Abstract

Creation of an arteriovenous fistula (AVF) for hemodialysis may result in cardiac failure due to dramatic increases in cardiac output. To investigate the quantitative relations between AVF flow, changes in cardiac output, myocardial stress and strain and resulting left ventricular adaptation, a computational model is developed. The model combines a one-dimensional pulse wave propagation model of the arterial network with a zero-dimensional one-fiber model of cardiac mechanics and includes adaptation rules to capture the effect of the baro-reflex and long-term structural remodelling of the left ventricle. Using generic vascular and cardiac parameters based on literature, simulations are done that illustrate the model's ability to quantitatively reproduce the clinically observed increase in brachial flow and cardiac output as well as occurence of eccentric hypertrophy. Patient-specific clinical data is needed to investigate the value of the computational model for personalized predictions.

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