OBJECTIVE: To assess the effectiveness of cilostazol, a selective inhibitor of phosphodiesterase type III, in preventing cerebral ischemia related to cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). METHODS: A total of six clinical studies met the inclusion criteria and were included in the meta-analysis. We calculated pooled risk ratios (RR) and 95% confidence intervals (CI) using random-effects models. The primary endpoint was cerebral ischemia related to vasospasm. Secondary endpoints were angiographic vasospasm, new cerebral infarct, mortality, and death or disability at the final follow-up. RESULTS: A total of 136 (22%) of 618 subjects (38 and 98 assigned to cilostazol and control treatments, respectively) with SAH developed cerebral ischemia related to vasospasm. The risk of cerebral ischemia related to vasospasm was significantly lower in subjects assigned to cilostazol treatment (RR 0.43; 95% CI 0.31-0.60; p< 0.001). The risks of angiographic vasospasm (RR 0.67, 95% CI 0.54-0.84, p< 0.001 ) and new cerebral infarct (RR 0.37, 95% CI 0.24-0.57, p< 0.001) were significantly lower in subjects assigned to cilostazol treatment. There was a significantly lower rate of death or disability in subjects assigned to cilostazol treatment at follow-up (PR 0.55, 95% 0.39-0.78, p = 0.001). CONCLUSION: The reduction in rates of cerebral ischemia related to vasospasm and death or disability at follow-up support further evaluation of oral cilostazol in patients with aneurysmal SAH in a large randomized clinical trial.
OBJECTIVE: To assess the effectiveness of cilostazol, a selective inhibitor of phosphodiesterase type III, in preventing cerebral ischemia related to cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). METHODS: A total of six clinical studies met the inclusion criteria and were included in the meta-analysis. We calculated pooled risk ratios (RR) and 95% confidence intervals (CI) using random-effects models. The primary endpoint was cerebral ischemia related to vasospasm. Secondary endpoints were angiographic vasospasm, new cerebral infarct, mortality, and death or disability at the final follow-up. RESULTS: A total of 136 (22%) of 618 subjects (38 and 98 assigned to cilostazol and control treatments, respectively) with SAH developed cerebral ischemia related to vasospasm. The risk of cerebral ischemia related to vasospasm was significantly lower in subjects assigned to cilostazol treatment (RR 0.43; 95% CI 0.31-0.60; p< 0.001). The risks of angiographic vasospasm (RR 0.67, 95% CI 0.54-0.84, p< 0.001 ) and new cerebral infarct (RR 0.37, 95% CI 0.24-0.57, p< 0.001) were significantly lower in subjects assigned to cilostazol treatment. There was a significantly lower rate of death or disability in subjects assigned to cilostazol treatment at follow-up (PR 0.55, 95% 0.39-0.78, p = 0.001). CONCLUSION: The reduction in rates of cerebral ischemia related to vasospasm and death or disability at follow-up support further evaluation of oral cilostazol in patients with aneurysmal SAH in a large randomized clinical trial.
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