Artikel
Aspirin treatment protects again inflammation in experimental bifurcation aneurysms with different wall conditions in New Zealand white rabbits
Aspirin-Einnahme schützt vor übermäßiger Entzündung in tierexperimentellen Bifurkationsaneurysmen unter Betrachtung verschiedener Wandcharakteristika
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Autoren
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Stefan Wanderer
- Kantonsspital Aarau, Neurosurgery, Aarau, Schweiz
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Basil Grüter
- Kantonsspital Aarau, Neurosurgery, Aarau, Schweiz
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Fabio Strange
- Kantonsspital Aarau, Neurosurgery, Aarau, Schweiz
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Gwendoline Boillat
- Kantonsspital Aarau, Neurosurgery, Aarau, Schweiz
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Sivani Sivanrupan
- Inselspital, Universitätsspital Bern, Cerebrovascular Research Group, Department for BioMedical Research, Bern, Schweiz
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Jeannine Rey
- Inselspital, Universitätsspital Bern, Cerebrovascular Research Group, Department for BioMedical Research, Bern, Schweiz
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Michael von Gunten
- Institute of Pathology Laenggasse, Bern, Schweiz
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Luca Remonda
- Kantonsspital Aarau, Division of Neuroradiology, Department of Radiology, Aarau, Schweiz
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Hans Rudolf Widmer
- Neurocenter and Regenerative Neuroscience Cluster, Department of Neurosurgery, Neurocenter and Regenerative Neuroscience Cluster, Bern, Schweiz
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Daniela Casoni
- Inselspital, Universitätsspital Bern, Cerebrovascular Research Group, Department for BioMedical Research, Bern, Schweiz
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Lukas Andereggen
- Kantonsspital Aarau, Neurosurgery, Aarau, Schweiz
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Javier Fandino
- Kantonsspital Aarau, Neurosurgery, Aarau, Schweiz
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Serge Marbacher
- Kantonsspital Aarau, Neurosurgery, Aarau, Schweiz
| Veröffentlicht: | 4. Juni 2021 |
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Gliederung
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Objective: In the past decades endovascular therapies have become increasingly popular in treating unruptured and ruptured intracranial aneurysms. Aneurysm wall degeneration is linked to aneurysm growth and rupture in preclinical and clinical studies. The aim of this study was to analyze the impact of aspirin (ASA) on the natural course of aneurysms with different wall conditions (vital, decellularized, elastase degraded) in a rabbit bifurcation model.
Methods: Bifurcation aneurysms were created in New Zealand White rabbits by suturing the right on the left carotid artery by end-to-side anastomosis with interposition of an arterial pouch (allograft or autograft). Study groups comprised vital, decellularized and elastase degraded aneurysms either with or without additional ASA treatment (n = 6). Animals were randomly allocated to one of these groups using a web-based randomization system. Primary outcomes were aneurysm patency and growth within 28 days. At follow-up contrast enhanced magnetic resonance and fluorescence angiography were performed. After harvesting the aneurysm underwent macroscopic and histological evaluation. Inflammation was assessed by semiquantitative cell count for neutrophils.
Results: We observed that none of the aneurysms ruptured during follow-up. Intraoperative fluorescence angiography revealed aneurysm patency in all cases (n = 44/44). After 28 days, patency of the aneurysm was confirmed in 92 % (n = 33/36) with magnetic resonance imaging. The vital (without ASA) and elastase (with and without ASA) groups revealed a significant increase in aneurysm size measured macroscopically. The decellularized series without ASA showed complete aneurysm thrombosis in only 50 % of cases (n = 3/6). Histological analysis revealed a significant reduced inflammation of the aneurysm complex in all groups receiving ASA.
Conclusion: Continuous ASA intake prevented inflammation of the periadventitial tissue layers as well as of the aneurysm wall, irrespective of initial wall condition. In aneurysms with vital walls, ASA significantly prevented aneurysm growth, whereas this preventive effect did not seem to play an important role in elastase degraded pouches. Considering these results, ASA intake in humans might have a potential preventive effect in the early phase of aneurysm formation in cases with healthy vessels but not if highly degenerative aneurysm wall is present.
