Spectral and Time-Domain Analyses of Heart-Rate Variability During Head-Upright Tilt-Table Testing in Children with Neurally Mediated Syncope

Abstract

Neurocardiac syncope (NS) is a common cause of syncope in children. The mechanism, though related to abnormalities in autonomic function, has not been fully elucidated, particularly in pediatric patients. This study assessed the heart-rate variability (HRV) response to head-upright tilt-table test (HUT) in children with NS and normal volunteers. Spectral and time-domain analysis of HRV was used to assess changes in autonomic function in 27 children (9 male, mean age 12.3 +/- 1.6 years) with a history of at least one episode of syncope and positive passive HUT and 27 age-matched normal volunteers with negative passive HUT before and during postural tilt and to attempt to relate such changes to specific types of hemodynamic response to tilt. Frequency-domain measurements of the high-(HF) and low-(LF) frequency bands and the ratio LF/HF were derived from Holter recordings and computed by fast Fourier analysis for 5-min intervals. Time-domain measurements of the SDNN, SDNNI, SDANN, RMSSD, and triangular index were derived from 24-h Holter recordings. There were no significant differences between clinical characteristics, time-domain, and basal frequency domain parameters of the groups. Mean values of LF and LF/HF ratio was increased and HF was decreased significantly in response to tilt in both patient and control groups. Mean values of LF and LF/HF ratio were higher and HF was lower compared to controls immediately after tilt. LF and LF/HF ratio showed a statistically significant decrease and a significant increase in HF during syncope in patients. The three subgroups of patients had similar patterns of changes in autonomic activity. The results of this study show that although the basal autonomic function was similar to that of the control group, patients with NS have a different pattern of response to the HUT. In our study, patients with NS demonstrated an exaggerated response to the HUT. This exaggerated response may be the factor that activates the pathological reflexes of NS. The pathological mechanism leading to NS appears to be independent of the specific type of hemodynamic response to HUT.