Research Papers

The Direct Incorporation of Perfusion Defect Information to Define Ischemia and Infarction in a Finite Element Model of the Left Ventricle

[+] Author and Article Information
Alexander I. Veress

Department of Mechanical Engineering,
University of Washington,
Stevens Way,
Box 352600,
Seattle, WA 98195
e-mail: averess@uw.edu

George S. K. Fung

Department of Radiology,
The Johns Hopkins University,
601 North Caroline Street,
JHOC Room 4263,
Baltimore, MD 21287-0859
e-mail: gfung2@jhmi.edu

Taek-Soo Lee

Department of Radiology,
The Johns Hopkins University,
601 North Caroline Street,
JHOC Room 4263,
Baltimore, MD 21287-0859
e-mail: tslee@jhmi.edu

Benjamin M. W. Tsui

Department of Radiology,
The Johns Hopkins University,
601 North Caroline Street,
JHOC Room 4263,
Baltimore, MD 21287-0859
e-mail: btsui@jhmi.edu

Gregory A. Kicska

Department of Radiology,
University of Washington,
1959 NE Pacific Street,
Seattle, WA 98195
e-mail: gkicska@gmail.com

W. Paul Segars

Carl E. Ravin Advanced Imaging Laboratories,
Duke University,
Duke University Hock Plaza,
2424 Suite 302, Erwin Road,
Durham, NC 27705
e-mail: paul.segars@duke.edu

Grant T. Gullberg

Structural Biology and Imaging Department,
Ernest Orlando Lawrence
Berkeley National Laboratory,
One Cyclotron Road, MS 55R0121,
Berkeley, CA 94720
e-mail: gtgullberg@lbl.gov

Manuscript received May 13, 2014; final manuscript received October 22, 2014; published online February 25, 2015. Assoc. Editor: Dalin Tang.

J Biomech Eng 137(5), 051004 (May 01, 2015) (10 pages) Paper No: BIO-14-1209; doi: 10.1115/1.4028989 History: Received May 13, 2014; Revised October 22, 2014; Online February 25, 2015

This paper describes the process in which complex lesion geometries (specified by computer generated perfusion defects) are incorporated in the description of nonlinear finite element (FE) mechanical models used for specifying the motion of the left ventricle (LV) in the 4D extended cardiac torso (XCAT) phantom to simulate gated cardiac image data. An image interrogation process was developed to define the elements in the LV mesh as ischemic or infarcted based upon the values of sampled intensity levels of the perfusion maps. The intensity values were determined for each of the interior integration points of every element of the FE mesh. The average element intensity levels were then determined. The elements with average intensity values below a user-controlled threshold were defined as ischemic or infarcted depending upon the model being defined. For the infarction model cases, the thresholding and interrogation process were repeated in order to define a border zone (BZ) surrounding the infarction. This methodology was evaluated using perfusion maps created by the perfusion cardiac-torso (PCAT) phantom an extension of the 4D XCAT phantom. The PCAT was used to create 3D perfusion maps representing 90% occlusions at four locations (left anterior descending (LAD) segments 6 and 9, left circumflex (LCX) segment 11, right coronary artery (RCA) segment 1) in the coronary tree. The volumes and shapes of the defects defined in the FE mechanical models were compared with perfusion maps produced by the PCAT. The models were incorporated into the XCAT phantom. The ischemia models had reduced stroke volume (SV) by 18–59 ml. and ejection fraction (EF) values by 14–50% points compared to the normal models. The infarction models, had less reductions in SV and EF, 17–54 ml. and 14–45% points, respectively. The volumes of the ischemic/infarcted regions of the models were nearly identical to those volumes obtained from the perfusion images and were highly correlated (R2= 0.99).

