A simple model for myocardial changes in a failing heart |
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| Affiliation: | 1. Department of Aerospace Engineering, University of Michigan, 1320 Beal Ave, Ann Arbor, MI 48109, USA;2. Department of Aerospace Engineering, University of Michigan, Ann Arbor, MI 48109, USA;3. Department of Mechanical Engineering, University of Michigan, Ann Arbor, MI 48109, USA;4. Department of Cardiac Surgery, University of Michigan, 1540 E. Hospital Dr. SPC 4204, Ann Arbor, MI 48109, USA;1. Advanced Product Development Team, R&D Center, Hankook Tire Co., 23-1 Jang-dong, Yuseong-gu, Daejeon 305-725, South Korea;2. The University of Akron, Akron, OH 44325-3909, USA;1. Department of Mechanical Engineering, University of Michigan, Ann Arbor, MI 48109, United States;2. William E Boeing Department of Aeronautics and Astronautics, Seattle, WA 98195-2400, United States;1. Institut de Recherche en Génie Civil et Mécanique (GeM), UMR CNRS 6183, École Centrale de Nantes, France;2. Michelin, Centre Technique de Ladoux, Clermont-Ferrand, France;1. Mechanical Engineering Department, Imperial College London, UK;2. AMME Department, University of Sydney, Australia;1. Centro de Estudios de Matemática para las Ciencias Técnicas (CEMAT), ISPJAE, 11500 La Habana, Cuba;2. Departamento de Matemáticas, Facultad de Matemática y Computación, Universidad de La Habana, 10400 La Habana, Cuba;3. Departamento de Mecánica de los Medios Continuos y T. Estructuras, E.T.S. de Caminos, Canales y Puertos, Universidad Politécnica de Madrid, 28040 Madrid, Spain;4. Center for Advancing Electronics (cfAED), Technische Universität Dresden, 01062 Dresden, Germany |
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| Abstract: | In a simplified setting, a multi-network model for remodeling in the left ventricle (LV) is developed that can mimic various pathologies of the heart. The model is an extension of the simple model introduced by Nardinocchi and Teresi 9], Nardinocchi et al. 10], 11] that results in an algebraic relation for LV pressure–volume–contraction. We considered two networks, the original tissue and a new tissue, each of which has its own volume fraction, stress-free reference configuration, elastic properties, and contractility. This is used to explore the consequences of microstructural changes in the muscle tissue on LV function in terms of the pressure–volume loop during a single cardiac cycle. Special attention is paid to the stroke volume, which is directly related to cardiac output, and changes in LV wall stress caused by various disease states, including wall thinning (dilated cardiomyopathy), wall thickening (hypertrophic cardiomyopathy), contractility degradation, and stiffness changes (scarring). Various scenarios are considered that are of clinical relevance, and the extent and nature of remodeling that could lead to heart failure are identified. |
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| Keywords: | Biomechanics Heart failure Multi-network hyperelasticity |
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