A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm

Department of Surgery, University of California, San Francisco, USA.
Journal of Biomechanical Engineering (Impact Factor: 1.78). 11/2009; 131(11):111001. DOI: 10.1115/1.3148464
Source: PubMed


A non-invasive method for estimating regional myocardial contractility in vivo would be of great value in the design and evaluation of new surgical and medical strategies to treat and/or prevent infarction-induced heart failure. As a first step towards developing such a method, an explicit finite element (FE) model-based formal optimization of regional myocardial contractility in a sheep with left ventricular (LV) aneurysm was performed using tagged magnetic resonance (MR) images and cardiac catheterization pressures. From the tagged MR images, 3-dimensional (3D) myocardial strains, LV volumes and geometry for the animal-specific 3D FE model of the LV were calculated, while the LV pressures provided physiological loading conditions. Active material parameters (T(max_B) and T(max_R)) in the non-infarcted myocardium adjacent to the aneurysm (borderzone) and in myocardium remote from the aneurysm were estimated by minimizing the errors between FE model-predicted and measured systolic strains and LV volumes using the successive response surface method for optimization. The significant depression in optimized T(max_B) relative to T(max_R) was confirmed by direct ex vivo force measurements from skinned fiber preparations. The optimized values of T(max_B) and T(max_R) were not overly sensitive to the passive material parameters specified. The computation time of less than 5 hours associated with our proposed method for estimating regional myocardial contractility in vivo makes it a potentially very useful clinical tool.

