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Neurological research · Jul 2015
Multicenter StudyCilostazol may prevent cardioembolic stroke in patients undergoing antiplatelet therapy.
- Nobutaka Horie, Makio Kaminogo, Tsuyoshi Izumo, Kentaro Hayashi, Akira Tsujino, and Izumi Nagata.
- Neurol. Res. 2015 Jul 1;37(7):619-23.
ObjectivesRandomised trials have shown the efficacy of antiplatelet therapy with cilostazol to prevent secondary ischaemic stroke. Recently, cilostazol has been reported to prevent the development and/or recurrence of atrial fibrillation (AF), which can potentially prevent cardioembolic stroke in patients undergoing antiplatelet therapy. Herein, we examined the impact of prior antiplatelet therapy with cilostazol on the incidence of cardioembolic stroke, which had not been fully investigated.MethodsUsing the multicenter retrospective study of stroke risk in antithrombotic therapy (RESTATE) database, we analysed consecutive patients with primary or secondary stroke under single antiplatelet therapy. We evaluated the characteristics of ischaemic stroke based on the type of antiplatelet agent used: aspirin, ticlopidine/clopidogrel or cilostazol.ResultsOf 1069 consecutive patients with primary or secondary stroke during antithrombotic therapy from January to December 2012, 615 patients received single antiplatelet therapy (293 and 322 cases of primary and secondary strokes, respectively). Interestingly, the percentage of cardioembolic infarction was significantly lower in patients taking cilostazol compared with other agents. Multivariate regression analysis found that age (OR: 1.03, 95% CI: 1.01-1.06, P = 0.0029), serum creatinine (OR: 1.17, 95% CI: 1.03-1.34, P = 0.0198), aspirin (OR: 1.75, 95% CI: 1.00-3.22, P = 0.0486), cilostazol (OR: 0.19, 95% CI: 0.03-0.73, P = 0.0125), and smoking (OR: 1.86, 95% CI: 1.16-2.94, P = 0.0102) were independently associated with cardioembolic stroke.ConclusionsCilostazol may prevent cardioembolic stroke in patients undergoing antiplatelet therapy. This could be a novel strategy for cardioembolic stroke prevention potentially by affecting cardiac remodelling, in contrast to secondary anticoagulant therapy.
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