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Veress, A. I., Segars, W. P., Weiss, J. A., Tsui, B. M., and Gullberg, G. T., 2006, “Normal and Pathological NCAT Image and Phantom Data Based on Physiologically Realistic Left Ventricle Finite-Element Models,” IEEE Trans. Med. Imaging, 25(12), pp. 1604–1616. [CrossRef] [PubMed]
Veress, A. I., Segars, W. P., Tsui, B. M., and Gullberg, G. T., 2011, “Incorporation of a Left Ventricle Finite Element Model Defining Infarction Into the XCAT Imaging Phantom,” IEEE Trans. Med. Imaging, 30(4), pp. 915–927. [CrossRef] [PubMed]
Holmes, J. W., Borg, T. K., and Covell, J. W., 2005, “Structure and Mechanics of Healing Myocardial Infarcts,” Annu. Rev. Biomed. Eng., 7(1), pp. 223–253. [CrossRef] [PubMed]
Pirzada, F. A., Ekong, E. A., Vokonas, P. S., Apstein, C. S., and Hood, W. B., Jr., 1976, “Experimental Myocardial Infarction. XIII. Sequential Changes in Left Ventricular Pressure–Length Relationships in the Acute Phase,” Circulation, 53(6), pp. 970–975. [CrossRef] [PubMed]
Vokonas, P. S., Pirzada, F. A., Robbins, S. L., and Hood, W. B., Jr., 1978, “Experimental Myocardial Infarction. XV. Segmental Mechanical Behavior and Morphology of Ischemic Myocardium During Hypothermia,” Am. J. Physiol., 235(6), pp. H736–H744. [PubMed]
Gillam, L. D., Franklin, T. D., Foale, R. A., Wiske, P. S., Guyer, D. E., and Hogan, R. D., and Weyman, A. E., 1986, “The Natural History of Regional Wall Motion in the Acutely Infarcted Canine Ventricle,” J. Am. Coll. Cardiol., 7(6), pp. 1325–1334. [CrossRef] [PubMed]
Fishbein, M. C., Maclean, D., and Maroko, P. R., 1978, “The Histopathologic Evolution of Myocardial Infarction,” Chest, 73(6), pp. 843–849. [CrossRef] [PubMed]
Fung, G. S. K., Segars, W. P., Lee, T., Veress, A. I., Gullberg, G. T., and Tsui, B. M., 2010, “A New Perfusion Heart Model for Realistic Simulation of Myocardial Perfusion Defects,” J. Nucl. Med., 51(Suppl. 2), p. 476.
Fung, G. S. K., Segars, W. P., Lee, T., Higuchi, T., Veress, A. I., Gullberg, G. T., and Tsui, B. M. W., 2010, “Realistic Simulation of Regional Myocardial Perfusion Defects for Cardiac SPECT Studies,” Nuclear Science Symposium Conference Record (NSS/MIC), Knoxville, TN, Oct. 30–Nov. 6, pp. 3061–3064. [CrossRef]
Fung, G. S., Segars, W. P., Gullberg, G. T., and Tsui, B. M., 2011, “Development of a Model of the Coronary Arterial Tree for the 4D XCAT Phantom,” Phys. Med. Biol., 56(17), pp. 5651–5663. [CrossRef] [PubMed]
Rasband, W. S., 1997–2014, IMAGEJ, U. S. National Institutes of Health, Bethesda, MD, see http://imagej.nih.gov/ij/
Kerckhoffs, R. C., McCulloch, A. D., Omens, J. H., and Mulligan, L. J., 2009, “Effects of Biventricular Pacing and Scar Size in a Computational Model of the Failing Heart With Left Bundle Branch Block,” Med. Image Anal., 13(2), pp. 362–369. [CrossRef] [PubMed]
Kerckhoffs, R. C., Neal, M. L., Gu, Q., Bassingthwaighte, J. B., Omens, J. H., and McCulloch, A. D., 2007, “Coupling of a 3D Finite Element Model of Cardiac Ventricular Mechanics to Lumped Systems Models of the Systemic and Pulmonic Circulation,” Ann. Biomed. Eng., 35(1), pp. 1–18. [CrossRef] [PubMed]