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Available from: Elaine Tseng, Jul 09, 2014
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    • "More precisely, Shimkunas et al. found that two weeks after induced anteroapical infarction, contractility in the BZ was reduced by 3162% compared to regions remote from the infarct. In our first step toward developing clinical tools for noninvasively estimating regional myocardial contractility in vivo [12], we studied a sheep heart 14 weeks after anteroapical infarction, which is well past the 8–12 weeks required for an aneurysm to fully develop. In that case, there is not enough MRI signal in the 1–3 mm thick LV aneurysm to measure myocardial strain, so we quantified aneurysmal material properties by using ex vivo biaxial mechanical testing. "
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    ABSTRACT: Heart failure is increasing at an alarming rate, making it a worldwide epidemic. As the population ages and life expectancy increases, this trend is not likely to change. Myocardial infarction (MI)-induced adverse left ventricular (LV) remodeling is responsible for nearly 70% of heart failure cases. The adverse remodeling process involves an extension of the border zone (BZ) adjacent to an MI, which is normally perfused but shows myofiber contractile dysfunction. To improve patient-specific modeling of cardiac mechanics, we sought to create a finite element model of the human LV with BZ and MI morphologies integrated directly from delayed enhancement magnetic resonance (DE-MR) images. Instead of separating the LV into discrete regions (e.g. the MI, BZ and remote regions) with each having a homogeneous myocardial material property, we assumed a functional relation between the DE-MR image pixel intensity and myocardial contractility. The finite element model was then comprehensively validated using measurements obtained from the same patient, namely, 3D strain measurements, using complementary spatial modulation of magnetization magnetic resonance (CSPAMM-MR) images. We demonstrate the utility of our method for quantifying smooth regional variations in myocardial contractility using cardiac DE-MR and CSPAMM-MR images acquired from a 78-year-old woman who experienced an MI approximately one year prior. We found a remote myocardial diastolic stiffness of 0.102 kPa, and a remote myocardial contractility of 146.9 kPa, which are both in the range of previously published normal human values. Moreover, we found a BZ extending over 30% of the normalized pixel intensity maps from the DE-MR images, which is consistent with the literature. Based on these regional myocardial material properties, we used our finite element model to compute unmeasurable patient-specific diastolic and systolic LV myofiber stress distributions. One of the main driving forces for adverse LV remodeling is assumed to be an abnormally high level of ventricular wall stress, and many existing and new treatments for heart failure fundamentally attempt to normalize LV wall stress. Thus, our non-invasive method for estimating smooth regional variations in myocardial contractility should be valuable for optimizing new surgical or medical strategies to limit the chronic evolution from infarction to heart failure.
    Full-text · Article · Nov 2014 · Journal of Biomechanical Engineering
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    • "8.2–62.4 [44] In Vivo MVO Tagged MRI 2 (ED, ES) Sheep 0.95 49.3 19.2 17.4 [9] a In Vivo MVO Tagged MRI, pressure wire 2 (MVO, ED) Dog 1.7 14.3 4.5 0.76 [24] In Vivo Zero pressure Tagged MRI, pressure wire 2 Human 0.3 41.7 9.1 51.5 [45] Passive inflation Mid Diastole PV-curves 3 Mouse 1.1 8.0 2.0 3.7 [15] a In vivo Calculated Tagged MRI, pressure wire 4–6 Human 2 19.3 10.7 12.8 Costa law b [46] a In vivo Ellipsoid Implanted markers 2 (ED, ES) Dog 1.8 6.0 3.0–12.0 3.0–7.0 "
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    ABSTRACT: The mouse is an important model for theoretical-experimental cardiac research, and biophysically based whole organ models of the mouse heart are now within reach. However, the passive material properties of mouse myocardium have not been much studied. We present an experimental setup and associated computational pipeline to quantify these stiffness properties. A mouse heart was excised and the left ventricle experimentally inflated from 0 to 1.44 kPa in seven steps, and the resulting deformation was estimated by echocardiography and speckle tracking. An in silico counterpart to this experiment was built using finite element methods and data on ventricular tissue microstructure from diffusion tensor MRI. This model assumed a hyperelastic, transversely isotropic material law to describe the force-deformation relationship, and was simulated for many parameter scenarios, covering the relevant range of parameter space. To identify well-fitting parameter scenarios, we compared experimental and simulated outcomes across the whole range of pressures, based partly on gross phenotypes (volume, elastic energy, and short- and long-axis diameter), and partly on node positions in the geometrical mesh. This identified a narrow region of experimentally compatible values of the material parameters. Estimation turned out to be more precise when based on changes in gross phenotypes, compared to the prevailing practice of using displacements of the material points. We conclude that the presented experimental setup and computational pipeline is a viable method that deserves wider application.
    Full-text · Article · Oct 2014 · Computers in Biology and Medicine
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    • "The material passive stiffness (C) and the tissue contractility (T max ) were chosen so that the predicted LV volumes (without injection) matched the corresponding EDV (197 ml) and ESV (122 ml) measured from the MR images. All other parameters had values equal to those used in large animal studies (Sun et al., 2009) and human study (Wenk et al., 2012). "
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    ABSTRACT: Injection of biomaterials into diseased myocardium has been associated with decreased myofiber stress, restored left ventricular (LV) geometry and improved LV function. However, its exact mechanism(s) of action remained unclear. In this work, we present the first patient-specific computational model of biomaterial injection that accounts for the possibility of residual strain and stress introduced by this treatment. We show that the presence of residual stress can create more heterogeneous regional myofiber stress and strain fields. Our simulation results show that the treatment generates low stress and stretch areas between injection sites, and high stress and stretch areas between the injections and both the endocardium and epicardium. Globally, these local changes are translated into an increase in average myofiber stress and its standard deviation (from 6.9±4.6 to 11.2±48.8kPa and 30±15 to 35.1±50.9kPa at end-diastole and end-systole, respectively). We also show that the myofiber stress field is sensitive to the void-to-size ratio. For a constant void size, the myofiber stress field became less heterogeneous with decreasing injection volume. These results suggest that the residual stress and strain possibly generated by biomaterial injection treatment can have large effects on the regional myocardial stress and strain fields, which may be important in the remodeling process.
    Full-text · Article · Jun 2014 · Journal of Biomechanics
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