H Yoneda1, S Shirao, T Kurokawa, H Fujisawa, S Kato, M Suzuki. 1. Department of Neurosurgery, Clinical Neuroscience, Yamaguchi University School of Medicine, Ube, Yamaguchi, Japan. yo-hiroshi@k9.dion.ne.jp
Abstract
BACKGROUND: Cerebral vasospasm following subarachnoid hemorrhage (SAH) is a significant cause of morbidity and mortality and recent studies indicate that Rho-kinase plays an important role in the occurrence of such cerebral vasospasm. Eicosapentaenoic acid (EPA), an n-3 polyunsaturated fatty acid, inhibits sphingosylphosphorylcholine (SPC)-induced Rho-kinase activation in vitro, so this study examined whether EPA prevented cerebral vasospasm occurrence after SAH in patients. METHODS: The trial population was 101 patients with SAH subjected to craniotomy and clip application. EPA was orally administered at a daily dose of 1800 mg EPA from day 4 to day 14 to 73 patients; the other 28 constituted the control group, receiving no EPA. RESULTS: EPA significantly curtailed both the occurrence of symptomatic vasospasm (14% EPA group, 36% control, P = 0.019) and of cerebral infarction because of cerebral vasospasm (4% EPA group, 29% control, P = 0.001). Moreover, the percentage of patients with a clinically good outcome was significantly higher in the EPA group (85%, P = 0.022) than in control (64%); there were no deaths in the EPA group but three (11%) in control (P = 0.020). CONCLUSION: These findings suggest EPA inhibits symptomatic cerebral vasospasm and cerebral infarction after SAH and also improves clinical prognosis.
BACKGROUND:Cerebral vasospasm following subarachnoid hemorrhage (SAH) is a significant cause of morbidity and mortality and recent studies indicate that Rho-kinase plays an important role in the occurrence of such cerebral vasospasm. Eicosapentaenoic acid (EPA), an n-3 polyunsaturated fatty acid, inhibits sphingosylphosphorylcholine (SPC)-induced Rho-kinase activation in vitro, so this study examined whether EPA prevented cerebral vasospasm occurrence after SAH in patients. METHODS: The trial population was 101 patients with SAH subjected to craniotomy and clip application. EPA was orally administered at a daily dose of 1800 mg EPA from day 4 to day 14 to 73 patients; the other 28 constituted the control group, receiving no EPA. RESULTS:EPA significantly curtailed both the occurrence of symptomatic vasospasm (14% EPA group, 36% control, P = 0.019) and of cerebral infarction because of cerebral vasospasm (4% EPA group, 29% control, P = 0.001). Moreover, the percentage of patients with a clinically good outcome was significantly higher in the EPA group (85%, P = 0.022) than in control (64%); there were no deaths in the EPA group but three (11%) in control (P = 0.020). CONCLUSION: These findings suggest EPA inhibits symptomatic cerebral vasospasm and cerebral infarction after SAH and also improves clinical prognosis.
Authors: Michaela C Pascoe; David W Howells; David P Crewther; Nicki Constantinou; Leeanne M Carey; Sarah S Rewell; Giovanni M Turchini; Gunveen Kaur; Sheila G Crewther Journal: Front Neurol Date: 2014-02-06 Impact factor: 4.003