Abstract

Introduction Narcolepsy with hypocretin deficiency is known to alter cardiovascular control during sleep. The underlying etiology has been disputed. To discriminate the effects of sleep architecture on cardiovascular autonomic control from the consequences of hypocretin-deficiency per se, the present study examined heart rate modulations while taking into account the effects of sleep state duration, and sleep state transitions. Materials and methods One-night ambulatory polysomnography was recorded from 12 hypocretin-deficient narcolepsy patients with cataplexy (11 male, 16–53 years) and 12 healthy controls (11 male, 19–55 years). Heart rate and its variability were calculated per 30-s epoch. Heart rate variability was computed through fast Fourier transforms. Respiratory frequency was derived from a thoracic respiratory band. Results Heart rate was continuously elevated in narcolepsy patients compared to controls. This effect was found in sleep stage 1 (Mean ± SEM, controls vs. patients: 54.3 ± 2.2 vs. 60.4 ± 3.1 ), sleep stage 2 ( 51.0 ± 2.1 vs. 57.8 ± 3.0 ), slow wave sleep ( 52.1 ± 2.3 vs. 59.5 ± 3.2 ), and rapid eye movement (REM) sleep ( 53.5 ± 2.1 vs. 61.5 ± 3.0 ). No substantial changes in sympathovagal balance were found between patients and controls, even if differences in respiration frequency were taken into account. Heart rate alterations after sleep state onset and during transitions from non-REM to REM sleep were comparable between cases and controls. However, patients showed a blunted heart rate augmentation in response to transitions from NREM to wake. Conclusion Heart rate was continuously elevated in patients, and was not only explained by sleep fragmentation. This indicates that autonomic changes are may also be attributable to a direct effect of hypocretin-deficiency. Acknowledgements We would like to thank Noortje van der Kleij – Corssmit, Hanno Pijl and Nienke Biermasz for their contribution to the data collection.

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