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research-article

Multiscale Computational Analysis of RV Mechanoenergetics

[+] Author and Article Information
Ryan J. Pewowaruk

ASME Student Member, Biomedical Engineering, University of Wisconsin − Madison, 2145 Engineering Centers Building, 1550 Engineering Drive, Madison, WI 53706, USA
pewowaruk@wisc.edu

Jennifer Philip

Surgery, University of Wisconsin − Madison, 2143 Engineering Centers Building, 1550 Engineering Drive, Madison, WI 53706, USA
philip@surgery.wisc.edu

Shivendra Tewari

Molecular & Integrative Physiology, University of Michigan – Ann Arbor, 2800 Plymouth Road, North Campus Research Center, Ann Arbor, MI 48109-5622, USA
tewarisg@gmail.com

Claire Chen

Mechanical Engineering, University of Wisconsin − Madison, 2145 Engineering Centers Building, 1550 Engineering Drive, Madison, WI 53706, USA
cchen394@wisc.edu

Mark Nyaeme

Biomedical Engineering, University of Wisconsin − Madison, 2145 Engineering Centers Building, 1550 Engineering Drive, Madison, WI 53706, USA
mnyaeme@wisc.edu

Zhijie Wang

Mechanical Engineering, Colorado State University, 1301 Campus Delivery, Fort Collins, CO 80521, USA
zhijie.wang@colostate.edu

Diana Tabima

Biomedical Engineering, University of Wisconsin − Madison, 2144 Engineering Centers Building, 1550 Engineering Drive, Madison, WI 53706, USA
dtabimamarti@wisc.edu

Anthony Baker

Medicine, University of California – San Francisco, 4150 Clement St, San Francisco, CA 94121
anthony.baker@ucsf.edu

Daniel Beard

Molecular & Integrative Physiology, University of Michigan – Ann Arbor, 2800 Plymouth Road, North Campus Research Center, Ann Arbor, MI 48109-5622, USA
beardda@med.umich.edu

Naomi Chesler

ASME Fellow, Biomedical Engineering, University of Wisconsin – Madison, Medicine, University of Wisconsin − Madison, 2146 Engineering Centers Building, 1550 Engineering Drive, Madison, WI 53706
naomi.chesler@wisc.edu

1Corresponding author.

ASME doi:10.1115/1.4040044 History: Received December 01, 2017; Revised April 13, 2018

Abstract

Right ventricular (RV) failure, which occurs in the setting of pressure overload, i.e. pulmonary hypertension (PH), is characterized by abnormalities in myofilament mechanics and energetic state. The effects of these cell level changes on organ level RV function are unknown. The primary aim of this study was to quantify the effects of metabolite concentrations as well as active and passive cardiac tissue mechanics on RV function using a multiscale model of the cardiovascular system. The model integrates metabolic environment, actin-myosin cross bridging, intracellular myofilament mechanics and extracellular tissue mechanics in a mechanistically realistic heart model coupled with a simple lumped parameter circulation. Three models of PH were simulated and compared to experiment. The model was able to capture a wide range of cardiovascular physiology and pathophysiology, from mild RV dysfunction to severe RV failure, as well as elevated RV afterload secondary to LV disease. Simulations predict that in response to pressure overload alone, the RV is able to maintain cardiac output and that alterations in RV active myofilament mechanics or RV energetic state are necessary to decrease cardiac output.

Copyright (c) 2018 by ASME
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