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

Abstract

Aims 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. Methods and results 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. Conclusion Implantation of current design LVAD does not consistently normalize sympathetic activity in patients with end‐stage heart failure despite haemodynamic improvement.

Baroreflex activation therapy with the Barostim™ device in patients with heart failure with reduced ejection fraction: a patient level meta‐analysis of randomized controlled trials

“… 23 , 24 , 25 , 26 This differential therapeutic effect between patients with lower NT‐proBNP versus higher NT‐proBNP, or more advanced HF, has been observed in other studies, and more recently in left ventricular assist devices. 24 , 25 , 26 , 27 , 28 , 29 Thus, the differential therapeutic effect observed may be due to the patients with higher NT‐proBNP having more advanced structural heart disease, as higher levels of natriuretic peptides correlate with greater left ventricular mass, worse left ventricular diastolic dysfunction and higher pulmonary pressure, as well as higher prevalence of comorbidities such as renal dysfunction and AF, and that they may, therefore, be less likely to respond to therapeutic interventions.…”

Vascular dysfunction in HFpEF: Potential role in the development, maintenance, and progression of the disease

“…Then, a bidirectional and maladaptive relationship between endothelial function and hyperactivity of the SNS could play a role in short- and long-term vascular dysfunction in HFpEF. Indeed, autonomic imbalance in HFpEF increases sympathetic vasomotor tone ( 6 ). The latter results in increased excitatory sympathetic activity to blood vessels changing the balance between vasodilator and vasoconstrictor molecules that regulate endothelial cell function and therefore, cardiovascular integrity ( 7 ).…”