Objective Some previous studies have found clinical benefit of dual antiplatelet
therapy with
aspirin and
cilostazol for prevention of secondary
stroke, but the physiological mechanism involved remains unknown. We aimed to clarify the effects of
aspirin/
cilostazol therapy on the platelet and endothelial functions of patients with acute noncardioembolic
ischemic stroke, in comparison to patients who were treated with
aspirin alone. Methods The present randomized prospective pilot study enrolled 24 patients within a week after the onset of noncardioembolic
ischemic stroke. The patients were randomly allocated to receive
aspirin (100 mg/day) (A group; 11 patients) or
cilostazol (200 mg/day) plus
aspirin (100 mg/day) (CA group; 13 patients). We measured platelet aggregation, platelet activation, and the
thrombomodulin (TM), highly sensitive
C-reactive protein (
hs-CRP),
intercellular adhesion molecule-1 (ICAM-1),
vascular cell adhesion molecule-1 (VCAM-1) and von Willebrand (vWF)
antigen levels and vWF activity over a 4-week period after enrollment. Results There was no significant difference in the platelet functions of the A and CA groups. However, the platelet aggregation induced by
adenosine diphosphate (
ADP) was decreased at 2 and 4 weeks (p<0.05)
after treatment in comparison to the pre-treatment values in the CA group, but not in the A group. Platelet activation, and the
hs-CRP, TM,
ICAM-1,
VCAM-1 and vWF values did not significantly decrease
after treatment in either group. Conclusion Although there were no significant differences in platelet aggregation, platelet activation or the endothelial
biomarker levels of the A and CA groups, dual
therapy with
aspirin and
cilostazol inhibited platelet aggregation in comparison to the pre-treatment values, similarly to patients who received
aspirin alone. This may suggest the clinical usefulness of dual
therapy with
aspirin and
cilostazol in the treatment of patients with noncardioembolic
ischemic stroke.