急性缺血性脑卒中血管内治疗无效再通的病理生理机制和潜在治疗策略  

Pathophysiological mechanisms of futile recanalization following endovascular therapy for acute ischemic stroke due to large vessel occlusion and potential targeted therapeutic strategy

作　　者：邓刚[1] 秦川[1] 田代实[1] Deng Gang;Qin Chuan;Tian Daishi(Department of Neurology,Tongji Hospital of Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China)

机构地区：[1]华中科技大学同济医学院附属同济医院神经内科,湖北430030

出　　处：《中华神经科杂志》2022年第12期1423-1430,共8页Chinese Journal of Neurology

基　　金：国家自然科学基金面上项目(81873743,82071380)。

摘　　要：血管内治疗是急性前循环大血管闭塞缺血性卒中的一线治疗方案。然而越来越多的研究表明,即使及时开通闭塞血管,仍有接近半数的患者后期功能恢复不佳,这一现象被称为“无效再通”。无效再通的病理生理机制复杂,可能包括组织无复流、早期动脉再闭塞、侧支循环不良、出血转化、脑血管自动调节功能受损以及低灌注体积较大等。针对这些机制的靶向治疗策略已经在基础研究中进行尝试,但其向临床的转化仍有待探索。文中针对无效再通的病理生理机制和靶向治疗策略作一综述,重点关注无复流现象的机制和靶向治疗策略,以加深对这一现象的全面认识,为改善血管内治疗的疗效提供新的转化研究思路和潜在干预靶点。Endovascular therapy is the standard treatment for acute ischemic stroke due to large vessel occlusion.However,an increasing number of studies have demonstrated that about half of patients had poor functional recovery despite successful recanalization,namely futile recanalization.Previous studies suggested that tissue no-reflow(lack of reperfusion despite recanalized large vessel),early re-occlusion,poor collateral status,hemorrhagic transformation,impaired cerebral autoregulation and large hypoperfusion volume may all contribute to futile recanalization.Targeted treatment strategies for these mechanisms have been attempted in pre-clinical researches but failed to translate into clinical practices.This review aimed to summarize the mechanisms of futile recanalization and potential targeted treatment strategies,particularly focus on the no-reflow phenomenon and its mechanisms,clinical evaluation,and treatment approaches,hoping to promote translational research and improve the status of stroke treatment.

关 键 词：卒中 脑缺血 动脉闭塞性疾病 侧支循环 无复流现象 

分 类 号：R743.3[医药卫生—神经病学与精神病学]