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research-article

Structural and Biomechanical Adaptations of Right Ventricular Remodeling - in Pulmonary Arterial Hypertension - Reduces Left Ventricular Rotation During Contraction: A Computational Study

[+] Author and Article Information
Vitaly Kheyfets

University of Colorado Anschutz Medical Campus, Children's Hospital Colorado
vitaly.kheyfets@ucdenver.edu

Uyen Truong

University of Colorado Anschutz Medical Campus, Children's Hospital Colorado
uyen.truong@childrenscolorado.org

Dunbar Ivy

University of Colorado Anschutz Medical Campus, Children's Hospital Colorado
dunbar.ivy@childrenscolorado.org

Robin Shandas

University of Colorado Anschutz Medical Campus, Children's Hospital Colorado
robin.shandas@ucdenver.edu

1Corresponding author.

ASME doi:10.1115/1.4042682 History: Received February 14, 2018; Revised January 24, 2019

Abstract

Pulmonary hypertension (PH) is a degenerative disease characterized by progressively increased right ventricular (RV) afterload that leads to ultimate functional decline [1]. Recent observational studies have documented a decrease in left ventricular (LV) torsion during ejection, with preserved LV ejection fraction (EF) in pediatric and adult PH patients [2-4]. The objective of this study was to develop a computational model of the bi-ventricular heart and use it to evaluate changes in LV torsion mechanics in response to mechanical, structural, and hemodynamic changes in the RV free-wall. The heart model revealed that LV apex rotation and torsion were decreased when increasing RV mechanical rigidity and during re-orientation of RV myocardial fibers. Furthermore, structural changes to the RV appear to have a notable impact on RV EF, but little influence on LV EF. Finally, RV pressure overload exponentially increased LV myocardial stress. The computational results found in this study are consistent with clinical observations in adult and pediatric PH patients, which reveal a decrease in LV torsion with preserved LV EF [3, 4]. Furthermore, discovered causes of decreased LV torsion are consistent with RV structural adaptations seen in PH rodent studies [5], which might also explain suspected stress-induced changes in LV myocardial gene/protein expression.

Copyright (c) 2019 by ASME
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