Changes in autonomic activity preceding onset of nonsustained ventricular tachycardia.
BACKGROUND
The triggering role of the autonomic nervous system in the initiation of ventricular tachycardia has not been established. To investigate the relationship between changes in autonomic activity and the occurrence of nonsustained ventricular tachycardia (NSVT) we examined heart rate variability (HRV) during the 2-hour period preceding spontaneous episodes of NSVT. Twenty-four subjects were identified retrospectively as having had one episode of NSVT during 24-hour Holter ECC recording.


METHODS
We measured the mean interval between normal heats (meanRR), the standard deviation of the intervals between beats (SD), the percentage of counts of sequential intervals between normal beats with a change of >50 ms (%RR50), the logarithms of low- and high-frequency spectral components (lnLF, lnHF) of HRV for sequential 10-minute segments preceding NSVT. The correlation dimension (CDim) of HRV was calculated similarly for sequential 20-minute segments. We assessed the significance of the time-course change of each marker over the 120-minute period prior to NSVT onset.


RESULTS
MeanRR (P < 0.05), lnLF (P < 0.0001), lnHF (P < 0.0001), the natural logarithm of the ratio of LF to HF (ln[LF/HF]; P < 0.05), and CDim (P < 0.05) showed significant time-course changes during that period, while SD and %RR50 did not. MeanRR, lnLF, lnHF, and CDim all decreased prior to the onset of NSVT, whereas ln(LF/HF) increased. We divided the subjects into two groups: one consisting of 12 patients with coronary artery disease; and the second group of 12 patients without known coronary artery disease. Both groups showed significant changes (P < 0.05) of CDim, lnLF, and lnHF preceding the episodes of NSVT.


CONCLUSIONS
Changes in the pattern of HRV prior to the onset of episodes of NSVT suggest that changes in autonomic activity may commonly play a role in the triggering of spontaneous episodes of NSVT in susceptible patients. The measured changes suggest a reduction in parasympathetic activity, perhaps in conjunction with an increase in sympathetic activity, may trigger NSVT.
Osaka
M
M
Harvard-MIT Division of Health Sciences and Technology, Cambridge, Massachusetts, USA.
Saitoh
H
H
Sasabe
N
N
Atarashi
H
H
Katoh
T
T
Hayakawa
H
H
Cohen
R J
RJ
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001341:Autonomic Nervous System / Q000473:pathology / Q000503:physiopathology*; D009202:Cardiomyopathies / Q000209:etiology* / Q000503:physiopathology; D016757:Death, Sudden, Cardiac / Q000209:etiology / Q000473:pathology; D015716:Electrocardiography, Ambulatory; D005260:Female; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012815:Signal Processing, Computer-Assisted; D017180:Tachycardia, Ventricular / Q000209:etiology* / Q000503:physiopathology