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The aim of this study was to confirm clinically a hypothesis that cilostazol i nhibits leukocyte Mac-1, leading to prevention of post stent restenosis. The p latelet phosphodiesterase III inhibitor called cilostazol also inhibits alpha g ranule release of P selectin in platelets. The P selectin mediated plateletle ukocyte interaction promotes activation and upregulation of leukocyte Mac 1 aft er coronary stenting, which plays a key role on the mechanism of restenosis. Thu s, cilostazols potential inhibition of this process may lead to prevention of restenosis. Using flow cytometric analysis of whole blood obtained from the coro nary sinus, the expression of platelet membrane glycoproteins and neutrophil adh esion molecules was observed in 70 consecutive patients undergoing coronary sten ting. The patients were randomly assigned to either a cilostazol or ticlopidine group before stent placement. The restenosis rate was lower (15%vs. 31%, p< 0. 05) in the cilostazol group (n=34)than in the ticlopidine group (n=32). A stent induced increase in platelet P selectin(CD62P) expression and an increase in neutrophil Mac-1 (CD11b) expression were suppressed in the cilostazol group com pared with the ticlopidine group. Angiographic late lumen loss was correlated wi th the relative changes in platelet P selectin and neutrophil Mac-1 at 48 h af ter coronary stenting. Cilostazol may have effects on suppression of P selectin mediated platelet activation, platelet leukocyte interaction, and subsequent Mac 1 mediated leukocyte activation, which might lead to a reduced restenosis rate after coronary stent implantation.
The aim of this study was to confirm clinically a hypothesis that cilostazol i nhibits leukocyte Mac-1, leading to prevention of post stent restenosis. The P latelet phosphodiesterase III inhibitor called cilostazol also inhibits alpha g ranule release of P selectin in platelets. The P selectin mediated plateletle ukocyte interaction promotes activation and upregulation of leukocyte Mac 1 aft coronary stenting, which plays a key role on the mechanism of restenosis. Thu s, cilostazol s potential inhibition of this process may lead to prevention of restenosis. Using flow cytometric analysis of whole blood obtained from the coro nary sinus, the expression of platelet membrane glycoproteins and neutrophil adh esion molecules was observed in 70 consecutive patients undergoing coronary stening. The patients were randomly assigned to either a cilostazol or ticlopidine group before stent placement. The restenosis rate was lower (15% vs. 31%, p <0.05) in the cilostazol group (n = 34) than i n the ticlopidine group (n = 32). A stent induced increase in platelet P selectin (CD62P) expression and an increase in neutrophil Mac-1 (CD11b) expression were suppressed in the cilostazol group com pared with the ticlopidine group. Angiographic late lumen loss was correlated wi th the relative changes in platelet P selectin and neutrophil Mac-1 at 48 h af ter coronary stenting. Cilostazol may have on suppression of P selectin mediated platelet activation, platelet leukocyte interaction, and subsequent Mac 1 mediated leukocyte activation, which might lead to reduced recovery rate after coronary stent implantation.