Yushkevich, P. A., Piven, J., Hazlett, H. C., Smith, R. G., Ho, S., Gee, J. C., and Gerig, G., 2006, “User-Guided 3D Active Contour Segmentation of Anatomical Structures: Significantly Improved Efficiency and Reliability,” Neuroimage, 31(3), pp. 1116–1128. [CrossRef] [PubMed]
XYZ Scientific Applications, Inc., 2012, TrueGrid, XYZ Scientific Applications, Inc., Livermore, CA.
Weiss, J. A., Maker, B. N., and Govindjee, S., 1996, “Finite Element Implementation of Incompressible, Transversely Isotropic Hyperelasticity,” Comput. Methods Appl. Mech. Eng., 135(1–2), pp. 107–128. [CrossRef]
Guccione, J. M., and McCulloch, A. D., 1993, “Mechanics of Active Contraction in Cardiac Muscle: Part I—Constitutive Relations for Fiber Stress That Describe Deactivation,” ASME J. Biomech. Eng., 115(1), pp. 72–81. [CrossRef]
Guccione, J. M., and McCulloch, A. D., 1993, “Mechanics of Active Contraction in Cardiac Muscle: Part II—Constitutive Relations for Fiber Stress That Describe Deactivation,” ASME J. Biomech. Eng., 115(1), pp. 82–90. [CrossRef]
Bathe, K.-J., 1982, Finite Element Procedures in Engineering Analysis, Prentice-Hall, Englewood Cliffs, NJ.
Jackson, B. M., Gorman, J. H., III, Salgo, I. S., Moainie, S. L., Plappert, T., St John-Sutton, M., Edmunds, L. H. Jr., and Gorman, R. C., 2003, “Border Zone Geometry Increases Wall Stress After Myocardial Infarction: Contrast Echocardiographic Assessment,” Am. J. Physiol. Heart. Circ. Physiol., 284(2), pp. H475–H479. [PubMed]
Lima, J. A., Becker, L. C., Melin, J. A., Lima, S., Kallman, C. A., Weisfeldt, M. L., and Weiss, J. L., 1985, “Impaired Thickening of Nonischemic Myocardium During Acute Regional Ischemia in the Dog,” Circulation, 71(5), pp. 1048–1059. [CrossRef] [PubMed]
Epstein, F. H., Yang, Z., Gilson, W. D., Berr, S. S., Kramer, C. M., and French, B. A., 2002, “MR Tagging Early After Myocardial Infarction in Mice Demonstrates Contractile Dysfunction in Adjacent and Remote Regions,” Magn. Reson. Med., 48(2), pp. 399–403. [CrossRef] [PubMed]
Garot, J., Lima, J. A., Gerber, B. L., Sampath, S., Wu, K. C., Bluemke, D. A., Prince, J. L., and Osman, N. F., 2004, “Spatially Resolved Imaging of Myocardial Function With Strain-Encoded MR: Comparison With Delayed Contrast-Enhanced MR Imaging After Myocardial Infarction,” Radiology, 233(2), pp. 596–602. [CrossRef] [PubMed]
Gilson, W. D., Yang, Z., French, B. A., and Epstein, F. H., 2005, “Measurement of Myocardial Mechanics in Mice Before and After Infarction Using Multislice Displacement-Encoded MRI With 3D Motion Encoding,” Am. J. Physiol. Heart Circ. Physiol., 288(3), pp. H1491–H1497. [CrossRef] [PubMed]
Kramer, W., Wizemann, V., Thormann, J., Bechthold, A., Schutterle, G., and Lasch, H. G., 1985, “Mechanisms of Altered Myocardial Contractility During Hemodialysis: Importance of Changes in the Ionized Calcium to Plasma Potassium Ratio,” Klin. Wochenschr., 63(6), pp. 272–278. [CrossRef] [PubMed]
Gallagher, K. P., Gerren, R. A., Choy, M., Stirling, M. C., and Dysko, R. C., 1987, “Subendocardial Segment Length Shortening at Lateral Margins of Ischemic Myocardium in Dogs,” Am. J. Physiol., 253(4), pp. H826–H837. [PubMed]
Gallagher, K. P., Gerren, R. A., Stirling, M. C., Choy, M., Dysko, R. C., McManimon, S. P., and Dunham, W. R., 1986, “The Distribution of Functional Impairment Across the Lateral Border of Acutely Ischemic Myocardium,” Circ. Res., 58(4), pp. 570–583. [CrossRef] [PubMed]
