Understanding the effects of myofibroblasts on the electrical and mechanical functions of the heart is important to understanding the long-term consequences of cardiac fibrosis and myocardial infarction, but the effects are difficult to quantify. Cardiac fibroblasts convert from their quiescent state to the larger and contractile myofibroblasts phenotype under conditions of hypertension and following myocardial infarction. The excess fibrous connective tissue produced by myofibroblasts stiffens heart muscle and the presence of the MFs disrupts the normal pattern of electrical excitation of the cardiomyoctyes. In a model tissue system we have developed in our laboratories (engineered heart tissues, EHTs), overgrowth of myofibroblasts leads to an increase in average (tonic) contractile stress and, eventually, a shut-down of periodic or twitch contractile stress. To understand how myofibroblast/cardiomyoctye interactions relate to conduction and contraction changes in EHTs, a series of coupled mechanical and electrophysiological simulations and experiments were performed.

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