Remodeling of cardiomyocytes in vitro (INVITED)

Abstract eng:
A feature of hypertrophy in heart disease is remodeling of cardiomyocytes. In hypertension, the heart wall tends to thicken as sarcomeres are added within cardiomyocytes in parallel, so that the heart can pump more effectively against high blood pressure. In volume overload, where the heart is called on to pump more blood, the heart tends to enlarge by adding sarcomeres within cardiomyocytes in series. This observation is duplicated in vitro in similar conditions imposed on excised animal myocardium. A model is presented for this response. Chemical kinetics accounts for the addition and subtraction of sarcomeres, while a contractile force is generated by an actomyosin simulator whose output also influences the chemical potentials driving remodeling. Results are presented for cyclic straining of myocardium subject to displacement boundary conditions to simulate volume overload, and force boundary conditions to simulate pressure overload. The results are consistent with the observation of remodeling in vitro.

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