Mazhari, R., Omens, J. H., Covell, J. W., and McCulloch, A. D., 2000, “Structural Basis of Regional Dysfunction in Acutely Ischemic Myocardium,” Cardiovasc. Res., 47(2), pp. 284–293. [CrossRef] [PubMed]
Sakai, K., Watanabe, K., and Millard, R. W., 1985, “Defining the Mechanical Border Zone: A Study in the Pig Heart,” Am. J. Physiol., 249(1), pp. H88–H94. [PubMed]
Van Leuven, S. L., Waldman, L. K., McCulloch, A. D., and Covell, J. W., 1994, “Gradients of Epicardial Strain Across the Perfusion Boundary During Acute Myocardial Ischemia,” Am. J. Physiol., 267(6), pp. H2348–H2362. [PubMed]
Weiss, J., Maker, B., and Govindjee, S., 1996, “Finite Element Implementation of Incompressible Transversely Isotropic Hyperelasticity,” Comput. Methods Appl. Mech. Eng., 135(1–2), pp. 107–128. [CrossRef]
Walker, J. C., Guccione, J. M., Jiang, Y., Zhang, P., Wallace, A. W., Hsu, E. W., and Ratcliffe, M. B., 2005, “Helical Myofiber Orientation After Myocardial Infarction and Left Ventricular Surgical Restoration in Sheep,” J. Thorac. Cardiovasc. Surg., 129(2), pp. 382–390. [CrossRef] [PubMed]
Chen, J., Song, S. K., Liu, W., McLean, M., Allen, J. S., Tan, J., Wickline, S. A., and Yu, X., 2003, “Remodeling of Cardiac Fiber Structure After Infarction in Rats Quantified With Diffusion Tensor MRI,” Am. J. Physiol. Heart Circ. Physiol., 285(3), pp. H946–H954. [PubMed]
Dang, A. B., Guccione, J. M., Mishell, J. M., Zhang, P., Wallace, A. W., Gorman, R. C., and Ratcliffe, M. B., 2005, “Akinetic Myocardial Infarcts Must Contain Contracting Myocytes: Finite-Element Model Study,” Am. J. Physiol. Heart Circ. Physiol., 288(4), pp. H1844–H1850. [CrossRef] [PubMed]
Dang, A. B., Guccione, J. M., Zhang, P., Wallace, A. W., Gorman, R. C., Gorman, J. H.III, and Ratcliffe, M. B., 2005, “Effect of Ventricular Size and Patch Stiffness in Surgical Anterior Ventricular Restoration: A Finite Element Model Study,” Ann. Thorac. Surg., 79(1), pp. 185–193. [CrossRef] [PubMed]
Guccione, J. M., Moonly, S. M., Wallace, A. W., and Ratcliffe, M. B., 2001, “Residual Stress Produced by Ventricular Volume Reduction Surgery Has Little Effect on Ventricular Function and Mechanics: A Finite Element Model Study,” J. Thorac. Cardiovasc. Surg., 122(3), pp. 592–599. [CrossRef] [PubMed]
Delaunay, B. N., 1934, “Sur la Sphère Vide, Vol. 7, Izvestia Akademia Nauk SSSR, VII Seria, Otdelenie Matematicheskii i Estestvennyka Nauk, pp. 793–800.
Moller, J. E., Pellikka, P. A., Hillis, G. S., and Oh, J. K., 2006, “Prognostic Importance of Diastolic Function and Filling Pressure in Patients With Acute Myocardial Infarction,” Circulation, 114(5), pp. 438–444. [CrossRef] [PubMed]
Moller, J. E., Brendorp, B., Ottesen, M., Kober, L., Egstrup, K., Poulsen, S. H., and Christian, T-P., 2003, “Congestive Heart Failure With Preserved Left Ventricular Systolic Function After Acute Myocardial Infarction: Clinical and Prognostic Implications,” Eur. J. Heart. Fail., 5(6), pp. 811–819. [CrossRef] [PubMed]
Rechavia, E., de Silva, R., Nihoyannopoulos, P., Lammertsma, A. A., Jones, T., and Maseri, A., 1995, “Hyperdynamic Performance of Remote Myocardium in Acute Infarction. Correlation Between Regional Contractile Function and Myocardial Perfusion,” Eur. Heart J., 16(12), pp. 1845–1850. [PubMed]
