Ogawa Shotaro, Koizumi Satoshi, Umekawa Motoyuki, Fujitani Shigeta, Ono Hideaki, Miyawaki Satoru, Saito Nobuhito
Department of Neurosurgery, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Interv Neuroradiol. 2025 Aug 6:15910199251362730. doi: 10.1177/15910199251362730.
Background and PurposeAlthough many studies have reported the efficacy of clazosentan in preventing delayed cerebral ischemia associated with cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH), recent studies have shown that its vasodilatory effect does not contribute to improved prognosis, leaving its efficacy controversial. In this study, we quantitatively measured vascular diameter changes during the vasospasm period at various vascular sites to investigate the association between the radiological and clinical effects of clazosentan.Materials and MethodsWe retrospectively analyzed 22 patients with aSAH classified as Fisher group 3, treated at our hospital. Clazosentan (10 mg/h) was administered to 12 patients, while 10 patients received conventional vasospasm management. Arterial diameters at 12 locations were measured at the onset and during the vasospasm period. Quantitative changes in vascular diameter were compared between the clazosentan and nonclazosentan groups.ResultsDuring the vasospasm period, mean arterial diameters increased in all regions, including the posterior circulation, except internal carotid artery (ICA) top in the clazosentan group, while they decreased across all regions in the nonclazosentan group (overall average: + 22.3% vs. -16.9%; = 0.005). Notably, in the clazosentan group, significant vasodilation was observed in distal arteries (M2: + 46.1%, = 0.003; M3: + 58.2%, = 0.001) compared to proximal arteries (ICAtop: -10.7%, = 0.33; M1p: + 0.38%, = 0.16; M1d: + 3.6%, = 0.07). Symptomatic vasospasm occurred exclusively in the nonclazosentan group; however, no significant difference was observed in modified Rankin Scale scores 3 months post-onset ( = 0.38).ConclusionsClazosentan demonstrated a significant vasodilatory effect compared to conventional treatments, particularly in distal arteries. However, its limited effect on proximal arteries suggests a need for supplementary treatments targeting these regions to improve clinical outcomes. Differences in vasodilatory effect at various sites may be associated with the controversy regarding clazosentan's clinical effects.
背景与目的
尽管许多研究报告了氯沙坦在预防动脉瘤性蛛网膜下腔出血（aSAH）后与脑血管痉挛相关的迟发性脑缺血方面的疗效，但最近的研究表明，其血管舒张作用对改善预后并无帮助，其疗效仍存在争议。在本研究中，我们定量测量了血管痉挛期不同血管部位的血管直径变化，以研究氯沙坦的影像学和临床效果之间的关联。
材料与方法
我们回顾性分析了我院收治的22例Fisher 3级aSAH患者。12例患者接受氯沙坦（10mg/h）治疗，10例患者接受传统的血管痉挛管理。在发病时和血管痉挛期测量12个部位的动脉直径。比较氯沙坦组和非氯沙坦组血管直径的定量变化。
结果
在血管痉挛期，氯沙坦组除颈内动脉（ICA）顶部外，包括后循环在内的所有区域平均动脉直径均增加，而非氯沙坦组所有区域的平均动脉直径均减小（总体平均值：+22.3%对-16.9%；P=0.005）。值得注意的是，在氯沙坦组中，与近端动脉（ICA顶部：-10.7%，P=0.33；M1p：+0.38%，P=0.16；M1d：+3.6%，P=0.07）相比，远端动脉（M2：+46.1%，P=0.003；M3：+58.2%，P=0.001）出现明显血管舒张。有症状的血管痉挛仅发生在非氯沙坦组；然而，发病后3个月改良Rankin量表评分无显著差异（P=0.38）。
结论
与传统治疗相比，氯沙坦显示出显著的血管舒张作用，尤其是在远端动脉。然而，其对近端动脉的作用有限，提示需要针对这些区域进行辅助治疗以改善临床结局。不同部位血管舒张作用的差异可能与氯沙坦临床效果的争议有关。
