The Influence of Sacubitril/Neprilysin Inhibition on Ventricular Assist Device Haemodynamics - A Case Report

Introduction Standard guideline-directed neurohumoral blocking therapy is often continued or initiated after left ventricular assist device (LVAD) implantation once haemodynamics are stabilised. Angiotensin/neprilysin inhibitors (ARNI) are well integrated into international guidelines, but the role of these agents in LVAD patients is unclear. In LVAD patients with high afterload sensitivity, small preload changes can lead to suboptimal LV filling and intermittent suction-mediated inflow cannula obstruction. Case Report We investigated the haemodynamic influence of ARNI on LVAD flow, as a surrogate marker of possible suction events, using the accessible logfile data from an in-vivo HeartWare(HW) device, which captures instantaneous power and derived flow every 15-minutes. We extracted the logfile data of a patient who, after stabilisation on ARNI therapy following LVAD implantation, ultimately ceased due to labile arterial pressures. Using the patient as their own control we calculated 1) the mean flow using a running average, 2) the pulsatility index (PI) from minimum/maximum flows, and 3) potential suction events (defined as outlier flow events two standard deviations from the mean). Mean flow was similar off (3.86±0.5l L/min) compared to on (3.78±0.7L/min) ARNI therapy. The PI was numerically higher on therapy (2.1±0.2 L/min) compared to no therapy (1.7±0.3 L/min). There were numerically many more outlier flow events with ARNI therapy (78) compared to no therapy (9), which may correlate with suction events, and suggests haemodynamic instability on therapy. Summary Whilst a few small studies have demonstrated general tolerability of ARNIs in LVAD patients, potent venodilatory and anti-hypertensive effects can cause unfavourable haemodynamics. We show evidence of increased haemodynamic instability evident from controller logfiles possibly due to a disproportionate reduction in preload relative to afterload with increased uncoupling of ventricular to arterial elastance.