Patient-specific predictions of aneurysm growth and remodeling in the ascending thoracic aorta using the homogenized constrained mixture model

TL;DR

This paper presents a novel patient-specific finite-element model using the constrained mixture model to predict aneurysm growth and remodeling in the ascending thoracic aorta, capturing complex biological responses and shape evolution.

Contribution

First implementation of a patient-specific constrained mixture model in finite-element analysis for predicting aortic aneurysm evolution, validated on canonical and real geometries.

Findings

Elastin proteolysis leads to typical aneurysm shape formation.

Stress transfer to adventitia due to elastin loss causes arterial stiffening.

Model predicts collagen deposition in regions of elastin degradation.

Abstract

In its permanent quest of mechanobiological homeostasis, our vascula-ture significantly adapts across multiple length and time scales in various physiological and pathological conditions. Computational modeling of vascular growth and remodeling (G\&R) has significantly improved our insights of the mechanobio-logical processes of diseases such as hypertension or aneurysms. However, patient-specific computational modeling of ascending thoracic aortic aneurysm (ATAA) evolution, based on finite-element models (FEM), remains a challenging scientific problem with rare contributions, despite the major significance of this topic of research. Challenges are related to complex boundary conditions and geometries combined with layer-specific G\&R responses. To address these challenges, in the current paper, we employed the constrained mixture model (CMM) to model the arterial wall as a mixture of different constituents such as elastin, collagen fiber families and smooth muscle cells (SMCs). Implemented in Abaqus as a UMAT, this first patient-specific CMM-based FEM of G\&R in human ATAA was first validated for canonical problems such as single-layer thick-wall cylindrical and bi-layer thick-wall toric arterial geometries. Then it was used to predict ATAA evolution for a patient-specific aortic geometry, showing that the typical shape of an ATAA can be simply produced by elastin proteolysis localized in regions of deranged hemodymanics. The results indicate a transfer of stress to the adventitia by elastin loss and continuous adaptation of the stress distribution due to change of ATAA shape. Moreover, stress redistribution leads to collagen deposition where the maximum elastin mass is lost, which in turn leads to stiffening of the arterial wall. As future work, the predictions of this G\&R framework will be validated on datasets of patient-specific ATAA geometries followed up over a significant number of years.