AuthorsO. Odeigah, J. Sundnes, M. Bennington and D. Valdez-Jasso
TitleA computational model of right ventricular remodelling in the presence of pulmonary arterial hypertension
AfilliationScientific Computing
Project(s)Department of Computational Physiology
Publication TypePoster
Year of Publication2022
Secondary TitleBiophysical Journal
Date Published02/2022
Place PublishedBiophysical Society Annual Meeting, San Francisco, California, USA

During early-stage pulmonary arterial hypertension (PAH), the right ventricle (RV) undergoes anatomical adaptation in the form of a thickened RV free wall, and material adaptation in the form of altered passive stiffness and contractility. The early-stage compensatory adaptations may help to preserve cardiac output but can later evolve into maladaptive remodelling and organ failure. The transition from compensatory to detrimental remodelling remains poorly understood.

Using in vivo hemodynamic and morphological data from normotensive and hypertensive rats, we built idealized bi-ventricular finite element models representing different disease stages. We built a total of eight models, with RV wall thickness based on ex vivo measurements and passive material properties prescribed based on planar biaxial mechanical data obtained from the same animals. A previously developed inverse finite element framework was then used to fit the biventricular models to the in-vivo hemodynamic data, resulting in passive stiffness and contractility optimized to provide the best possible fit with the combined hemodynamic and biaxial data.

Model simulations were then used to study how the presence of PAH affects the stress distribution in the right ventricular free wall, and how wall stress and RV function are altered by the induced changes in morphology, passive stiffness and contractility. Further numerical experiments were conducted to gain insight into the relative contribution of geometric and material adaptation to maintaining RV function in early-stage PAH, as well as the role of the septal wall. Such insights can facilitate a more comprehensive understanding of the compensatory remodeling that occurs during the disease progression.

Citation Keyodeigah2022computational