Abstract 15992: Nonpulsatile Flow Among Patients With Continuous-Flow Left Ventricular Assist Devices Leads to Greater Levels of Sympathetic Neural Activity Through Unloading of Arterial Baroreceptors
Background: Patients with continuous-flow (CF) left ventricular assist devices (LVADs) have elevated sympathetic neural activity (SNA). We hypothesized that this hyperadrenergic environment is related to unloading of arterial baroreceptors resulting from reduced pulsatility. The purpose of this study was to quantify differences in carotid arterial (CA) distortion and wall tension at the level of the arterial baroreceptors in patients with CF-LVADs and healthy controls and determine how these variables influence muscle (M)SNA burst frequency (bursts/min).
Methods: Eleven CF-LVAD subjects and nine healthy controls underwent measurements of CA diameter using high-resolution ultrasonography and MSNA by microneurography during head-up tilt (HUT) at supine, 30o and 60o.
Results: CF-LVAD patients had higher mean arterial pressure (MAP) at the level of the CA, higher MSNA and a lower pulse pressure than healthy controls during HUT (P<0.05 at all positions). Pulsatile diameter of the CA (defined as diametersystole - diameterdiastole) was greater in healthy controls than CF-LVADs (P<0.05), however, static wall tension (defined as the product of MAP and mean carotid radius) was greater in CF-LVADs than healthy controls (P<0.05). Among healthy controls, MSNA was inversely correlated with pulsatile diameter (r = -0.42, P<0.05) and static wall tension (r = -0.68, P<0.05); however, among CF-LVADs, MSNA was inversely correlated with static wall tension (r =-0.53, P<0.05) but not pulsatile diameter (figure).
Conclusions: In the absence of a meaningful pulse, the sympathetic neural response to HUT among patients with CF-LVADs is related to changes in static wall tension of the CA. These data suggest that incorporation of pulsatile flow through automated modulations in pump speed in next-generation LVADs might reduce some of the risks associated with CF-LVADs (e.g. uncontrolled blood pressure) through enhanced baroreceptor distortion.
Author Disclosures: W.K. Cornwell: None. T. Tarumi: None. V. Aengevaeren: None. C. Ayers: None. P. Divanji: None. Q. Fu: None. D. Palmer: None. M. Drazner: None. D. Meyer: None. B. Bethea: None. J. Hastings: None. N. Fujimoto: None. S. Shibata: None. R. Zhang: None. D.W. Markham: Research Grant; Significant; Thoratec. B.D. Levine: None.
- © 2014 by American Heart Association, Inc.