18014
Heart Rate Variability during Sleep in Children with Autism Spectrum Disorders

Friday, May 16, 2014
Atrium Ballroom (Marriott Marquis Atlanta)
R. Harder1, A. Diedrich2, F. Baudenbacher2, A. Halbower3, L. Goodpaster2, S. E. Goldman4, D. B. Fawkes2, L. Wang2, Y. Shi2 and B. A. Malow4, (1)Electrical Engineering / BME, Vanderbilt University, Nashville, TN, (2)Vanderbilt University, Nashville, TN, (3)Children's Hospital Colorado Pulmonary Medicine, Aurora, CO, (4)Vanderbilt Kennedy Center, Vanderbilt University Medical Center, Nashville, TN
Background:

Studies have implicated autonomic nervous system dysfunction in autism spectrum disorders (ASD), including alterations in heart rate at baseline. Alterations in autonomic activity during sleep in children with ASD have received less attention, despite an evolving literature on the importance of sleep for restoring homeostatic function.

Objectives:

The objective is to study heart rate and heart rate variability during sleep in children with ASD.

Methods:

We studied 24 children with ASD, with age of 7.7±1.9 years (mean ± standard deviation, SD) and 23 typically developing medication-free children (TD med-free) with age 8.0±1.9 years, who underwent overnight polysomnography including heart rate monitoring in the Vanderbilt or Colorado Clinical Research Centers.

Automatic R-R peak detection in electrocardiogram with manual verification was performed. Heart rate (HR) and heart rate variability (HRV) was computed for each sleep stage (W, N2, N3, and REM) in the first sleep cycle. HRV spectral components were calculated for low frequency (LF), high frequency (HF), and the LF/HF ratio based on common standards (TASK FORCE 1997). Multivariate statistical tests were performed with adjustment for age. Significance was set at p = 0.05.

Results:

HR decreases with onset of sleep, with minimum heart rate during N2 sleep, and increases during REM sleep in TD as well in ASD. Children with ASD had a similar heart rate dynamic during sleep but with a significant offset of higher heart rates through all sleep stages (median HR in bpm with 25th-75thpercentile ASD vs. TD for W: 85.05 (79.07-89.58) vs. 86.77 (83.58-94.95), N2: 70.16 (66.89-77.47) vs. 76.19(71.10-87.50) p<0.05, N3: 72.19 (69.85-81.10) vs. 78.93-(73.78-88.13) p<0.05, REM: 74.46(70.41-83.70) vs. 80.91(76.04-87.29) p<0.05).

 Absolute LF power of HRV decreases during N3 and increases during REM. Children with ASD had a lower increase and lower power during REM (median LF in msec2 with 25th-75thpercentile ASD vs. TD for W: 696.44(462.10-1269.49) vs. 806.00 (389.15-1327.63), N2: 742.23(472.00-1154.58), N3: 377.36 (212.95-732.901) vs 314.11(154.06-856.07), REM: 643.94 (437.51-918.24) vs. 894.50 (574.80-2130.664) p<0.05). No significant differences could be detected for HF, and LF/HF ratio.

LF and HF power increases with age in TD and ASD for wake. For REM, ASD showed a tendency of lower increase of LF and no change in HF with increasing age. 

 

Conclusions:

Children with ASD showed higher heart rates during sleep and wakefulness. Analysis of HRV showed an abolished increase of LF during REM sleep, which could indicate a possible lack of sympathetic activation during restorative REM sleep in children with ASD. Age dependent changes in HRV during REM sleep are abolished for LF or not present for HF in ASD. This could indicate that the sympathetic and vagal branch of the autonomic system is affected during aging in ASD. Therefore, parameters of HRV during REM sleep are a potential biomarker of developmental trajectory and may be used to detect early signs and progression of ASD.