Right Ventricular Fiber Structure as a Compensatory Mechanism in Experimental Pressure Overload: A Computational Study

[+] Author and Article Information
Arnold D. Gomez

ASME Member Johns Hopkins University, Electrical and Computer Engineering Department 3400 North Charles Street, RM Clark 201B Baltimore, MD 21218, USA

Huashan Zou

University of Utah, Bioengineering Department 36 S. Wasatch Dr., SMBB RM 3100 Salt Lake City, UT 84112-2101

Megan E. Bowen

University of Utah, Surgery Department 30 N 1900 E, RM 3B205 Salt Lake City, UT 84112-2101

Xiaoqing Liu

University of Utah, Surgery Department, Cardiothoracic Division 2000 Circle of Hope, RM LL376 Salt Lake City, UT 84112-2101

Edward W. Hsu

University of Utah, Bioengineering Department 36 S. Wasatch Dr., SMBB RM 1242 Salt Lake City, UT 84112-2101

Stephen H. McKellar

University of Utah, Surgery Department, Cardiothoracic Division 30 N 1900 E, RM 3B205 Salt Lake City, UT 84112-2101

1Corresponding author.

ASME doi:10.1115/1.4036485 History: Received November 07, 2016; Revised April 07, 2017


Right ventricular failure (RVF) is a lethal condition in diverse pathologies. Pressure overload is the most common etiology of RVF, but our understanding of the tissue structure remodeling and other biomechanical factors involved in RVF is limited. Some remodeling patterns are interpreted as compensatory mechanisms including myocyte hypertrophy, extracellular fibrosis, and changes in fiber orientation. However, the specific implications of these changes, especially in relation to clinically observable measurements, are difficult to investigate experimentally. In this computational study, we hypothesized that, with other variables constant, fiber orientation alteration provides a quantifiable and distinct compensatory mechanism during RV pressure overload. Numerical models were constructed using a rabbit model of chronic pressure overload RVF based on intraventricular pressure measurements, CINE magnetic resonance imaging (MRI), and diffusion tensor MRI (DT-MRI). Biventricular simulations were conducted under normotensive and hypertensive boundary conditions using variations in RV wall thickness, tissue stiffness, and fiber orientation to investigate their effect on RV pump function. Our results show that a longitudinally aligned myocardial fiber orientation contributed to an increase in RV ejection fraction (RVEF). This effect was more pronounced in response to pressure overload. Likewise, models with longitudinally aligned fiber orientation required a lesser contractility for maintaining a target RVEF against elevated pressures. In addition to increased wall thickness and material stiffness (diastolic compensation), systolic mechanisms in the forms of myocardial fiber realignment and changes in contractility are likely involved in the overall compensatory responses to pressure overload.

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