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J Thorac Cardiovasc Surg 2008;135:1094-1102
© 2008 The American Association for Thoracic Surgery
Surgery for Acquired Cardiovascular Disease |
a Joint Graduate Group in Bioengineering, University of California, San Francisco and Berkeley, Calif
b Department of Surgery, University of California, San Francisco, Calif
c Department of Anesthesia, University of California, San Francisco, Calif
d Department of Radiology, University of California, San Francisco, Calif
e Department of Veterans Affairs Medical Center, San Francisco, Calif
f Department of Biomedical Engineering, Duke University, Durham, NC
Received for publication May 10, 2007; revisions received October 27, 2007; accepted for publication November 15, 2007. * Address for reprints: Julius M. Guccione, PhD, Division of Surgical Services (112D), VA Medical Center, 4150 Clement Street, San Francisco, CA 94121. (Email: GuccioneJ{at}surgery.ucsf.edu).
Objective: Linear repair of left ventricular aneurysm has been performed with mixed clinical results. By using finite element analysis, this study evaluated the effect of this procedure on end-systolic stress.
Methods: Nine sheep underwent myocardial infarction and aneurysm repair with a linear repair (13.4 ± 2.3 weeks postmyocardial infarction). Satisfactory magnetic resonance imaging examinations were obtained in 6 sheep (6.6 ± 0.5 weeks postrepair). Finite element models were constructed from in vivo magnetic resonance imaging-based cardiac geometry and postmortem measurement of myofiber helix angles using diffusion tensor magnetic resonance imaging. Material properties were iteratively determined by comparing the finite element model output with systolic tagged magnetic resonance imaging strain measurements.
Results: At the mid-wall, fiber stress in the border zone decreased by 39% (sham = 32.5 ± 2.5 kPa, repair = 19.7 ± 3.6 kPa, P = .001) to the level of remote regions after repair. In the septum, however, border zone fiber stress remained high (sham = 31.3 ± 5.4 kPa, repair = 23.8 ± 5.8 kPa, P = .29). Cross-fiber stress at the mid-wall decreased by 41% (sham = 13.0 ± 1.5 kPa, repair = 7.7 ± 2.1 kPa, P = .01), but cross-fiber stress in the un-excluded septal infarct was 75% higher in the border zone than remote regions (remote = 5.9 ± 1.9 kPa, border zone = 10.3 ± 3.6 kPa, P < .01). However, end-diastolic fiber and cross-fiber stress were not reduced in the remote myocardium after plication.
Conclusion: With the exception of the retained septal infarct, end-systolic stress is reduced in all areas of the left ventricle after infarct plication. Consequently, we expect the primary positive effect of infarct plication to be in the infarct border zone. However, the amount of stress reduction necessary to halt or reverse nonischemic infarct extension in the infarct border zone and eccentric hypertrophy in the remote myocardium is unknown.
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