The interplay between pulsatility, sympathetic regulation and renal physiology: Implications for left ventricular assist devices

Abstract

Left ventricular assist devices have gained traction both as a bridge therapy and as a destination therapy in the management of heart failure. Many of these devices reinstate blood flow in a continuous manner as opposed to the pulsatile flow present in normal physiology. This loss of pulsatility can alter the arterial baroreflex and sympathetic nervous system as well as modify release of nitric oxide. This review focuses on the relationship between pulsatility and sympathetic nerve activity with an emphasis on how this may alter kidney function. Our findings indicate that, in the clinical context of ventricular dysfunction and mechanical circulatory support, pulsatile flow may lower levels of sympathetic nerve activity and theoretically improve nitric oxide function. While there are inhibitory effects on sympathetic nerve activity during pulsatile flow, the downstream effects on renal function remain inconclusive with the caveat that these studies are often underpowered retrospective observational studies that use indirect measures of renal function. We suggest that future studies need to incorporate more sensitive markers of tubular and glomerular function to establish if pulsatility indeed has positive outcomes on renal function. Based on current data, we speculate that the improvement in cardiac output and redistribution of blood flow within the kidney may override putative beneficial effects of altered pulsatility observed in experimental studies.