Beyersdorf, F., Okamoto, F., Buckberg, G. D., Sjostrand, F., Allen, B. S., Acar, C., Young, H. H., and Bugyi, H. I., 1989, “Studies on Prolonged Acute Regional Ischemia. II. Implications of Progression From Dyskinesia to Akinesia in the Ischemic Segment,” J. Thorac. Cardiovasc. Surg., 98(2), pp. 224–233. [PubMed]
Kerckhoffs, R. C., Campbell, S. G., Flaim, S. N., Howard, E. J., Sierra-Aguado, J., Mulligan, L. J., and McCulloch, A. D., 2009, “Multi-Scale Modeling of Excitation–Contraction Coupling in the Normal and Failing Heart,” Conf. Proc. IEEE Eng. Med. Biol. Soc., 2009, pp. 4281–4282.
Kerckhoffs, R. C., Lumens, J., Vernooy, K., Omens, J. H., Mulligan, L. J., Delhaas, T., Arts, T., McCulloch, A. D., and Prinzen, F. W., 2008, “Cardiac Resynchronization: Insight From Experimental and Computational Models,” Prog. Biophys. Mol. Biol., 97(2–3), pp. 543–561. [CrossRef] [PubMed]
Lee, J. T., Ideker, R. E., and Reimer, K. A., 1981, “Myocardial Infarct Size and Location in Relation to the Coronary Vascular Bed at Risk in Man,” Circulation, 64(3), pp. 526–534. [CrossRef] [PubMed]
Diwan, A., and Dorn, G. W.II, 2007, “Decompensation of Cardiac Hypertrophy: Cellular Mechanisms and Novel Therapeutic Targets,” Physiology (Bethesda), 22(1), pp. 56–64. [CrossRef] [PubMed]
Frey, N., and Olson, E. N., 2003, “Cardiac Hypertrophy: The Good, the Bad, and the Ugly,” Annu. Rev. Physiol., 65(1), pp. 45–79. [CrossRef] [PubMed]
Frey, N., Katus, H. A., Olson, E. N., and Hill, J. A., 2004, “Hypertrophy of the Heart: A New Therapeutic Target?,” Circulation, 109(13), pp. 1580–1589. [CrossRef] [PubMed]
Farzaneh-Fara, A., and Kwong, R. Y., 2011, “Detecting Acute Coronary Syndromes by Magnetic Resonance Imaging,” Met. Imaging, 50, pp. 15–19.
Saraste, A., Nekolla, S., and Schwaiger, M., 2008, “Contrast-Enhanced Magnetic Resonance Imaging in the Assessment of Myocardial Infarction and Viability,” J. Nucl. Cardiol., 15(1), pp. 105–117. [CrossRef] [PubMed]
Takase, B., Kihara, T., Noya, K., Abe, Y., Nagata, M., Ohsuzu, F., and Ishihara, M., 2006, “Usefulness of Cardiac Magnetic Resonance Imaging for Detecting Acute Myocardial Infarction in Patients With No Significant Electrocardiogram Changes,” Heart Vessels, 21(2), pp. 131–134. [CrossRef] [PubMed]
Kwong, R. Y., Schussheim, A. E., Rekhraj, S., Aletras, A. H., Geller, N., Davis, J., Christian, T. F., Balaban, R. S., and Arai, A. E., 2003, “Detecting Acute Coronary Syndrome in the Emergency Department With Cardiac Magnetic Resonance Imaging,” Circulation, 107(4), pp. 531–537. [CrossRef] [PubMed]
Veress, A. I., Raymond, G. M., Gullberg, G. T., and Bassingthwaighte, J. B., 2009, “Coupled Modeling of the Left Ventricle and the Systemic Circulatory System,” SIAM NEWS, 42(5).
Veress, A. I., Raymond, G. M., Gullberg, G. T., and Bassingthwaighte, J. B. B., 2013, “Left Ventricular Finite Element Model bounded by a Systemic Circulation Model,” ASME J. Biomech. Eng., 135(5), p. 054502. [CrossRef]
Jaffe, R., Charron, T., Puley, G., Dick, A., and Strauss, B. H., 2008, “Microvascular Obstruction and the No-Reflow Phenomenon After Percutaneous Coronary Intervention,” Circulation, 117(24), pp. 3152–3156. [CrossRef] [PubMed]


