Computational modeling reveals inflammation-driven dilatation of the pulmonary autograft in aortic position.
Lauranne MaesThibault VervenneLucas Van HoofElizabeth Anne Vincent JonesFilip R RegaNele FamaeyPublished in: Biomechanics and modeling in mechanobiology (2023)
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.
Keyphrases
- aortic valve
- pulmonary hypertension
- transcatheter aortic valve replacement
- aortic valve replacement
- transcatheter aortic valve implantation
- aortic stenosis
- anterior cruciate ligament reconstruction
- pulmonary artery
- oxidative stress
- bone mineral density
- left ventricular
- coronary artery
- minimally invasive
- adipose tissue
- pulmonary arterial hypertension
- heart failure
- case report
- aortic dissection
- insulin resistance
- stress induced
- weight loss
- skeletal muscle