Sympathetic vasoconstrictor activity before and after left ventricular assist device implantation in patients with end-stage heart failure.

Abstract

Sympathetic overactivity, which predicts poor outcome in patients with heart failure, normalizes following cardiac transplantation. We tested the hypothesis that haemodynamic improvement following left ventricular assist device (LVAD) implantation is also associated with reductions in centrally generated sympathetic activity. In eight patients with heart failure (two women, six men, age 44-66 years), we continuously recorded electrocardiogram, beat-to-beat finger blood pressure, respiration, and muscle sympathetic nerve activity (MSNA) before and after implantation of the continuous-flow LVAD devices HeartWare HVAD (n= 4) and HeartMate II (n= 2), and the non-continuous-flow device HeartMate 3 (n= 2). LVAD implantation increased cardiac output by 1.29 ± 0.88 L/min (P= 0.060) and mean arterial pressure by 16.2± 7.9 mmHg (P< 0.001), while reducing pulse pressure by 25.3± 9.8 mmHg (P< 0.001). LVAD implantation did not change MSNA burst frequency (-1.3± 7.5 bursts/min, P= 0.636), total activity (+0.62 ± 1.83 au, P= 0.369), or normalized activity (+0.63 ± 4.23, P= 0.685). MSNA burst incidence was decreased (-7.8± 9.3 bursts/100 heart beats, P= 0.049). However, cardiac ectopy altered MSNA bursting patterns that could be mistaken for sympatholysis. Implantation of current design LVAD does not consistently normalize sympathetic activity in patients with end-stage heart failure despite haemodynamic improvement.