ArticleAJNR. American journal of neuroradiology2014
Complex hemodynamic insult in combination with wall degeneration at the apex of an arterial bifurcation contributes to generation of nascent aneurysms in a canine model.
Article in AJNR. American journal of neuroradiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Imaging of intracranial aneurysms in animals: a systematic review of modalities.Neurosurgical review · 2023Pooled it
- Impact of geometric factors and shear stress on endothelial function: Hemodynamic insights from human cerebral arterial bifurcations.Physiological reports · 2026Article
- Clinical relevance of critical plasma homocysteine levels in predicting rupture risk for small and medium-sized intracranial aneurysms.Scientific reports · 2024Article
- A Hemodynamic Mechanism Correlating with the Initiation of MCA Bifurcation Aneurysms.AJNR. American journal of neuroradiology · 2020Article
- Nomogram for Stability Stratification of Small Intracranial Aneurysm Based on Clinical and Morphological Risk Factors.Frontiers in neurology · 2020Article
- Hemodynamic Characteristics Regarding Recanalization of Completely Coiled Aneurysms: Computational Fluid Dynamic Analysis Using Virtual Models Comparison.Neurointervention · 2016Article
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7 authors.
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Abstract
background and purposeThe detailed mechanisms of cerebral aneurysm generation remain unclear. Our aim was to investigate whether specific hemodynamic insult in combination with arterial wall degeneration leads to the development of aneurysms in a canine model. MATERIALS AND
methodsNew branch points in the common carotid artery were created in 18 dogs. Nine animals subsequently received elastase insult at the arterial bifurcation apex (elastase-treated bifurcation group); the control bifurcation group (n=9) received saline, and 3 dogs received an elastase insult to both straight common carotid arteries (elastase-treated straight group). Angiographic and hemodynamic analysis was performed immediately and 12 and 24 weeks' postsurgery; histologic response was evaluated at 12 and 24 weeks.
resultsAngiography revealed nascent aneurysms (mean, 3.2±0.4 mm) at the arterial bifurcation apices in 5/9 models of the elastase-treated bifurcation group (versus 0 in the control bifurcation group and elastase-treated straight group) without any observed aneurysm rupture. Histologic analysis revealed internal elastic lamina discontinuity, elastic fiber disruption, a thinner muscular layer, reduced smooth-muscle cell proliferation, increased inflammatory cell (macrophage) infiltration, and expression of matrix metalloproteinase-2 and matrix metalloproteinase-9 in the media of the elastase-treated bifurcation group compared with that in either the control bifurcation group or the elastase-treated straight group (P<.001). Hemodynamic analysis after surgery indicated that the apex experienced extremely low wall shear stress and flow velocity and the highest relative and total pressure in the elastase-treated bifurcation group, while the values returned to normal after arterial wall remodelling.
conclusionsIn our study, combined hemodynamic insult and arterial wall degeneration at arterial bifurcations are required for the generation of aneurysms in a canine model.
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