Abstract
ObjectivesEndovascular treatment (EVT) has become the standard of care for acute ischemic stroke. Despite successful recanalization, a limited subset of patients benefits from the new treatment. Human MRI studies have shown that during removal of the thrombus, a shower of microclots is released from the initial thrombus, possibly causing new ischemic lesions. The aim of the current study is to quantify tissue damage following microembolism. Materials and methodsIn a rat model, microembolism was generated by injection of a mixture of polystyrene fluorescent microspheres (15, 25 and 50 µm in diameter). The animals were killed at three time-points: day 1, 3 or 7. AMIRA and IMARIS software was used for 3D reconstruction of brain structure and damage, respectively. ResultsMicroscopic analysis of 500 µm thick brain volumes revealed multiple ischemic, hypoxic and infarcted regions. Both the number and total volume of hypoxic and ischemic areas declined over time, whereas the infarcts remained. ConclusionsMicroembolism induces ischemia, hypoxia and infarction. Infarcted areas persist, but hypoxic regions recover over time suggesting that repair processes in the brain rescue the regions at risk.
Highlights
Acute ischemic stroke accounts for about 80% of stroke cases.[1]
We found that microembolism induces ischemia, hypoxia and infarction, yet hypoxic regions became significantly less pronounced over time, indicating that the brain has the capacity to recover from hypoxic injury
We found that microspheres of sizes relevant for endovascular treatment (EVT) induced persistent neuronal damage, which did not change in terms of number and size over time
Summary
Acute ischemic stroke accounts for about 80% of stroke cases.[1] The introduction of endovascular treatment (EVT), where a thrombus is removed by means of a retrieval device, has led to a breakthrough for the therapy of acute ischemic stroke.[2] in the large majority of cases successful recanalization of the occluded vessel is attained[3,4], only one third of patients is left with a good clinical outcome, defined as modified Rankin Scale from 0 to 2 at 90 days follow-up.[5]. From the Amsterdam UMC, University of Amsterdam, Biomedical Engineering and Physics, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands.
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