Taha Aladdin, Nagy Magdolna, Hund Hajo M, van Doormaal Pieter Jan, van Noorden Khay, Spronk Henri M H, Ceulemans Angelique, van Oostenbrugge Robert J, Duncker Dirk J, Ten Cate Hugo, Dippel Diederik, van Es Adriaan C G M, Bobi Joaquim, van Beusekom Heleen M M
Department of Cardiology, Division Experimental Cardiology, Erasmus MC University Medical Center, Rotterdam, The Netherlands.
Department of Neurology, Stroke Center, Erasmus MC University Medical Center, Rotterdam, The Netherlands.
BMJ Neurol Open. 2025 Mar 21;7(1):e000989. doi: 10.1136/bmjno-2024-000989. eCollection 2025.
Endovascular catheters and devices used for thrombectomy in patients who had a stroke can damage the vessel lumen leading to microthrombi. During stroke recanalisation, microthrombi could migrate distally and occlude cerebral microvasculature, potentially limiting the benefit of recanalisation therapy.
To describe vascular injury occurring after endovascular therapy (EVT), with stent retrievers (SR) and direct aspiration (DA), to open up avenues for further improvement of EVT technique.
SR and DA were performed according to clinical procedures in extracranial vessels in a swine model of thromboembolic arterial occlusion. Treated vessels were collected at 2 hours or 3 days post-EVT to assess respectively acute injury and early healing (remnant vascular injury) as assessed by Evans-Blue (EB) dye exclusion. The presence of microthrombi was quantified using scanning electron microscopy. Markers of coagulation activation were measured periprocedurally in plasma.
Both SR and DA induced vascular injury. SR tended to result in larger EB positive areas than DA at 2 hours (99.5 vs 84.5; p=0.072) which reached statistical significance at day 3 (78.6 vs 48.6; p=0.040) post-EVT. Both EVT methods similarly yielded microthrombi in treated areas which were still observed at 3 days post-EVT. In addition, both EVT methods immediately increased systemic plasma levels of complexes of intrinsic-pathway coagulation activation: thrombin, Factor IX and Factor Xa:Antithrombin.
In this preclinical thromboembolic model, SR thrombectomy and DA lead to acute vascular injury, yield microthrombi and trigger contact activation of the coagulation system. At 3 days after intervention, healing remains incomplete, showing remnant vascular injury in the treated arteries, especially in SR thrombectomy.
用于中风患者血栓切除术的血管内导管和装置可能会损伤血管腔，导致微血栓形成。在中风再通期间，微血栓可能会向远端迁移并阻塞脑微血管，从而可能限制再通治疗的益处。
描述血管内治疗（EVT）后使用支架取栓器（SR）和直接抽吸（DA）所发生的血管损伤，为进一步改进EVT技术开辟途径。
在血栓栓塞性动脉闭塞的猪模型中，根据临床操作在颅外血管中进行SR和DA。在EVT后2小时或3天收集治疗的血管，分别通过伊文思蓝（EB）染料排除法评估急性损伤和早期愈合（残余血管损伤）。使用扫描电子显微镜对微血栓的存在进行定量。在手术过程中在血浆中测量凝血激活标志物。
SR和DA均会导致血管损伤。在EVT后2小时，SR导致的EB阳性面积往往比DA更大（99.5对84.5；p = 0.072），在第3天达到统计学显著性（78.6对48.6；p = 0.040）。两种EVT方法在治疗区域产生的微血栓相似，在EVT后3天仍可观察到。此外，两种EVT方法均立即增加了内源性凝血激活复合物的全身血浆水平：凝血酶、因子IX和因子Xa：抗凝血酶。
在这个临床前血栓栓塞模型中，SR血栓切除术和DA会导致急性血管损伤，产生微血栓并触发凝血系统的接触激活。干预后3天，愈合仍不完全，在治疗的动脉中显示出残余血管损伤，尤其是在SR血栓切除术中。
