title: The effects of rate and irregularity on sympathetic nerve activity in human subjects.
abstract: BACKGROUND
  We have recently shown that atrial fibrillation is associated with an increase in sympathetic nerve activity (SNA) compared with sinus rhythm. It remains unclear, however, whether these findings are true at various rates and whether the magnitude of sympathoexcitation is related to the degree of irregularity.
  
  
  OBJECTIVE
  To determine the role of irregularity in mediating the SNA changes at various pacing rates. Univariate analysis showed that as the irregularity increased, SBP increased (r = 0.44, P < .001) but that MAP and DBP did not change significantly.
  
  
  METHODS
  Using custom-made software, atrioventricular sequential pacing with predetermined rates (100, 120, and 140 bpm) and irregularities (standard deviation = 0%, 5%, 15%, and 25% of mean cycle length) was performed in 23 patients referred for electrophysiologic evaluation. Pacing at each rate/irregularity was performed for 2 minutes, with 2 minutes of recovery in between. Systolic, diastolic, and mean arterial blood pressure (SBP, DBP, and MAP), central venous pressure (CVP), and SNA were measured at baseline and during pacing.
  
  
  RESULTS
  Univariate analysis showed that as the irregularity increased, SBP increased (r = 0.44, P < .001 but that MAP and DBP did not change significantly. A significant correlation was found between the pacing irregularity and SNA, with greater sympathoexcitation noted at greater degrees of irregularity (r = 0.2, P = .04). A five-variable linear model using DBP, MAP, CVP, and degree of pacing irregularity to predict SNA was highly statistically significant (r = 0.46, P < .001). After controlling for hemodynamic changes, for every 1% increase in irregularity, there was a 6.1% increase in SNA.
  
  
  CONCLUSIONS
  We have shown that greater degrees of irregularity cause greater sympathoexcitation and that the effects of irregular pacing on SNA are independent of the hemodynamic changes.
authors.affiliation: University of Utah, Salt Lake City, Utah, USA.
authors.forename: Nathan M
authors.initials: NM
authors.lastname: Segerson
authors.forename: Niraj
authors.initials: N
authors.lastname: Sharma
authors.forename: Michael L
authors.initials: ML
authors.lastname: Smith
authors.forename: Stephen L
authors.initials: SL
authors.lastname: Wasmund
authors.forename: Robert C
authors.initials: RC
authors.lastname: Kowal
authors.forename: Moeen
authors.initials: M
authors.lastname: Abedin
authors.forename: John F
authors.initials: JF
authors.lastname: Macgregor
authors.forename: Rakesh K
authors.initials: RK
authors.lastname: Pai
authors.forename: Roger A
authors.initials: RA
authors.lastname: Freedman
authors.forename: Richard C
authors.initials: RC
authors.lastname: Klein
authors.forename: T Scott
authors.initials: TS
authors.lastname: Wall
authors.forename: Gregory
authors.initials: G
authors.lastname: Stoddard
authors.forename: Mohamed H
authors.initials: MH
authors.lastname: Hamdan
mesh_terms: D001281:Atrial Fibrillation / Q000503:physiopathology*; D001794:Blood Pressure; D002304:Cardiac Pacing, Artificial; D002496:Central Venous Pressure / Q000502:physiology; D005260:Female; D006339:Heart Rate / Q000502:physiology*; D006352:Heart Ventricles / Q000294:innervation / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D013564:Sympathetic Nervous System / Q000503:physiopathology*