Abstract

Abstract Background Short sleep duration and poor sleep quality has been reported to be associated with increased cardiovascular risk and increased incidence of cardiovascular events. Purpose Whether and what extent the pathophysiology of this association includes sympathetic abnormalities has never been examined via microneurography. Methods In 28 untreated mild-to moderate essential hypertensives aged 66.4±3.1 (mean±SEM) without other cardiovascular or non-cardiovascular disease (including obstructive sleep apnea) recruited from the outpatient clinic and referred for short sleep duration, we directly assessed at patients home via actigraphy (actiwatch spectrum activity monitor, Phillips) time sleep duration and efficiency. Measurements, performed during a day preceding or following the 7 day actigraphy evaluation, included microneurographic recording of efferent postganglionic sympathetic nerve traffic (MSNA), venous plasma norepinephrine (HPLC), clinic, 24 hour and beat to beat blood pressure and heart rate values. Sleep diary and a sleep questionnaire were also administered. Results Nine patients slept less than 6 hours per night (LSD), while the remaining ones between 6 to 7 (MSD, n=8) or more than 7 hours (GSD,N=11). The 3 groups showed similar age and gender distribution and a body mass index amounting to 28.1±0.8, 28.6±0.5 and 27.3±0.5 kg/m2 (P=NS). For similar mean blood pressure values LSD showed MSNA values significantly greater than GSD (53.4±4.9 vs 40.1±3.8bs/100hb, P<0.03), this being the case also for MSD (49.7±4.4, P<0.05 vs GSD but not SLD). HR was significantly elevated only in LSD group when compared to GSD, while no significant difference was found in plasma NE between the 3 groups. Conclusions The present study provides the first microneurographic direct evidence that short sleep duration is linked to a marked sympathetic activation, which may participate at the high cardiovascular risk of these subjects. The sympathetic overdrive affects both the cardiac and peripheral district but is not reflected by NE, which thus does not represent in this condition a valuable adrenergic marker.

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