S C Malpas1, G L Purdie. 1. Department of Medicine, Wellington School of Medicine, New Zealand.
Abstract
STUDY OBJECTIVE: The aim of the study was to examine the circadian variation in heart rate variability and to test the hypothesis that the variation is due to vagal influence. DESIGN: Human subjects, some with vagal neuropathy, underwent ambulatory 24 h electrocardiographic monitoring, the recordings being played back through an analyser which identified and timed successive pulse (R-R) intervals. Heart rate variability was measured for each 30 min period over 24 h as the standard deviation of the successive differences between R-R intervals, which filtered out low frequency components of heart rate variability that were not autonomic in origin. Modelled curves of heart rate variability were compared using analysis of variance. SUBJECTS: The subjects were aged between 33 and 65 years and were matched in three groups for age and sex. There were 11 healthy controls, 12 insulin dependent diabetics and seven alcoholics with vagal neuropathy. RESULTS: A significant circadian variation in heart rate variability was present, characterised by a rise during sleep. Mean heart rate variation was significantly reduced in groups with vagal neuropathy, although the amplitude of the cycle and time of peak variability was not significantly different. The circadian variation was sustained regardless of the degree of vagal neuropathy. CONCLUSIONS: The cycle of heart rate variability is not dependent on vagal interaction. It may be due to fluctuations in sympathetic activity affecting beat to beat variability.
STUDY OBJECTIVE: The aim of the study was to examine the circadian variation in heart rate variability and to test the hypothesis that the variation is due to vagal influence. DESIGN:Human subjects, some with vagal neuropathy, underwent ambulatory 24 h electrocardiographic monitoring, the recordings being played back through an analyser which identified and timed successive pulse (R-R) intervals. Heart rate variability was measured for each 30 min period over 24 h as the standard deviation of the successive differences between R-R intervals, which filtered out low frequency components of heart rate variability that were not autonomic in origin. Modelled curves of heart rate variability were compared using analysis of variance. SUBJECTS: The subjects were aged between 33 and 65 years and were matched in three groups for age and sex. There were 11 healthy controls, 12 insulin dependent diabetics and seven alcoholics with vagal neuropathy. RESULTS: A significant circadian variation in heart rate variability was present, characterised by a rise during sleep. Mean heart rate variation was significantly reduced in groups with vagal neuropathy, although the amplitude of the cycle and time of peak variability was not significantly different. The circadian variation was sustained regardless of the degree of vagal neuropathy. CONCLUSIONS: The cycle of heart rate variability is not dependent on vagal interaction. It may be due to fluctuations in sympathetic activity affecting beat to beat variability.
Authors: Xian Li; Michele L Shaffer; Sol M Rodríguez-Colón; Fan He; Edward O Bixler; Alexandros N Vgontzas; Deborah L Wolbrette; Chuntao Wu; Richard W Ball; Duanping Liao Journal: Auton Neurosci Date: 2011-03-27 Impact factor: 3.145