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Role of Sympathovagal Balance in the Initiation of Idiopathic Ventricular Tachycardia Originating from Right Ventricular Outflow Tract
Authors:HIDEKI HAYASHI  AKIRA FUJIKI  MASANAO TANI  KOICHI MIZUMAKI  MAYUMI SHIMONO  HIROSHI INOUE
Affiliation:Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan
Abstract:
VT originating from the right ventricular outflow tract (RVOT) is prone to occur when sympathetic nervous activity is increased. β-Blockade is, therefore, effective in suppressing this VT. The purpose of this study was to determine the role of sympathovagal balance assessed by heart rate variability (HRV) in the spontaneous initiation of repetitive premature ventricular contractions (PVCs) and VT (five or more consecutive PVCs) arising from RVOT in seven patients without structural heart diseases. Frequency-domain measures of HRV were determined by analyzing 24-hour Holter electrocardiographic recording with the maximum entropy method over α 1,280-second period immediately before the onset of 35 single PVCs, 26 episodes of 2-4 consecutive PVCs, and 21 episodes of VT. High frequency component (HF: 0.15–0.40 Hz) was used as an index of parasympathetic activity, and the ratio of low frequency component (LF: 0.04–0.15 Hz) to HF (LF/HF ratio), as an index of sympathovagal balance. NN50(%), a time-domain variable of parasympathetic activity, was also determined. Mean RR interval and any measures of HRV did not change significantly before single PVCs. Mean RR interval shortened and HF decreased prior to repetitive PVCs and VT. The LF/HF ratio, however, increased only before the onset of VT. NN50(%) tended to decrease before repetitive PVCs and decreased significantly before VT. With propranolol (30–60 mg/day), frequency of repetitive PVCs was suppressed from 2,048 ± 1,201 to 746 ± 658/day and VT was totally abolished, but frequency of single PVCs did not change significantly. In conclusion, sympathetic predominance plays an important role in the initiation of repetitive PVCs and VT originating from RVOT in patients without structural heart diseases.
Keywords:heart rate variability    idiopathic VT    β-blockade
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