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Research Papers

Cardiac Assist With a Twist: Apical Torsion as a Means to Improve Failing Heart Function

[+] Author and Article Information
Dennnis R. Trumble, Walter E. McGregor, Roy C. P. Kerckhoffs, Lewis K. Waldman

 Allegheny-Singer Research and the McGinnis Cardiovascular Institutes, Allegheny General Hospital, West Penn Allegheny Health System, Pittsburgh, PA 15212; Biomedical Engineering Department,  Carnegie Mellon University, Pittsburgh, PA 15213 e-mail: trumble@wpahs.org Allegheny-Singer Research and the McGinnis Cardiovascular Institutes, Allegheny General Hospital, West Penn Allegheny Health System, Pittsburgh, PA 15212 e-mail: wmcgrego@wpahs.orgDepartment of Bioengineering,  University of California San Diego, La Jolla, CA 92093 e-mail: roy@bioeng.ucsd.edu Insilicomed, Inc., 7825 Fay Avenue, Suite 200, La Jolla, CA 92037 e-mail: lwaldman@san.rr.com

J Biomech Eng 133(10), 101003 (Oct 31, 2011) (10 pages) doi:10.1115/1.4005169 History: Received January 03, 2011; Accepted September 05, 2011; Published October 31, 2011; Online October 31, 2011

Changes in muscle fiber orientation across the wall of the left ventricle (LV) cause the apex of the heart to turn 10–15 deg in opposition to its base during systole and are believed to increase stroke volume and lower wall stress in healthy hearts. Studies show that cardiac torsion is sensitive to various disease states, which suggests that it may be an important aspect of cardiac function. Modern imaging techniques have sparked renewed interest in cardiac torsion dynamics, but no work has been done to determine whether mechanically augmented apical torsion can be used to restore function to failing hearts. In this report, we discuss the potential advantages of this approach and present evidence that turning the cardiac apex by mechanical means can displace a clinically significant volume of blood from failing hearts. Computational models of normal and reduced-function LVs were created to predict the effects of applied apical torsion on ventricular stroke work and wall stress. These same conditions were reproduced in anesthetized pigs with drug-induced heart failure using a custom apical torsion device programmed to rotate over various angles during cardiac systole. Simulations of applied 90 deg torsion in a prolate spheroidal computational model of a reduced-function pig heart produced significant increases in stroke work (25%) and stroke volume with reduced fiber stress in the epicardial region. These calculations were in substantial agreement with corresponding in vivo measurements. Specifically, the computer model predicted torsion-induced stroke volume increases from 13.1 to 14.4 mL (9.9%) while actual stroke volume in a pig heart of similar size and degree of dysfunction increased from 11.1 to 13.0 mL (17.1%). Likewise, peak LV pressures in the computer model rose from 85 to 95 mm Hg (11.7%) with torsion while maximum ventricular pressures in vivo increased in similar proportion, from 55 to 61 mm Hg (10.9%). These data suggest that: (a) the computer model of apical torsion developed for this work is a fair and accurate predictor of experimental outcomes, and (b) supra-physiologic apical torsion may be a viable means to boost cardiac output while avoiding blood contact that occurs with other assist methods.

FIGURES IN THIS ARTICLE
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Copyright © 2011 by American Society of Mechanical Engineers
Topics: Torsion , Rotation , Fibers
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Figures

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Figure 1

Drawing of an apical torsion device attached to the heart via a transcostal drive shaft. In this configuration the drive motor would be located outside the chest wall. For longer-term applications the actuator could be placed inside the chest and powered via a percutaneous driveline.

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Figure 2

Finite element model of the left ventricle constructed in the form of a prolate spheroid. Left: Prolate spheroidal coordinates (λ, μ, θ), a = major radius, b = minor radius, d = focal length = a2  − b2 . Right: Cross-sectional view showing the mesh configuration and the location of the four inter-element surface nodes used to define circumferential displacement of the apex (dark dots). Shown also are the locations of the central Gauss points used to calculate stress across the myocardial wall (light dots).

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Figure 3

Mesh configuration of the prolate spheroid LV model. The 18 elements are arranged in a 6x3 grid with six elements between apex and base and three across the ventricular wall. Myocardial stresses and strains are calculated at 27 Gauss points per element (486 total) at each time point in the simulation run.

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Figure 4

Top: Computer-controlled rotary servomotor used to drive a custom apical torsion suction device. The “SmartMotor” actuator can be programmed to turn through any angle with velocities, accelerations, and dwell times set by the user. Coordination of rotations with cardiac systole is accomplished by triggering off the ECG directly or via an external pacing signal. Bottom left: Top view of the suction cup apparatus (apical interface device) used to grip the apex of the heart. Bottom right: Side view of the device showing the housing profile, vacuum line, and pressure tubing used to connect to the motor drive shaft.

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Figure 5

Calculated pressure-volume loops showing changes in stroke work in normal (top) and reduced-function hearts (bottom) with 90° apical rotation. Unassisted beats are traced with solid lines, assisted beats with broken lines. In these simulations increases in stroke work were 14.8% and 25.2% for normal and reduced-function hearts respectively.

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Figure 6

Fiber stress distributions plotted across the LV free wall in normal (top) and reduced-function hearts with and without apical torsion. Data for endocardial, midwall, and epicardial regions were taken at end systole from the central Gauss point of model elements 13, 15, and 17, respectively. Heart rate  = 80 bpm.

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Figure 7

Fiber stress distributions plotted from apex to base in the endocardium (top), midwall (middle), and epicardium (bottom) in normal, reduced-function, and assisted hearts. Data are taken from the central Gauss point of each model element at end systole. Longitudinal position along the LV is expressed as the ratio of the mu (μ) coordinate to its maximum value (120° ) at the base. (Note: μ = 0° at the apex.)

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Figure 8

Plots of fiber stress distribution over time (one cardiac cycle) in the central region of the LV model (elements 13, 15, and 17) for normal (top), reduced-function (middle), and assisted (bottom) conditions

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Figure 9

Hemodynamic waveforms measured under conditions of severe heart failure (propranolol) before and after application of apical torsion (90° rotation over 25% of the cardiac cycle). * indicates non = assisted beats. LV = left ventricle, Ao = Aorta, PA = pulmonary artery.

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