Korean Circ J.  2009 Jan;39(1):21-25. 10.4070/kcj.2009.39.1.21.

Clinical Effects of Additional Cilostazol Administration After Drug-Eluting Stent Insertion

Affiliations
  • 1Department of Internal Medicine, College of Medicine, Dong-A University, Busan, Korea. kimmh@dau.ac.kr
  • 2Department of Laboratory Medicine, College of Medicine, Dong-A University, Busan, Korea.

Abstract

BACKGROUND AND OBJECTIVES: Cilostazol, a selective inhibitor of phosphodiesterase III (PDE III), prevents inactivation of the intracellular second messenger cyclic adenosine monophosphate (cAMP) and irreversibly inhibits platelet aggregation and vasodilation. Hence, we performed this prospective randomized study to evaluate the clinical effects of additional cilostazol administration in patients receiving dual antiplatelet therapy after drug-eluting stent (DES) insertion.
SUBJECTS AND METHODS
Between December 2003 and June 2006, we enrolled a total 603 consecutive patients who underwent successful percutaneous coronary intervention (PCI) with DES insertion at Dong-A University Hospital. Study patients received dual antiplatelet therapy (aspirin and clopidogrel, n=301) for at least six months or dual antiplatelet therapy (six months) combined with cilostazol medication for one month (triple therapy, n=302) after PCI. We investigated the incidence of major adverse cardiac events (MACE) at one month and six months after the initiation of medical therapy. MACE was defined as a composite of death, myocardial infarction (MI), stent thrombosis, and target lesion revascularization (TLR). Platelet function was evaluated in 66 patients (dual therapy group, n=40; triple therapy group, n=26) using a Chrono-Log platelet aggregometer and the VerifyNow P2Y12 assay system.
RESULTS
The MACE rate was 0.66% in the triple therapy group (death only, 0.67%) and 1.67% in the dual therapy group (death, 0.67%; MI, 0.67%; stent thrombosis, 0.99%; TLR, 0.99%) at one month after PCI (p=0.087). At six months, there were no differences in the MACE rate between the two groups (triple group vs. dual group=2.65% vs. 3.99%, p=0.864). In laboratory tests, platelet aggregation induced by agonists of ADP (27.92+/-13.04% vs. 40.9+/-15.78%, p=0.0008), collagen (13.73+/-6.95% vs. 27.43+/-14.87%, p=0.03), and epinephrine (10.38+/-7.82% vs. 15.5+/-10.45%, p=0.0000) were lower in the triple therapy group versus the dual therapy group. However, platelet aggregation induced by agonists of arachidonic acid (3.23+/-1.07% vs. 3.78+/-2.12%, p=0.23) and ristocetin (29.19+/-35.55% vs. 44.78+/-32.65%, p=0.07) and aspirin reaction unit (412.96+/-96.25 vs. 427.93+/-76.24, p=0.48) measured by VerifyNow were not different in the triple group versus the dual group.
CONCLUSION
Additional administration of cilostazol did not decrease the MACE rate when compared to dual therapy six months after PCI in patients with DES.

Keyword

Drug-eluting stents; Platelet aggregation; Cilostazol

MeSH Terms

Adenosine Diphosphate
Adenosine Monophosphate
Arachidonic Acid
Aspirin
Blood Platelets
Collagen
Cyclic Nucleotide Phosphodiesterases, Type 3
Drug-Eluting Stents
Epinephrine
Humans
Incidence
Myocardial Infarction
Percutaneous Coronary Intervention
Platelet Aggregation
Prospective Studies
Ristocetin
Second Messenger Systems
Stents
Tetrazoles
Thrombosis
Ticlopidine
Vasodilation
Adenosine Diphosphate
Adenosine Monophosphate
Arachidonic Acid
Aspirin
Collagen
Cyclic Nucleotide Phosphodiesterases, Type 3
Epinephrine
Ristocetin
Tetrazoles
Ticlopidine

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