Patient-Specific Finite Element Modeling of Aneurysmal Dilatation After Chronic Type B Aortic Dissection

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.

A computational study of the effects of size, location, and number of tears on haemodynamics in surgically repaired type A aortic dissection

“…Elevated LPD (>5 mmHg) has been potentially associated with progressive aortic dilatation ( 26 ). A recent numerical study has also shown that at least 50% reduction in the pressure between the true and false channel is needed to stabilize a dissection ( 31 ). In both patients examined here, the overall best performance was achieved by increasing the size of re-entry tear (LRT-1 and LRT-2), especially for patient 2, the maximum LPD was reduced to 4.4 mmHg from 11.8 mmHg (62.7% reduction).…”

Finite‐element simulation of in‐plane tear propagation in the dissected aorta: Implications for the propagation mechanism

“…Different axial lengths (11,12,13,18, and 23 mm) were set for the baseline model (η = 150 , t = 0.4, s = 10 mm) to investigate the influence of the boundary condition on dissection propagation, corresponding to an axial margin of 1, 2, 3, 8, and 13 mm for the initial tear. While the propagation took place in a different location near the axial constraint for 1 mm margin, the critical pressure was 79, 130, 130, 130 kPa for 2, 3, 8, and 13 mm margin respectively.…”

“…Wang et al 16 studied dissection propagation with a 2D plane‐strain residually stressed two‐layer arterial model and reported that residual stress protected the arterial wall from dissection by increasing the critical pressure. Zhang et al 17 , 18 proposed a three‐dimensional (3D) model of aortic dissection, where high stiffness springs were utilized to model the bonding between media and adventitia. The model was utilized to create the false lumen so that aortic expansions following dissection can be investigated.…”