Autonomic nervous system activity and the spontaneous initiation of ventricular tachycardi

Objectives. We hypothesized that neurohormonal activity contributes to the initiation of sustained ventricular tachycardi (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 ultr 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 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.