Effects of Cilostazol on Platelet Activation in Coronary Stenting Patients Who Already Treated with Aspirin and Clopidogrel.
- Author:
Jeong Cheon AHN
1
;
Woo Hyuk SONG
;
Jung Ah KWON
;
Chang Gyu PARK
;
Hong Seok SEO
;
Dong Joo OH
;
Young Moo RHO
Author Information
1. Department of Internal Medicine, Ansan Hospital, Korea University College of Medicine, Seoul, Korea. hhansin@korea.ac.kr
- Publication Type:Original Article
- Keywords:
Antiplatelet therapy;
Coronary stent
- MeSH:
Aspirin/*therapeutic use;
Dose-Response Relationship, Drug;
Drug Therapy, Combination;
Female;
Humans;
Male;
Middle Aged;
Myocardial Ischemia/surgery;
P-Selectin/blood;
Platelet Aggregation Inhibitors/*therapeutic use;
Platelet Glycoprotein GPIIb-IIIa Complex/analysis;
Stents;
Tetrazoles/*therapeutic use;
Thrombosis/blood/*prevention & control;
Ticlopidine/*analogs & derivatives/*therapeutic use
- From:The Korean Journal of Internal Medicine
2004;19(4):230-236
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: A recent study has shown that triple anti-platelet therapy (cilostazol+clopidogrel+aspirin) resulted in a significantly lower restenosis rate after coronary stenting than did conventional therapy (clopidogrel+aspirin). However, the anti-platelet effects of cilostazol, when combined with clopidogrel and aspirin, have not been evaluated. METHODS: Low dose cilostazol (50 mg/BID) was given to 47 patients who had already been taking clopidogrel (75 mg/day) and aspirin (100 mg/day) for more than 1 month subsequent to coronary stenting due to AMI and unstable angina. Markers of platelet activation, P-selectin and activated GPIIb/IIIa on platelets, were measured at baseline and 2 weeks after cilostazol treatment. We empirically divided patients into tertiles (low, n=16; moderate, n=14; high group, n=17), according to the baseline P-selectin expression. We then performed a comparative assessment of the anti-platelet effects of cilostazol at baseline and after 2 weeks of cilosatzol administration. RESULTS: P-selectin was significantly decreased after 2 weeks of cilostazol treatment in total patients (n=47, 3.2 +/- 2.4% to 2.0 +/- 1.9%, p=0.03). This inhibition of P-selectin expression was mainly achieved in the moderate and high P-selectin groups (low group; 1.4 +/- 0.5 to 1.9 +/- 1.3%, p> 0.05, moderate group; 2.5 +/- 0.3 to 1.3 +/- 0.3%, p< 0.05, high group; 5.4 +/- 2.7 to 2.7 +/- 2.8%, p< 0.05). Activated GPIIb/IIIa was not significantly changed (13.5% to 17.6%, p> 0.05). Underlying disease, cardiovascular risk factors, concomitant medication including statin, and hsCRP were not related to the degree of P-selectin expression. CONCLUSION: Our data demonstrated that cilostazol treatment in addition to conventional anti-platelet therapy provides more effective suppression of platelet P-selectin expression in patients with relatively high platelet activity.
