Cardiovascular autonomic control in patients undergoing left ventricular assist device (LVAD) support and pharmacologic therapy

Abstract

Objectives: The objective of the study is to determine cardiac autonomic control in patients undergoing assessment for and/or LVAD therapy. Methods: Heart rate variability (HRV) was measured in 17 explanted LVAD, 17 implanted LVAD and 23 NYHA III-IV classified chronic heart failure (CHF) patients and ten healthy matched controls under three conditions: supine free breathing, standing and supine controlled breathing. Five measures of HRV were assessed: mean R-R interval (mR-R), high frequency (HF) and low frequency (LF) spectral power, LF in normalised units (LFnu), and LF to HF (LF:HF) ratio. Results: Repeat measures ANOVA showed significant (p b 0.05) differences in HRV between all three conditions within groups. Lower values were observed in CHF for LF(in log natural units) compared with explanted patients (− 1.4 [95% CI − 2.6 to − 0.7], p = 0.04) and controls (− 2.1 [− 3.5 to −0.7], p = 0.001) and for LF: HF compared with implanted patients under paced breathing conditions (z = − 2.7, p = 0.007) and controls in standing (z = − 2.9, p = 0.004) and paced breathing conditions (z = −2.3, p = 0.02). However, no significant differences were seen between explanted, implanted and control groups under any condition. Conclusions: Patients implanted with an LVAD and explanted from a LVAD following myocardial recovery demonstrate a more normal dynamic response to autonomic stimuli and have a lower HRV risk profile compared to CHF patients.

Orthostatic Hypotension in Patients With Left Ventricular Assist Devices: Acquired Autonomic Dysfunction

“…The dysregulation of the autonomic tone with an abnormal sympathetic tone follows (6,7) and results in loss of compensatory mechanisms with positional changes (6,8). Restoration of pulsatility or device explantation reverses the measured baroreceptor dysfunction (9,10). Autonomic dysregulation and elevated baseline heart rate likely explain the lack of compensatory heart rate elevation through a similar pathophysiology (11).…”