ArticleBMJ neurology open2025
Vascular injury and occurrence of microthrombi after endovascular therapy for acute ischaemic stroke in a thromboembolic model.
Article in BMJ neurology open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Microvascular Occlusion and Postrecanalization Hyperperfusion in a Swine Model of Acute Ischemic Stroke.Journal of the American Heart Association · 2025Article
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14 authors.
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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.
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