Grahic Jump Location
Fig. 3

Thresholding was used to isolate the ischemic/infarcted regions of the myocardium. A midventricular, short axis slice of the 3D perfusion map for the proximal LAD with a 90% occlusion is shown on the left. The ischemic/infarcted region is shown on the right with threshold values of 6% (lower cutoff) and 90% (upper cutoff) of the maximum intesity.

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Fig. 2

The location of the occlusions (top) used to define the perfusion maps in the PCAT. Arrows indicate the location of the vessel occlusions. The resulting bull's eye maps (bottom) showing the extent of the perfusion defects.

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Fig. 4

The locations of the integration points within a hexahedral element

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Fig. 5

A 5 voxel Gaussian blur was applied to the thresholded image (left) to increase the size of the lesions (middle). This image was processed in order to define the BZ (right) which is the region with normal perfusion that borders the infarcted region.

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Fig. 1

Infarct model with simplified infarct region (black) surrounded by a one element thick BZ (white). This type of model was demonstrated in our previous work [2].

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Fig. 6

The ischemic/infarcted regions of the FE models show similar size and shape compared with the renderings of the perfusion maps. The ischemic/infarcted regions are defined as the blue interior regions for the models. The BZ is the continuous region surrounding the infarct. RCA segment 1 has had the RV removed from the rendered images.

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Fig. 7

The comparison of the ischemic and infarcted volumes given in Table 2 shows a slight tendency toward underestimation

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Fig. 8

Positive fiber strain result from the aneurysmic deformations associated with the ischemic (left column) and infarcted (right column) regions (positive fiber strains—elongation) as demonstrated in these midventricular short axis slices. This is in contrast to the deformations of the normal model (right column—top) which shows fiber contraction (negative fiber strains).

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Fig. 9

This demonstrates how the ischemia mechanical model was defined from the PCAT perfusion data. The deformations predicted by this mechanical model were then used to define the LV within the XCAT phantom. This was used to create simulated SPECT images, in this case noise-free, which can reproduce the dyskinetic (aneurysmic) deformations of acute ischemia.

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Fig. 10

Short axis cine reconstructed images corresponding to each perfusion defect. PCAT derived perfusion images (left), 4D XCAT reconstructed using FBP (center) and OS–EM reconstruction.

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Fig. 11

Thresholding was used to isolate the enhanced region of the myocardium. (a) The delayed enhanced MRI image with an anterior defect. (b) A thresholding value of 185 (lower threshold) was used to isolate the enhanced perfusion region. (c) A 3 voxel Gaussian blur was applied to the thresholded image to smooth the boundary of the enhanced region. (d) The image theresholded to isolate the enhanced region.

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Fig. 12

Thresholding was used to isolate the no-reflow zone of the myocardium in this (a) perfusion MRI image. (b) A 5 voxel Gaussian blur was applied to the image. (c) The contrast was enhanced and (d) a thresholding value of 190 was used to isolate the no reflow region. The underlying cause of no reflow is microvascular obstruction, which is confined to the irreversibly damaged necrotic zone of the infarct [54].



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