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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