Abstract

The pulsatile hemodynamics resulting from the interaction of a left ventricular assist device (LVAD) with a ventricle and an arterial system is quite complex. This complexity compounds with chronic adaptation. To simplify, investigators have focused on characterizing how altered arterial mechanical properties affect pulsatile pressure, or how altered pulsatile pressure affects ventricular mechanical properties. In a radically different approach, we modified a classical model of the arterial circulation to explore adaptation of the vasculature to decreased pulsatility induced by an LVAD. Each artery was assumed to adapt to circumferential wall stress and endothelial shear stress. The model resulted in values of radii, thicknesses, and stiffnesses as well as pulsatile pressures and flows consistent with reported values. Decreasing pulsatility of input flow to simulate LVAD implantation led to an acute decrease in regional pulse pressures. Arterial adaptation subsequently increased arterial stiffness and partially restored pulsatile pressures. These findings suggest that increases in arterial stiffness (and thus cardiac afterload) may negatively impact cardiac recovery and transplantation. More importantly, the current work reveals a new hemostatic principle: vascular adaptation to circumferential wall stress maintains pulsatility.

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