Dose-Dependent Inhibitory Effects of Cilostazol on Delayed Cerebral Infarction After Aneurysmal Subarachnoid Hemorrhage.
Dose-Dependent Inhibitory Effects of Cilostazol on Delayed Cerebral Infarction After Aneurysmal Subarachnoid Hemorrhage.
复制标题
西洛他唑对动脉瘤性蛛网膜下腔出血后迟发性脑梗死的剂量依赖性抑制作用。
DOI：
10.1007/s12975-018-0650-y
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发表时间：
2019
影响因子：
6.9
通讯作者：
Toma N.
中科院分区：
文献类型：
--
作者：
Suzuki H;Nakatsuka Y;Yasuda R;Shiba M;Miura Y;Terashima M;Suzuki Y;Hakozaki K;Goto F;Toma N.
西洛他唑是一种选择性磷酸二酯酶III抑制剂，下调腱生蛋白-C（TNC），一种基质细胞蛋白，可能导致蛛网膜下腔出血（SAH）后迟发性脑梗死。作者增加西洛他唑的剂量，并评价西洛他唑对SAH患者迟发性脑梗死和结局的剂量依赖性作用。这是一项单中心回顾性队列研究。分析了2007年至2017年期间100例连续的五十六例SAH患者，包括67例在SAH后48小时内接受蛛网膜下腔闭塞的入院世界神经外科医生联合会IV-V级患者。从夹闭后或弹簧圈栓塞后1天至第14天或之后给予西洛他唑（0 - 300 mg/天）。西洛他唑治疗剂量依赖性地减少迟发性脑梗死，并倾向于改善结局，尽管西洛他唑不影响其他结局指标，包括血管造影性血管痉挛。在多变量分析中，300 mg/天（100 mg 3次）西洛他唑独立地降低了迟发性脑梗死并改善了3个月的预后，但其他方案包括200 mg/天（100 mg 2次）西洛他唑不是独立的预后因素。倾向评分匹配分析显示，与非西洛他唑组相比，300 mg/d西洛他唑组血浆TNC水平较低，迟发性脑梗死发生率较低，结局较好。300 mg/d西洛他唑可能通过降低血浆TNC水平和延迟性脑梗死而改善SAH后结局，但不包括血管痉挛。进一步的研究是必要的，以调查是否300毫克/天西洛他唑是更有益的SAH后的结果比通常剂量的200毫克/天西洛他唑，被证明是有效的随机对照试验。
Cilostazol is a selective inhibitor of phosphodiesterase type III that downregulates tenascin-C (TNC), a matricellular protein, which may cause delayed cerebral infarction after aneurysmal subarachnoid hemorrhage (SAH). The authors increased the dosage and evaluated the dose-dependent effects of cilostazol on delayed cerebral infarction and outcomes in SAH patients. This was a retrospective cohort study in a single center. One hundred fifty-six consecutive SAH patients including 67 patients of admission World Federation of Neurological Surgeons grades IV–V who underwent aneurysmal obliteration within 48 h post-SAH from 2007 to 2017 were analyzed. Cilostazol (0 to 300 mg/day) was administered from 1-day post-clipping or post-coiling to day 14 or later. Cilostazol treatment dose-dependently decreased delayed cerebral infarction and tended to improve outcomes, although cilostazol did not affect other outcome measures including angiographic vasospasm. On multivariate analyses, 300 mg/day (100 mg three times) cilostazol independently decreased delayed cerebral infarction and improved 3-month outcomes, but other regimens including 200 mg/day (100 mg twice) cilostazol were not independent prognostic factors. Propensity score-matched analyses showed that the 300 mg/day cilostazol cohort had lower plasma TNC levels and a lower incidence of delayed cerebral infarction associated with better outcomes compared with the non-cilostazol cohort. The 300 mg/day cilostazol may improve post-SAH outcomes by reducing plasma TNC levels and delayed cerebral infarction, but not vasospasm. Further studies are warranted to investigate if 300 mg/day cilostazol is more beneficial to post-SAH outcomes than a usual dose of 200 mg/day cilostazol that was demonstrated to be effective in randomized controlled trials.