Computational modeling reveals inflammation-driven dilatation of the pulmonary autograft in aortic position.

Abstract

The pulmonary autograft in the Ross procedure, where the aortic valve is replaced by the patient's own pulmonary valve, is prone to failure due to dilatation. This is likely caused by tissue degradation and maladaptation, triggered by the higher experienced mechanical loads in aortic position. In order to further grasp the causes of dilatation, this study presents a model for tissue growth and remodeling of the pulmonary autograft, using the homogenized constrained mixture theory and equations for immuno- and mechano-mediated mass turnover. The model outcomes, compared to experimental data from an animal model of the pulmonary autograft in aortic position, show that inflammation likely plays an important role in the mass turnover of the tissue constituents and therefore in the autograft dilatation over time. We show a better match and prediction of long-term outcomes assuming immuno-mediated mass turnover, and show that there is no linear correlation between the stress-state of the material and mass production. Therefore, not only mechanobiological homeostatic adaption should be taken into account in the development of growth and remodeling models for arterial tissue in similar applications, but also inflammatory processes.