Aladdin Taha, Magdolna Nagy, Hajo M Hund, Pieter Jan van Doormaal, Khay van Noorden, Henri M H Spronk, Angelique Ceulemans, Robert J van Oostenbrugge, Dirk J Duncker, Hugo Ten Cate, Diederik Dippel, Adriaan C G M van Es, Joaquim Bobi, Heleen M M van Beusekom
{"title":"Vascular injury and occurrence of microthrombi after endovascular therapy for acute ischaemic stroke in a thromboembolic model.","authors":"Aladdin Taha, Magdolna Nagy, Hajo M Hund, Pieter Jan van Doormaal, Khay van Noorden, Henri M H Spronk, Angelique Ceulemans, Robert J van Oostenbrugge, Dirk J Duncker, Hugo Ten Cate, Diederik Dippel, Adriaan C G M van Es, Joaquim Bobi, Heleen M M van Beusekom","doi":"10.1136/bmjno-2024-000989","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Objectives: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":52754,"journal":{"name":"BMJ Neurology Open","volume":"7 1","pages":"e000989"},"PeriodicalIF":2.1000,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11931897/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"BMJ Neurology Open","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1136/bmjno-2024-000989","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: 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.
Objectives: 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.
Methods: 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.
Results: 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.
Conclusions: 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.