Key result
The addition of a hemodynamic feedback mechanism to a multi-scale model of left ventricular growth restored hemodynamic function to homeostatic levels in 10 out of 12 stable stimuli combinations.
Why the study?
Predicting chronic cardiac growth is clinically relevant, but predictive models lack consensus on the stimulus-effect relation, and previous models showed an unphysiological decline in pump function in response to valve disease.
A computational model incorporating hemodynamic feedback demonstrates that a combination of stress and strain stimuli best predicts physiological cardiac growth and pump function restoration.
Mixed stress-strain stimuli yield stable LV growth restoring pump function in valve disease; leaves open optimal laws for patient-specific FE models.
Cardiac growth is an important mechanism for the human body to respond to changes in blood flow demand. Being able to predict the development of chronic growth is clinically relevant, but so far models to predict growth have not reached consensus on the stimulus-effect relation. In a previously published study, we modeled cardiac and hemodynamic function through a lumped parameter approach. We evaluated cardiac growth in response to valve disease using various stimulus-effect relations and observed an unphysiological decline pump function. Here we extend that model with a model of hemodynamic feedback that maintains mean arterial pressure and cardiac output through adaptation of peripheral resistance and circulatory unstressed volume. With the combined model, we obtain stable growth and restoration of pump function for most growth laws. We conclude that a mixed combination of stress and strain stimuli to drive cardiac growth is most promising since it (1) reproduces clinical observations on cardiac growth well, (2) requires only a small, clinically realistic adaptation of the properties of the circulatory system and (3) is robust in the sense that results were fairly insensitive to the exact choice of the chosen mechanics loading measure. This finding may be used to guide the choice of growth laws in more complex finite element models of cardiac growth, suitable for predicting the response to spatially varying changes in tissue load. Eventually, the current model may form a basis for a tool to predict patient-specific growth in response to spatially homogeneous changes in tissue load, since it is computationally inexpensive.
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Rondanina et al. (2020) studied Valve disease (Aortic stenosis, Aortic regurgitation, Mitral regurgitation). Hemodynamic feedback model vs. Growth-only model (without hemodynamic feedback) was evaluated on Restoration of hemodynamic function (cardiac output and mean arterial pressure). The addition of a hemodynamic feedback mechanism to a multi-scale model of left ventricular growth restored hemodynamic function to homeostatic levels in 10 out of 12 stable stimuli combinations.
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