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TECHNICAL PAPERS

Effects of Ischemia on Epicardial Deformation in the Passive Rabbit Heart

[+] Author and Article Information
Glenn R. Gaudette

Department of Biomedical Engineering, Institute of Molecular Cardiology

Irvin B. Krukenkamp

Department of Biomedical Engineering, Division of Cardiothoracic Surgery, Institute of Molecular Cardiology

Evren U. Azeloglu

Department of Biomedical Engineering, Department of Mechanical Engineering

Adam E. Saltman

Division of Cardiothoracic Surgery, The Institute for Molecular Cardiology, The State University of New York at Stony Brook, Stony Brook, NY

Miriam Lense

Ward Melville High School, East Setauket, NY

Joseph Todaro

Department of Mechanical Engineering

Fu-Pen Chiang

Department of Biomedical Engineering, Department of Mechanical Engineering, Division of Cardiothoracic Surgery, Institute for Molecular Cardiology, The State University of New York at Stony Brook, Stony Brook, NY

J Biomech Eng 126(1), 70-75 (Mar 09, 2004) (6 pages) doi:10.1115/1.1645524 History: Received February 12, 2002; Revised September 04, 2003; Online March 09, 2004
Copyright © 2004 by ASME
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References

Figures

Grahic Jump Location
Shown above (top) is a schematic diagram of the experimental setup. The image on the bottom left shows a typical heart with the silicone carbide particles (approximately 40 μ in diameter) applied. The bottom right image shows an enlarged view of the region of interest. The cut out region in the lower left represents a 90×90-pixel area.
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Comparison between principal strain (from 10 to 20 mmHg intracavitary pressure) obtained with or without an intracavitary balloon in the passive rabbit heart. The use of an intracavitary balloon did not affect the strain on the ventricle, suggesting a highly compliant balloon.
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Representative data sets of myocardial deformation of a passive rabbit heart when the intracavitary pressure was increased from 0 to 10 mmHg. Note each contour represents 10 μ displacement. Numbers represent actual displacements in microns. (a) u and v displacements, respectively, at 20 minutes of perfusion in the arrested heart. (b) u and v displacements, respectively, at 15 minutes of global ischemia in the arrested heart. (c) u and v displacements, respectively, at 15 minutes of reperfusion in the arrested heart.
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Principal strain (E1) and the first invariant of the 2-D strain (I1) for hyperkalemic hearts as a function of the perfusion status. Hearts were loaded from 10 to 20 mmHg pressure.
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Deformation map of a regional ischemic rabbit heart. The images show the displacement for an intracavitary pressure increase from 0 to 25 mmHg. Each contour line represents 20 μm displacement. The image of the heart shown is captured with a wider zoom for representation purposes. The approximate ischemic border is delineated with the dashed line. (a) Regionally ischemic heart with u displacements. The approximate dimension of the analyzed region is given. (b) Regionally ischemic heart with v displacements. The invariant of the 2-D strain tensor was determined in the highlighted regions and their values are shown. The region in the upper right hand corner is in the perfused zone, and the region in the lower left hand corner is in the ischemic zone.

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