Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Aging Dis. 2023 Dec 1;14(6):2096-2112. doi: 10.14336/AD.2023.0321-1.
Endovascular therapy is the first-line treatment for acute ischemic stroke. However, studies have shown that, even with the timely opening of occluded blood vessels, nearly half of all patients treated with endovascular therapy for acute ischemic stroke still have poor functional recovery, a phenomenon called "futile recanalization.". The pathophysiology of futile recanalization is complex and may include tissue no-reflow (microcirculation reperfusion failure despite recanalization of the occluded large artery), early arterial reocclusion (reocclusion of the recanalized artery 24-48 hours post endovascular therapy), poor collateral circulation, hemorrhagic transformation (cerebral bleeding following primary ischemic stroke), impaired cerebrovascular autoregulation, and large hypoperfusion volume. Therapeutic strategies targeting these mechanisms have been attempted in preclinical research; however, translation to the bedside remains to be explored. This review summarizes the risk factors, pathophysiological mechanisms, and targeted therapy strategies of futile recanalization, focusing on the mechanisms and targeted therapy strategies of no-reflow to deepen the understanding of this phenomenon and provide new translational research ideas and potential intervention targets for improving the efficacy of endovascular therapy for acute ischemic stroke.
血管内治疗是急性缺血性卒中的一线治疗方法。然而，研究表明，即使及时开通闭塞的血管，接受血管内治疗的急性缺血性卒中患者中仍有近一半的患者功能恢复不佳，这种现象被称为“无效再通”。无效再通的病理生理学机制复杂，可能包括组织无再流（尽管闭塞的大动脉再通，但微循环再灌注失败）、早期动脉再闭塞（血管内治疗后 24-48 小时再通的动脉再次闭塞）、侧支循环不良、出血性转化（原发性缺血性卒中后脑内出血）、脑血管自动调节功能受损和大的低灌注体积。针对这些机制的治疗策略已在临床前研究中进行了尝试；然而，向床边的转化仍有待探索。本综述总结了无效再通的危险因素、病理生理机制和靶向治疗策略，重点关注无再流的机制和靶向治疗策略，以加深对这一现象的理解，并为提高急性缺血性卒中血管内治疗的疗效提供新的转化研究思路和潜在的干预靶点。
