Details

Autor(en) / Beteiligte

• Sugimoto, Kazutaka
• Nomura, Sadahiro
• Shirao, Satoshi
• Inoue, Takao
• Ishihara, Hideyuki
• Kawano, Reo
• Kawano, Akiko
• Oka, Fumiaki
• Suehiro, Eiichi
• Sadahiro, Hirokazu
• Shinoyama, Mizuya
• Oku, Takayuki
• Maruta, Yuichi
• Hirayama, Yuya
• Hiyoshi, Koichiro
• Kiyohira, Miwa
• Yoneda, Hiroshi
• Okazaki, Koki
• Dreier, Jens P.
• Suzuki, Michiyasu

Titel

Cilostazol decreases duration of spreading depolarization and spreading ischemia after aneurysmal subarachnoid hemorrhage

Ist Teil von

• Annals of neurology, 2018-12, Vol.84 (6), p.873-885

Ort / Verlag

United States: Wiley Subscription Services, Inc

Erscheinungsjahr

2018

Quelle

Wiley InterScience Journals

Beschreibungen/Notizen

• Objective Traditionally, angiographic vasospasm (aVS) has been thought to cause delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH). However, successful treatment of aVS alone does not result in improved neurological outcome. Therefore, there may be other potential causes of poor neurological outcome, including spreading depolarization (SD). A recent study showed beneficial effects of cilostazol on DCI and neurological outcome. The present prospective clinical trial and experimental study focused on effects of cilostazol on SDs. Methods Fifty aSAH patients were treated with clip ligation and randomly assigned to a cilostazol (n = 23) or control group (n = 27). Effects of cilostazol on DCI, aVS, and SDs, measured with subdural electrodes, were examined. The effect of cilostazol on SD‐induced perfusion deficits (spreading ischemia) was assessed in an aSAH‐mimicking model. Results There was a trend for less DCI in the cilostazol group, but it did not reach our threshold for statistical significance (13.0% vs 40.0%, odds ratio = 0.266, 95% confidence interval [CI] = 0.059–1.192, p = 0.084). However, the total SD‐induced depression duration per recording day (22.2 vs 30.2 minutes, β = −251.905, 95% CI = −488.458 to −15.356, p = 0.043) and the occurrence of isoelectric SDs (0 vs 4 patients, β = −0.916, 95% CI = −1.746 to −0.085, p = 0.037) were significantly lower in the cilostazol group. In rats, cilostazol significantly shortened SD‐induced spreading ischemia compared to vehicle (Student t test, difference = 30.2, 95% CI = 5.3–55.1, p = 0.020). Interpretation Repair of the neurovascular response to SDs by cilostazol, as demonstrated in the aSAH‐mimicking model, may be a promising therapy to control DCI. Ann Neurol 2018;84:873–885