Published online before print November 27, 2006, doi: 10.1161/CIRCULATIONAHA.106.657270
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(Circulation. 2006;114:2627-2635.)
© 2006 American Heart Association, Inc.
Heart Failure |
Theoretical Impact of the Injection of Material Into the Myocardium
A Finite Element Model Simulation
From the University of California at Berkeley/San Francisco, Joint Graduate Group in Bioengineering (S.T.W., J.C.W., K.E.H., M.B.R., J.M.G.); Departments of Material Science and Engineering (K.E.H.) and Bioengineering (K.E.H.), University of California at Berkeley; Department of Surgery, University of California at San Francisco (M.B.R., J.M.G.); and Veterans Affairs Medical Center, San Francisco, Calif (M.B.R., J.M.G.).
Correspondence to Julius M. Guccione, PhD, SFVAMC M/C 112D, 4150 Clement St, San Francisco, CA 94121. E-mail Julius.Guccione{at}med.va.gov
Received August 8, 2006; revision received September 27, 2006; accepted October 5, 2006.
Background— To treat cardiac injuries created by myocardial infarcts, current approaches seek to add cells and/or synthetic extracellular matrices to the damaged ventricle to restore function. Because definitive myocardial regeneration remains undemonstrated, we propose that cardiac changes observed from implanted materials may result from altered mechanisms of the ventricle.
Methods and Results— We exploited a validated finite element model of an ovine left ventricle with an anteroapical infarct to examine the short-term effect of injecting material to the left ventricular wall. The model’s mesh and regional material properties were modified to simulate expected changes. Three sets of simulations were run: (1) single injection to the anterior border zone; (2) therapeutic multiple border zone injections; and (3) injection of material to the infarct region. Results indicate that additions to the border zone decrease end-systolic fiber stress proportionally to the fractional volume added, with stiffer materials improving this attenuation. As a potential therapy, small changes in wall volume (
4.5%) reduce elevated border zone fiber stresses from mean end-systole levels of 28.2 kPa (control) to 23.3 kPa (treatment), similar to levels of 22.5 kPA computed in remote regions. In the infarct, injection improves ejection fraction and the stroke volume/end-diastolic volume relationship but has no effect on the stroke volume/end-diastolic pressure relationship.
Conclusions— Simulations indicate that the addition of noncontractile material to a damaged left ventricular wall has important effects on cardiac mechanics, with potentially beneficial reduction of elevated myofiber stresses, as well as confounding changes to clinical left ventricular metrics.
CLINICAL PERSPECTIVE
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