TY - JOUR
T1 - Restoration of pulsatile flow reduces sympathetic nerve activity among individuals with continuous-flow left ventricular assist devices
AU - Cornwell, William K.
AU - Tarumi Ph.D., Takashi
AU - Stickford, Abigail
AU - Lawley, Justin
AU - Roberts, Monique
AU - Parker, Rosemary
AU - Fitzsimmons, Catherine
AU - Kibe, Julius
AU - Ayers, Colby
AU - Markham, David
AU - Drazner, Mark H
AU - Fu, Qi
AU - Levine, Benjamin D
PY - 2015
Y1 - 2015
N2 - Background-Current-generation left ventricular assist devices provide circulatory support that is minimally or entirely nonpulsatile and are associated with marked increases in muscle sympathetic nerve activity (MSNA), likely through a baroreceptor-mediated pathway. We sought to determine whether the restoration of pulsatile flow through modulations in pump speed would reduce MSNA through the arterial baroreceptor reflex. Methods and Results-Ten men and 3 women (54±14 years) with Heartmate II continuous-flow left ventricular assist devices underwent hemodynamic and sympathetic neural assessment. Beat-to-beat blood pressure, carotid ultrasonography at the level of the arterial baroreceptors, and MSNA via microneurography were continuously recorded to determine steady-state responses to step changes (200-400 revolutions per minute) in continuous-flow left ventricular assist device pump speed from a maximum of 10 480±315 revolutions per minute to a minimum of 8500±380 revolutions per minute. Reductions in pump speed led to increases in pulse pressure (high versus low speed: 17±7 versus 26±12 mm Hg; P0.01), distension of the carotid artery, and carotid arterial wall tension (P0.05 for all measures). In addition, MSNA was reduced (high versus low speed: 41±15 versus 33±16 bursts per minute; P0.01) despite a reduction in mean arterial pressure and was inversely related to pulse pressure (P=0.037). Conclusions-Among subjects with continuous-flow left ventricular assist devices, the restoration of pulsatile flow through modulations in pump speed leads to increased distortion of the arterial baroreceptors with a subsequent decline in MSNA. Additional study is needed to determine whether reduction of MSNA in this setting leads to improved outcomes.
AB - Background-Current-generation left ventricular assist devices provide circulatory support that is minimally or entirely nonpulsatile and are associated with marked increases in muscle sympathetic nerve activity (MSNA), likely through a baroreceptor-mediated pathway. We sought to determine whether the restoration of pulsatile flow through modulations in pump speed would reduce MSNA through the arterial baroreceptor reflex. Methods and Results-Ten men and 3 women (54±14 years) with Heartmate II continuous-flow left ventricular assist devices underwent hemodynamic and sympathetic neural assessment. Beat-to-beat blood pressure, carotid ultrasonography at the level of the arterial baroreceptors, and MSNA via microneurography were continuously recorded to determine steady-state responses to step changes (200-400 revolutions per minute) in continuous-flow left ventricular assist device pump speed from a maximum of 10 480±315 revolutions per minute to a minimum of 8500±380 revolutions per minute. Reductions in pump speed led to increases in pulse pressure (high versus low speed: 17±7 versus 26±12 mm Hg; P0.01), distension of the carotid artery, and carotid arterial wall tension (P0.05 for all measures). In addition, MSNA was reduced (high versus low speed: 41±15 versus 33±16 bursts per minute; P0.01) despite a reduction in mean arterial pressure and was inversely related to pulse pressure (P=0.037). Conclusions-Among subjects with continuous-flow left ventricular assist devices, the restoration of pulsatile flow through modulations in pump speed leads to increased distortion of the arterial baroreceptors with a subsequent decline in MSNA. Additional study is needed to determine whether reduction of MSNA in this setting leads to improved outcomes.
KW - blood pressure
KW - heart failure
KW - pressoreceptors
KW - sympathetic nervous system
KW - ventricular assist device
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U2 - 10.1161/CIRCULATIONAHA.115.017647
DO - 10.1161/CIRCULATIONAHA.115.017647
M3 - Article
C2 - 26510698
AN - SCOPUS:84952630110
SN - 0009-7322
VL - 132
SP - 2316
EP - 2322
JO - Circulation
JF - Circulation
IS - 24
ER -