CONSTITUENT BASED MODELLING OF ARTERIAL WALL MECHANICS

In the preclinical setting, Angiotensin-II infusion has been the most popular model for mouse aneurysm research in the last 15 years. Nonetheless, little is known about the ascending aortic aneurysm pathobiology of this model and several lingering questions regarding the abdominal aortic aneurysm pa...

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Bibliographic Details
Main Authors: Lydia Aslanidou, Rodrigo Araujo Fraga da Silva, Patrick Segers, Nikos Stergiopulos
Format: Article
Language:English
Published: BMC 2016-11-01
Series:Artery Research
Online Access:https://www.atlantis-press.com/article/125930378/view
Description
Summary:In the preclinical setting, Angiotensin-II infusion has been the most popular model for mouse aneurysm research in the last 15 years. Nonetheless, little is known about the ascending aortic aneurysm pathobiology of this model and several lingering questions regarding the abdominal aortic aneurysm pathology (AAA) have long remained unaddressed, namely the suprarenal location of the murine AAA, the large morphological variation of the lesions and the presence of intramural thrombus. Technological advancements in both in vivo and ex vivo imaging techniques have significantly enhanced our understanding of the mechanisms driving the Angiotensin-II mouse model pathology. Our implementation of the groundbreaking PCXTM imaging modality has challenged the existing paradigm on this model while yielding unprecedented insight into previous observations on murine dissecting AAA. The detailed 3D PCXTM images have unveiled a previously unknown pivotal role for small, supraceliac and thoracic side branches to the onset of the disease. Mural ruptures in the vicinity of small side branches lead to apparent luminal dilatation and intramural hematoma. The PCXTM-based observations are in line with -seemingly incongruous- previous findings obtained with other imaging techniques, thereby raising a point on the importance of the implemented imaging modality when characterizing this aneurysm model.
ISSN:1876-4401