Michael S. Sacks
W.A. Moncrief Chair in Simulation Based Engineering Sciences
Professor of Biomedical Engineering
Oden Institute for Computational Sciences and Engineering
The University of Texas at Austin

“Structural remodeling and volumetric growth in the heart”

Abstract:

Many cardiac diseases impose pressure overload leading to ventricular enlargement via the growth of cardiac myocytes and remodeling of the collagen fiber architecture. One such disease is pulmonary arterial hypertension (PAH), which primarily affects the right ventricle (RV). The effects of PAH on the functional behavior of the RV free wall (RVFW) on RV organ-level cardiac function remain largely unexplored. Computational rodent heart models (RHM) of the normal and hypertensive states can be quite valuable in gaining insights into the pathophysiology of myocardium remodeling. Recently, we developed high-fidelity biventricular finite-element RHMs using extensive data collected from rat hearts at normal and post-PAH time points. In this study, we extended our model to predict the time-course adaptations of RV under PAH from normal state to post-PAH state. Our model accounted for growth processes driven by sarcomerogenesis and collagen fibrosis, coupled with myo- and collagen fiber reorientation events. We used our model to investigate the correlations between the alterations in the wall stress, the remodeling of the RVFW microstructure, and the shape changes in the RV during the development of PAH. To the best of our knowledge, this is the first work to investigate the interaction between fiber remodeling and volumetric growth in the heart. Ultimately, the detailed description of organ-level remodeling patterns predicted by in-silico models such as ours could replace the traditional measures of RV dimensions and volume that often lead to gross and limited information on cardiac performance. Future directions of the research will also be presented.