학술대회 안내 사전등록 안내 초록등록 안내 초록등록/관리 숙박및교통 안내


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ǥ : ڻ ȣ - 500717   8 
The effect of additional cilostazol for the ADP induced platelet aggregation and soluble CD40L in patients with primary percutaneous coronary intervention.
연세대학교 원주의과대학 원주기독병원 순환기내과
이경훈, 이승환, 신명상, 유호열, 안민수, 최현민, 김장영, 이승환, 윤정한, 최경훈
Background: Recent evidences suggest that 5-45 % of taking aspirin or clopidogrel have inadequate antiplatelet activity which is related poor outcome of ischemic heart disease. Cilostazol can reduce the signal transduction of ADP induced platelet aggregation and might be potentate the antiplatelet efficacy of clopidogrel. We examined the effect of additional cilostazol for the ADP induced platelet aggregation and soluble CD40 ligand(sCD40L) in patients with acute myocardial infarction(AMI). Methods: Patients with AMI were randomly assigned 28 of dual antiplatelet therapy (aspirin and clopidogrel, age; 62.3±10.3) and 26 of triple regimen (dual plus cilostazol, age; 62.3±10.9). Loading dosage (aspirin 300mg, clopidogrel 600mg and cilostazol 400mg in triple regimen) was medicated prior to 1-2 hours before emergent PCI. Aspirin 100mg and clopidogrel 75mg qd was administrated in dual and additional cilostazol 100mg bid was administrated in triple . Aspirin and clopidogrel resistance were evaluated by VerifyNow™ tests(Accumetrics, CA). The aspirin resistance results were expressed quantitatively in Aspirin Reaction Units(ARU) based on the degree of platelet aggregation. Clopidogrel resistance was expressed % inhibition of ADP-mediated aggregation specific to the platelet P2Y12 receptor compared to aggregation of the thrombin receptor activating peptide. The sCD40L was measured by ELISA method(R&D systems, MN).Results: Baseline clinical and laboratory characteristics were similar in both groups including initial sCD40L (387.6±596.2 vs. 435.2±469.8 pg/mL, p=0.75). ARU was not different in both groups (dual; 419.6 ± 44.3 vs. 425.8±66.2ARU, p=0.71). Percent inhibition of ADP-mediated aggregation was significantly higher in triple group (24.2±19.8 vs. 43.9±21.2, p=0.03). The values of sCD40L (day 1) was lower in triple (104.9±54.5 pg/mL) than dual group (164.3±147.1 pg/mL), but there was no statistical difference.(p=0.055) Conclusions: Additional administration of cilostazol was synergistically inhibiting P2Y12 mediated platelet aggregation and the trend of lowering overall antiplatelet activity in the early phase of AMI. These results suggested that cilostazol might improve the clopidogrel resistance in AMI.


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