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The sleep apnoea/hypopnoea syndrome depresses waking vagal tone independent of sympathetic activation

¹ School of Engineering, University of Warwick, Coventry, UK, Depts of ² Clinical Biochemistry, ³ Cardiology and ⁴ Respiratory Medicine, Birmingham Heartlands Hospital, ⁵ Sleep Disorders Program, Circadian, Neuroendocrine and Sleep Disorders Section, Brigham and Women's Hospital/Harvard Medical School, Boston, MA, USA

CORRESPONDENCE: M. Hilton, Circadian, Neuroendocrine and Sleep Disorders Section, Sleep Disorders Program, Brigham and Women's Hospital, RFB-486, 221 Longwood Avenue, Boston, MA, 02115, USA. Fax: 1 6179750809

Keywords: apnoea, autonomic nervous system, heart, heart rate variability, sympathetic, vagus

Received: February 1, 2000
Accepted March 15, 2001

This work was supported by the Mathematics in Medicine Initiative (MiMl) from the University of Warwick and the British Medical Association, Board of Science and Education, Edith Walsh and Ivy Powell Research Grant Award.

The modest daytime hypertension and sympathetic upregulation associated with the sleep apnoea/hypopnoea syndrome (SAHS), does not explain the relatively large increased risk of cardiac morbidity and mortality in the SAHS patients population. Therefore, efferent vagal and sympathetic activity was evaluated during wakefulness in SAHS subjects and matched healthy controls, in order to determine if vagal downregulation may play a role in the aetiology of cardiac disease in the SAHS.

The awake autonomic nervous system function of 15 male subjects, with mild-to-moderate SAHS was compared to that of 14 healthy controls matched for age, body mass index, gender and blood pressure. All subjects were free from comorbidity. Vagal activity was estimated from measurements of heart rate variability high frequency power (HF) and sympathetic activity was measured from urine catecholamine excretion.

The %HF power was significantly (p<0.03) reduced in SAHS patients (10±1.6 (mean±sem)) as compared to controls (17±3). In addition, HF power correlated with the apnoea/hypopnoea index in the SAHS subjects (R=–0.592, p=0.02). There was no statistically significant difference in the daytime excretion of nonadrenaline between control (242±30 nmol·collection^–1) and SAHS (316±46 nmol·collection^–1) subjects (p=0.38).

In these sleep apnoea/hypopnoea syndrome patients there was limited evidence of increased waking levels of urine catecholamines. The principal component altering waking autonomic nervous system function, in the sleep apnoea/hypopnoea syndrome subjects, was a reduced daytime efferent vagal tone.

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