Clinical Studies
Antiplatelet Effect of Ticlopidine After Coronary Stenting

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Abstract

Objectives. This study sought to investigate the contribution of ticlopidine to the inhibition of platelet activation after coronary stent placement.

Background. After coronary stenting, antiplatelet therapy with aspirin and ticlopidine improves stent patency compared with anticoagulation. However, the specific role of ticlopidine has not been elucidated.

Methods. After successful coronary stent placement, we randomized 22 patients to receive ticlopidine and aspirin (ticlopidine group) and 25 to receive aspirin alone (aspirin group). Surface expression on platelets of the activated fibrinogen receptor and of P-selectin was assessed by flow cytometry.

Results. In the aspirin group the percent of platelets with activated fibrinogen receptors increased between days 1 and 5 (p = 0.001), whereas there were no substantial changes in the ticlopidine group. The percent of P-selectin–positive platelets did not change significantly in the aspirin group but decreased in the ticlopidine group (p = 0.019). At day 5 after the intervention, the percent of platelets with activated fibrinogen receptors in the ticlopidine group was significantly lower (median [interquartile range]: 8.5 [3.1 to 17.8] vs. 18.1 [8.5 to 35.5], p = 0.025), and there was a trend to fewer P-selectin–positive platelets than in the aspirin group (5.8 [3.4 to 9.5] vs. 8.8 [4.0 to 15.8], p = 0.073).

Conclusions. Combined antiplatelet therapy with ticlopidine plus aspirin is superior to treatment with aspirin alone in suppressing platelet activation after coronary stenting.

(J Am Coll Cardiol 1997;29:1515–9)

Abbreviations

CD
cluster of differentiation
FITC
fluorescein isothiocyanate
GP
glycoprotein
LIBS1
ligand-induced binding site 1
PTCA
percutaneous transluminal coronary angioplasty

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This study was supported by Grants Ne 540/1-1 and Ga 381/2-1 from the Deutsche Forschungsgemeinschaft, Bonn-Bad Godesberg, Germany and by Grant HL-48728 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Anti-LIBS1 monoclonal antibody was provided by Scripps Clinic, La Jolla, California.