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Paper title Loss of Mural Cells Leads to Impaired Thrombus Remodeling and Prolonged Aneurysm Cicatrisation in a Rabbit Arterial Sidewall Aneurysm Model
Paper code P39
Authors
  1. Fabio von Faber-Castell UniversitätsSpital & Universität Zürich Speaker
  2. Basil E. Grüter Kantonsspital Aarau Speaker
  3. Michael von Gunten Institute of Pathology Laenggasse
  4. Hans Rudolf Widmer Inselspital, Universitätsspital Bern
  5. Jatta Berberat Kantonsspital Aarau
  6. Luca Remonda Kantonsspital Aarau AG
  7. Javier Fandino Neurochirurgie Zentrum Zürich, Klinik Hirslanden
  8. Daniel Coluccia Kantonsspital Aarau
  9. S. Marbacher Kantonsspital Aarau
Form of presentation Poster
Topics
  • Joint SSNR | SSNS
Abstract text Aims:
Previous studies have demonstrated that ruptured aneurysms show a significant cell loss in the vessel wall when compared to unruptured aneurysms. Decellularized aneurysms have been confirmed to be prone to growth and rupture, when compared with vital aneurysms in a rat model. The exact mechanism of thrombus and vessel wall interaction and aneurysm growth is yet insufficiently understood. The authors therefore investigated this in a rabbit arterial sidewall aneurysm model.

Methods: Sidewall aneurysms were created bilaterally on the carotid artery of New Zealand White Rabbits. Aneurysms vessel walls were vital (n=6) or decellularized (n=12), of which 6 animals received additionally acetylsalicylic acid (ASA) in the drinking water. For decellularization, vessel pouches from a donor animal were incubated in 1% sodium dodecyl sulfate (SDS) for 6 hours to destroy cells of the vessel wall but not the extracellular matrix. Follow-up time was 1 month. Aneurysm growth was monitored with transcutaneous ultrasound on a weekly basis and all animals received an MR angiography prior to the euthanasia. Histological analyses of the aneurysms were used to assess the role of periadventitial environment, aneurysm wall and thrombus remodeling.

Results:
During the study period, no aneurysm were ruptured. All aneurysms showed a significant decrease in volume, more pronounced in vital aneurysms as compared to decellularized aneurysms (p=0.045). Histologically, decellularized aneurysms demonstrated a tendency towards a higher wall inflammation when compared to vital aneurysms. The administration of ASA was associated with a non-significant trend towards fewer wall hematoma and reduced wall inflammation.

Conclusion:
Although aneurysm growth and rupture did not occur, the absence of mural cells led to impaired intraluminal thrombus organization and neointima formation in the rabbit arterial sidewall aneurysm model. The excessive inflammation in decellularized aneurysms may partially be attenuated by administration of ASA and therefore potentially support aneurysm healing.