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Research Papers

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 O. Kheyfets

University of Colorado Anschutz Medical Campus,
Children's Hospital Colorado,
Aurora, CO 80045
e-mail: vitaly.kheyfets@ucdenver.edu

Uyen Truong

University of Colorado Anschutz Medical Campus,
Children's Hospital Colorado,
Aurora, CO 80045
e-mail: Uyen.Truong@childrenscolorado.org

Dunbar Ivy

University of Colorado Anschutz Medical Campus,
Children's Hospital Colorado,
Aurora, CO 80045
e-mail: Dunbar.Ivy@childrenscolorado.org

Robin Shandas

University of Colorado Anschutz Medical Campus,
Children's Hospital Colorado,
Aurora, CO 80045
e-mail: robin.shandas@ucdenver.edu

1Corresponding author.

Manuscript received February 14, 2018; final manuscript received January 24, 2019; published online March 25, 2019. Assoc. Editor: Alison Marsden.

J Biomech Eng 141(5), 051002 (Mar 25, 2019) (10 pages) Paper No: BIO-18-1089; doi: 10.1115/1.4042682 History: Received February 14, 2018; Revised January 24, 2019

Pulmonary hypertension (PH) is a degenerative disease characterized by progressively increased right ventricular (RV) afterload that leads to ultimate functional decline. 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. The objective of this study was to develop a computational model of the biventricular 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 torsion and apical rotation were decreased when increasing RV mechanical rigidity and during re-orientation of RV myocardial fibers, both of which have been demonstrated in PH. 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. Furthermore, discovered causes of decreased LV torsion are consistent with RV structural adaptations seen in PH rodent studies, which might also explain suspected stress-induced changes in LV myocardial gene and protein expression.

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Figures

Grahic Jump Location
Fig. 1

Finite element model of the heart, with the left (darker mesh) and right (lighter mesh) ventricles meshed as separate, but connected, bodies. Each node on the base is connected to a virtual six-degrees-of-freedom spring element that is fixed on the other end.

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Fig. 2

(a) Computation of fiber orientation within the local coordinate system, as it rotates across the myocardium according to Eq. (1). Red vectors represent local coordinate system before rotation (no rotation at the epicardium), and blue vectors represent the local coordinate system after rotation. Fibers are orientated −66.5 deg from the A⇀ axis; (b) Representation of fiber orientation superimposed on the heart model. Yellow lines show fiber orientation along the epi/endocardium walls.

Grahic Jump Location
Fig. 3

(a) Stress versus stretch curves along the fiber (ff) and sheet (ss) axis. Data are extracted from Ref. [14], obtained from passive RV myocardial tissue during an equal-biaxial mechanical testing experiment. (b) Stress versus stretch data computed to obtain Mooney–Rivlin (M–R) material constants at peak contraction. These data were created from data in (a), but modified by multiplying stress along the fiber direction tenfold at each stretch measurement. (c) Waveform describing the time variation in tissue stiffness during contraction (extracted from the elastance function in Ref. [20]), E(t). Values in boxes show M–R material constants at end diastole and end ejection.

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Fig. 4

(a) Pressure waveforms applied to the RV endocardial surface under different simulations conditions and (b) pressure waveform applied to the LV endocardium in all reported simulations

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Fig. 5

(a) Simulated changes in RV and LV volume during normal systolic contraction and (b) simulated apex and base rotation during normal systolic contraction

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Fig. 6

Left ventricular apex rotation (a) and LV twisting (b) at end ejection for eight simulated conditions. (c) Evidence of progressively worse septal flattening for Sim 4a-c, which still revealed progressively increasing LV apex rotation.

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Fig. 7

(a) Stress distribution under normal RV/LV ejection. (b) Stress distribution under severely hypertensive RV, with normal LV, ejection. Each plot shows a heat map of the first principal component of stress (P1) superimposed on the endocardial surface viewing the ventricle from the base (left) and at four planes cut along the short axis of the heart (right). (c) Exponential (although near-linear) correlation between maximum RV pressure and the temporal/spatial maximum of P1.

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