V. Shusterman et al., Autonomic nervous system activity and the spontaneous initiation of ventricular tachycardia, J AM COL C, 32(7), 1998, pp. 1891-1899
Citations number
67
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Objectives. We hypothesized that neurohormonal activity contributes to the
initiation of sustained ventricular tachycardia (VT) as reflected in indice
s 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 a
nd examined for changes before the onset of VT. Heart rate variability indi
ces in the frequency domain included ultra low frequency power (PP) (ULFP):
0-0.0033 Hz; very low FP (VLFP): 0.0033-0.01 Hz; low PP (LFP): 0.04-0.15 H
z; high FP (HFP): 0.15-0.4 Hz; total power (TP); normalized LFP (LFPn); nor
malized HFP (HFPn), and the ratio: LFP/HFP.
Results. Heart rate variability indices were severely diminished: TP: 12,00
9 +/- 11,076 ms(2); ULFP: 10,087 +/- 9,565 ms(2); VLFP: 1,416 +/- 1,571 ms(
2); LFP: 544 +/- 620 ms(2); HFP: 161 +/- 176 ms(2), and dLFP/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: -435 +/- 13.7%, p = 0.04). LFPn and the LFP/HFP ratio decreased sign
ificantly 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 (1.29 +/-
29.9%, p = 0.097).
Conclusions. Heart rate rose, whereas LFP, LFPn and LFP/ HFP fell before th
e onset of VT. This pattern of changes could be explained by a rise in symp
athetic activity and saturation of the HRV signal resulting in dissociation
of the average and rhythmical effects of sympathetic activity. These findi
ngs suggest that alterations in autonomic activity contributed to arrhythmo
genesis in this group of patients. (J Am Coll Cardiol 1998;32:1891-9) (C) 1
998 by the American College of Cardiology.