing primary percutaneous coronary intervention

AU - Kim, Jang Young

AU - Lee, Kyounghoon

AU - Shin, Myungsang

AU - Ahn, Minsoo

AU - Choe, Hyunmin

AU - Yoo, Byung Su

AU - Yoon, Junghan

AU - Choe, Kyung Hoon

AU - Lee, Seung Hwan

PY - 2007/12/20

Y1 - 2007/12/20

N2 - 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, 24h 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.

AB - 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, 24h 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.

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