Response by Luby et al to Letter Regarding Article, "Frequency of Blood-Brain Barrier Disruption Postendovascular Therapy and Multiple Thrombectomy Passes in Acute Ischemic Stroke Patients".
Response by Luby et al to Letter Regarding Article, "Frequency of Blood-Brain Barrier Disruption Postendovascular Therapy and Multiple Thrombectomy Passes in Acute Ischemic Stroke Patients".
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Luby 等人对有关文章“急性缺血性中风患者血管内治疗后血脑屏障破坏和多次血栓切除术的频率”的信件的回应。
DOI：
10.1161/strokeaha.119.027214
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发表时间：
2019
期刊：
影响因子：
8.3
通讯作者：
Latour,LawrenceL
中科院分区：
文献类型：
--
作者：
Luby,Marie;Hsia,AmieW;Latour,LawrenceL
我们衷心感谢Renú、Laredo和Amaro的来信以及他们对我们的文章《急性缺血性中风患者血管内治疗和多次血栓切除术后血脑屏障破坏的频率》的兴趣。我们感谢Renúet al提请我们注意他们的工作和重要出版物。特别是，他们非常有价值和相关的文章，血管壁增强和急性缺血性卒中机械取栓术后血脑脊液屏障的破坏，强调了血脑屏障破坏与快速再灌注的临床相关性，以及需要进一步的策略来解决继发性损伤反应。Renú等人重申了我们文章中的关键发现，即多次血栓切除与血脑屏障(BBB)破坏的显着增加独立相关，血脑屏障破坏被定义为高强度急性再灌注损伤标记物。1高强度急性再灌注损伤标记物代表脑脊液间隙(包括脑沟和皮质表面间隙)的延迟强化，1和Renú等人所指出的蛛网膜下腔和硬膜下间隙，2在机械取栓后24小时，对比剂液体减弱的反转恢复。Renúet al和我们的工作在多项研究中都有值得称赞的发现。我们在文章中建议，在未来的辅助治疗临床试验中，当有效地防止血脑屏障中断时，高强度急性再灌注损伤标记物可以作为二级损伤标记物和替代结局。1为了了解机械取栓促进快速血运重建的病理生理机制，1评价高强度急性再灌注损伤标志物作为继发性损伤的影像标志物具有重要价值，并可能用于了解有效和及时的辅助治疗对血脑屏障的保护作用。Renúet al描述了由于出血转化和脑水肿的可能性增加，以及由此导致的相关临床恶化，包括早期神经恶化和功能不良，血脑屏障中断对限制再灌注治疗疗效的影响。2，3Renú等人就血脑屏障损伤的来源展开了一场令人信服的辩论，原因要么是微循环的直接损害，要么是由于血栓取回器设备的部署而对血管壁造成的机械损伤，4或可能两者兼而有之。然而，正如Renú等人所建议的，造成损伤的机制可能不同，因此辅助治疗将需要考虑在快速血管重建条件下靶向神经保护的各种途径，以防止BBB中断。
We sincerely appreciate the letter by Renú, Laredo, and Amaro and their interest in our article,“Frequency of Blood-Brain Barrier Disruption Post-Endovascular Therapy and Multiple Thrombectomy Passes in Acute Ischemic Stroke Patients.” We thank Renú et al for bringing their work and important publications to our attention. In particular, their extremely valuable and relevant article, Vessel Wall Enhancement and Blood-Cerebrospinal Fluid Barrier Disruption After Mechanical Thrombectomy in Acute Ischemic Stroke, emphasized the clinical relevance of BBB disruption with rapid reperfusion and the need for further strategies to address the secondary injury responses. Renú et al reiterated the key finding from our article that multiple thrombectomy passes were independently associated with a significant increase in blood-brain barrier (BBB) disruption defined as hyperintense acute reperfusion injury marker. 1 Hyperintense acute reperfusion injury marker represents the presence of delayed enhancement of the cerebrospinal fluid spaces including sulcal and cortical surface spaces1 and as noted by Renú et al, the subarachnoid and subpial spaces, 2 at 24 hours post-mechanical thrombectomy on post-contrast fluid-attenuated inversion recovery. Renú et al and our work have complimentary findings across studies. We suggested in our article that hyperintense acute reperfusion injury marker may serve as a secondary injury marker and surrogate outcome when BBB disruption is effectively prevented in future clinical trials for adjunctive therapies. 1 To understand the pathophysiologic mechanisms associated with rapid revascularization facilitated by mechanical thrombectomy, 1 evaluation for hyperintense acute reperfusion injury marker is invaluable as an imaging marker of secondary injury and could possibly be used to understand the protection of the BBB with effective and timely adjunctive therapies. Renú et al describes the impact BBB disruption has on limiting the efficacy of reperfusion therapies given the increased likelihood of hemorrhagic transformation and cerebral edema, and the resulting associated clinical worsening including early neurological deterioration and poor functional outcome. 2, 3Renú et al begins a compelling debate on the source of the BBB damage, either because of direct damage to the microcirculation or mechanical injury to the vessel wall3, 4 because of deployment of the clot retriever devices, 4 or likely both. However, as Renú et al suggests, the mechanisms responsible for the damage may differ and therefore adjunctive therapies will need to consider various pathways for targeting neuroprotection under rapid revascularization conditions for prevention of BBB disruption.