Technical Brief

Numerical Evaluation of Myofiber Orientation and Transmural Contractile Strength on Left Ventricular Function

[+] Author and Article Information
Xiaoyan Zhang

Department of Mechanical Engineering,
University of Kentucky,
Lexington, KY 40506;
Center for Computational Sciences,
University of Kentucky,
Lexington, KY 40506

Premi Haynes, Kenneth S. Campbell

Department of Physiology,
University of Kentucky,
Lexington, KY 40506;
Center for Muscle Biology,
University of Kentucky,
Lexington, KY 40506

Jonathan F. Wenk

Department of Mechanical Engineering,
University of Kentucky,
269 Ralph G. Anderson Building,
Lexington, KY 40506;
Department of Surgery,
University of Kentucky,
Lexington, KY 40506
e-mail: wenk@engr.uky.edu

1Corresponding author.

Manuscript received June 24, 2014; final manuscript received October 30, 2014; published online February 5, 2015. Assoc. Editor: Jonathan Vande Geest.

J Biomech Eng 137(4), 044502 (Apr 01, 2015) (6 pages) Paper No: BIO-14-1291; doi: 10.1115/1.4028990 History: Received June 24, 2014; Revised October 30, 2014; Online February 05, 2015

The left ventricle (LV) of the heart is composed of a complex organization of cardiac muscle fibers, which contract to generate force and pump blood into the body. It has been shown that both the orientation and contractile strength of these myofibers vary across the ventricular wall. The hypothesis of the current study is that the transmural distributions of myofiber orientation and contractile strength interdependently impact LV pump function. In order to quantify these interactions a finite element (FE) model of the LV was generated, which incorporated transmural variations. The influences of myofiber orientation and contractile strength on the Starling relationship and the end-systolic (ES) apex twist of the LV were assessed. The results suggest that reductions in contractile strength within a specific transmural layer amplified the effects of altered myofiber orientation in the same layer, causing greater changes in stroke volume (SV). Furthermore, when the epicardial myofibers contracted the strongest, the twist of the LV apex was greatest, regardless of myofiber orientation. These results demonstrate the important role of transmural distribution of myocardial contractile strength and its interplay with myofiber orientation. The coupling between these two physiologic parameters could play a critical role in the progression of heart failure.

Copyright © 2015 by ASME
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Grahic Jump Location
Fig. 1

A 3D FE model was created to simulate the function of LV. (a) Wireframe view of the LV, which was represented by an ellipsoidal morphology; (b) view with half of the model removed to show the LV wall with three transmural layers of equal thickness, outermost = epicardium, middle = midwall, and innermost = endocardium; (c) epicardial view of model with transmural variation in myofiber orientation (white lines within elements) and a radial–circumferential plane near the apex where the LV twist was assessed, and (d) example of the rotation angles of two specific nodes on the inner and outer surface of LV wall from end-diastolic to ES states.

Grahic Jump Location
Fig. 2

The transmural distribution of myocardium contractile strength altered the effects of myofiber orientation on the Starling relationship of LV. With the helical angle of epi-myofibers fixed at −30 deg, the effects of changes in endo-myofiber helical angle on the Starling curve of LV were assessed when Tmax for epi-, mid-, and endocardium was 150, 110, and 70 kPa, respectively, [case (i); (a)], and 70, 110, and 150 kPa, respectively, [case (ii); (b)]. The effects of epi-myofiber helical angle on LV Starling curve were assessed when the endo-myofibers were set at 60 deg for cases i (c) and ii (d), respectively.

Grahic Jump Location
Fig. 3

The transmural variations of myofiber orientation and contractile strength interdependently influenced the systolic twist angles of left ventricular apex. The apex twist angle of the LV from ED to ES was determined at EDP = 15 mmHg and ESP = 90 mmHg. The effects of endo-myofiber (a) and epi-myofiber (b) helical angles on LV apex twist were examined, respectively, for cases (i) and (ii).




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