Abstract
Cardiac growth is the natural capability of the heart to change size in response to changes in blood flow demand of the growing body. Cardiac diseases can trigger the same process leading to an abnormal type of growth. Prediction of cardiac growth would be clinically valuable, but so far published models on cardiac growth differ with respect to the stimulus-effect relation and constraints used for maximum growth. In this study, we use a zero-dimensional, multiscale model of the left ventricle to evaluate cardiac growth in response to three valve diseases, aortic and mitral regurgitation along with aortic stenosis. We investigate how different combinations of stress- and strain-based stimuli affect growth in terms of cavity volume and wall volume and hemodynamic performance. All of our simulations are able to reach a converged state without any growth constraint, with the most promising results obtained while considering at least one stress-based stimulus. With this study, we demonstrate how a simple model of left ventricular mechanics can be used to have a first evaluation on a designed growth law.
Highlights
Cardiac growth is a natural process through which the heart adapts to deal with a change in blood flow demand of the body, which can be related either to changes in physical exercise (Rawlins et al 2009) or cardiovascular diseases
The aim of this study is to evaluate the capability of several combinations of growth stimuli, based on myocardial tissue stress and strain, to reproduce a clinically realistic and stable changes of left ventricular (LV) geometry, i.e., 1 3 Vol.:(0123456789)
The aim of this study is to evaluate the capability of several combinations of growth stimuli to reproduce a clinically
Summary
Cardiac growth is a natural process through which the heart adapts to deal with a change in blood flow demand of the body, which can be related either to changes in physical exercise (Rawlins et al 2009) or cardiovascular diseases. It has been demonstrated how pressure overload promotes thickening of the cardiac wall, defined as concentric type of growth, while volume overload generates a dilated heart with a thinning of the wall, defined as eccentric growth (Cantor et al 2005). We find both unconstrained growth laws (Bovendeerd et al 2006; Kroon et al 2009; Taber 1998) and constrained laws, the latter being motivated from experimental observations on myocyte properties (Göktepe et al 2010; Kerckhoffs et al 2012; Rausch et al 2011) as well as availability of nutrients (Bellomo et al 2012).
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