Key result
Dual therapy with aspirin and cilostazol did not significantly differ from aspirin alone in platelet aggregation or activation, but it significantly inhibited ADP-induced platelet aggregation compared to baseline.
Why the study?
Does dual therapy with cilostazol and aspirin improve platelet aggregation and endothelial function compared to aspirin alone in patients with acute noncardioembolic ischemic stroke?
RCT (n=24)
Open-label
RAND function of Microsoft Excel
No
Does dual therapy with cilostazol and aspirin improve platelet aggregation and endothelial function compared to aspirin alone in patients with acute noncardioembolic ischemic stroke?
p-value: p=>0.05
Dual therapy with aspirin and cilostazol did not significantly differ from aspirin alone in between-group platelet aggregation, but it did significantly reduce ADP-induced platelet aggregation from baseline in patients with noncardioembolic stroke.
Dual therapy adds no platelet inhibition benefit over aspirin alone in acute noncardioembolic stroke; challenges adjunctive cilostazol and warrants outcome-focused trials.
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.
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Ohnuki et al. (2017) conducted an RCT in Acute noncardioembolic ischemic stroke (n=24). Cilostazol plus aspirin vs. Aspirin 100 mg/day was evaluated on Differences in platelet aggregation, platelet activation, and biomarkers at 2 and 4 weeks (p=>0.05). Dual therapy with aspirin and cilostazol did not significantly differ from aspirin alone in platelet aggregation or activation, but it significantly inhibited ADP-induced platelet aggregation compared to baseline.
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