Patient-specific Finite Element Modeling of Aneurysmal dilatation after chronic type B aortic dissection

TL;DR

This study develops a patient-specific finite element model to simulate aneurysmal dilatation after chronic type B aortic dissection, highlighting the role of growth and remodeling parameters in stability and expansion.

Contribution

It introduces a novel 3D finite-element G&R model for cTBAD that incorporates mechanobiological equations and demonstrates its application to idealized and patient-specific geometries.

Findings

G&R triggers aneurysmal dilatation to restore tension.

Gain parameter influences stability of aortic expansion.

Wide tears and high false lumen pressure promote instability.

Abstract

Progressive aneurysmal dilatation is a well-recognized complication in patients with chronic type B aortic dissection (cTBAD), which may lead to a delayed rupture and create a life-threatening condition. However, our understanding of such aortic expansion in cTBAD remains weak. In the present paper, we propose to use numerical simulations to study the role of growth and remodeling (G\&R) in aneurysmal dilatation after cTBAD. We set up a 3D finite-element model of G\&R for aortic dissection within an open-source code. Constitutive equations, momentum balance equations, and equations related to the mechanobiology of the artery were formulated based on the homogenized constrained mixture theory. The model was first applied to idealized aortic geometries with cylindrical and toric shapes to demonstrate its feasibility and efficiency. The model was then applied to a patient-specific aortic segment to show its potential in more relevant and complex patient-specific clinical applications. It was found that the G\&R tends to naturally trigger the aneurysmal dilatation after dissection, in order to restore its tensional equilibrium. Our results indicated that the value of the gain parameter, related to collagen G\&R, plays an important role in the stability of aortic expansion after cTBAD. A small gain parameter will induce an excessive aneurysmal degeneration whilst a large gain parameter helps to recover a stabilized state of the artery after dissection. Finally, it was found that other mechanobiology-related parameters, such as the circumferential length of the dissection, as well as the pressure in the false lumen, may also be determinant for the stability of aneurysmal dilatation after cTBAD. Both a wide tear and an elevated false lumen pressure favor an unstable development of aortic expansion after cTBAD. As future work, the present model will be validated through predictions of aneurysmal dilatation in patient-specific clinical cases, in comparison with datasets followed over a significant period of time.