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Effects of cilostazol on platelet activation in coronary stenting patients who already treated with aspirin and clopidogrel.
Korean Journal of Internal Medicine 2004 December
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). Underying 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.
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). Underying 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.
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