ArticleFrontiers in bioengineering and biotechnology2020
Computational Study of Growth and Remodeling in Ascending Thoracic Aortic Aneurysms Considering Variations of Smooth Muscle Cell Basal Tone.
Article in Frontiers in bioengineering and biotechnology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 21 citations in OpenAlex.
- Mechanisms driving thoracic aortic aneurysm instability.Biomechanics and modeling in mechanobiology · 2026Article
- Mechanisms Driving Thoracic Aortic Aneurysm Stability.bioRxiv : the preprint server for biology · 2025Article
- Irregular anatomical features can alter hemodynamics in Takayasu arteritis.JVS-vascular science · 2023Article
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3 authors at 1 institution in 1 country.
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Abstract
In this paper, we investigate the progression of Ascending Thoracic Aortic Aneurysms (ATAA) using a computational model of Growth and Remodeling (G&R) taking into account the composite (elastin, four collagen fiber families and Smooth Muscle Cells-SMCs) and multi-layered (media and adventitia) nature of the aorta. The G&R model, which is based on the homogenized Constrained Mixture theory, is implemented as a UMAT in the Abaqus finite-element package. Each component of the mixture is assigned a strain energy density function: nearly-incompressible neo-Hookean for elastin and Fung-type for collagen and SMCs. Active SMCs tension is additionally considered, through a length-tension relationship having a classic inverted parabola shape, in order to investigate its effects on the progression of ATAA in a patient-specific model. A sensitivity analysis is performed to evaluate the potential impact of variations in the parameters of the length-tension relationships. These variations reflect in variations of SMCs normal tone during ATAA progression, with active stress contributions ranging between 30% (best case scenario) and 0% (worst case scenario) of the total wall circumferential stress. Low SMCs active stress in the worst case scenarios, in fact, affect the rates of collagen deposition by which the elastin loss is gradually compensated by collagen deposition in the simulated ATAA progression, resulting eventually in larger aneurysm diameters. The types of length-tension relationships leading to a drop of SMCs active stress in our simulations reveal a critical condition which could also result in SMCs apoptosis.
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