TY - JOUR
T1 - Effects of cilostazol on platelet activation in coronary stenting patients who already treated with aspirin and clopidogrel
AU - Ahn, Jeong Cheon
AU - Song, Woo Hyuk
AU - Kwon, Jung Ah
AU - Park, Chang Gyu
AU - Seo, Hong Seok
AU - Oh, Dong Joo
AU - Rho, Young Moo
PY - 2004/12
Y1 - 2004/12
N2 - 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.
AB - 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.
KW - Antiplatelet therapy
KW - Coronary stent
UR - http://www.scopus.com/inward/record.url?scp=14844328650&partnerID=8YFLogxK
U2 - 10.3904/kjim.2004.19.4.230
DO - 10.3904/kjim.2004.19.4.230
M3 - Article
C2 - 15683111
AN - SCOPUS:14844328650
SN - 1226-3303
VL - 19
SP - 230
EP - 236
JO - Korean Journal of Internal Medicine
JF - Korean Journal of Internal Medicine
IS - 4
ER -