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): 00.0033 Hz; very low FP (VLFP): 0.00330.04 Hz; low FP (LFP): 0.040.15 Hz; high FP (HFP): 0.150.4 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.
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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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