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J Am Coll Cardiol, 1998; 32:1891-1899
© 1998 by the American College of Cardiology Foundation
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CLINICAL STUDIES

Autonomic nervous system activity and the spontaneous initiation of ventricular tachycardia

Vladimir Shusterman, MD, PhDa, Benhur Aysin, MSa, Venkateshwar Gottipaty, MD, PhDa, Raul Weiss, MDa, Susan Brode, MDa, David Schwartzman, MDa, Kelley P. Anderson, MD, FACCa for the ESVEM Investigators*

a Cardiac Electrophysiology Program, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

Manuscript received January 27, 1998; revised manuscript received July 30, 1998, accepted August 6, 1998.

Address for correspondence: Kelley P. Anderson, MD, Cardiac Electrophysiology Program, University of Pittsburgh, Presbyterian University Hospital Room B535, Pittsburgh, Pennsylvania 15213-2582
anders{at}ep1.bwing.upmc.edu

Objectives. We hypothesized that neurohormonal activity contributes to the initiation of sustained ventricular tachycardia (VT) as reflected in indices of heart rate variability (HRV).

Background. Autonomic nervous system activity participates in experimental arrhythmias but clinical studies have been inconsistent.

Methods. Holter electrocardiograms from 53 patients with VT were analyzed. Heart rate variability indices were determined over 5 and 15 min and 24 h and examined for changes before the onset of VT. Heart rate variability indices in the frequency domain included ultra low frequency power (FP) (ULFP): 0–0.0033 Hz; very low FP (VLFP): 0.0033–0.04 Hz; low FP (LFP): 0.04–0.15 Hz; high FP (HFP): 0.15–0.4 Hz; total power (TP); normalized LFP (LFPn); normalized HFP (HFPn), and the ratio: LFP/HFP.

Results. Heart rate variability indices were severely diminished: TP: 12,009 ± 11,076 ms2; ULFP: 10,087 ± 9,565 ms2; VLFP: 1,416 ± 1,571 ms2; LFP: 544 ± 620 ms2; HFP: 161 ± 176 ms2, and LFP/HFP: 3.68 ± 2.83. Heart rate increased before VT (80.4 ± 17.3 to 85.3 ± 17.4 bpm, p < 0.001). Several HRV variables declined 30 min before VT compared to 24-h values (VLFP: –5.89 ± 17.81%, p = 0.031; LFP: –5.23 ± 14.3%, p = 0.003; HFP: –4.35 ± 13.7%, p = 0.04). LFPn and the LFP/HFP ratio decreased significantly before the onset of VT (–17.7 ± 46.9%, p = 0.035 and –8.24 ± 38.8%, p = 0.037, respectively), whereas HFPn increased slightly (4.29 ± 29.9%, p = 0.097).

Conclusions. Heart rate rose, whereas LFP, LFPn and LFP/HFP fell before the onset of VT. This pattern of changes could be explained by a rise in sympathetic activity and saturation of the HRV signal resulting in dissociation of the average and rhythmical effects of sympathetic activity. These findings suggest that alterations in autonomic activity contributed to arrhythmogenesis in this group of patients.

Abbreviations and Acronyms
  ANOVA = analysis of variance
  ESVEM = Electrophysiologic Study Versus Electrocardiographic Monitoring
  HFP = high frequency power
  HFPn = normalized high frequency power
  HR = heart rate
  HRV = heart rate variability
  LFP = low frequency power
  LFPn = normalized low frequency power
  pNN50 = percentage of differences between adjacent normal RR intervals that are >50 ms
  r-MSSD = square root of the mean of the squared differences between adjacent normal RR intervals
  SDANN = standard deviation index of the average normal RR-intervals for all 5-minute segments
  SDANN index = SD of the average normal RR intervals for all 5 minute segments
  SDNN = standard deviation (SD) of normal RR-intervals in the entire 24-hour ECG recording
  SDNN index = mean of the SDs of normal RR-intervals for all 5-minute segments
  TP = total power
  ULFP = ultra low frequency power
  VLFP = very low frequency power
  VT = Sustained monomorphic ventricular tachycardia




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