Background: Patients with obstructive sleep apnea (OSA) are characterized by deranged cardiovascular variability, a well-established marker of cardiovascular risk. While long-term treatment with continuous positive airway pressure leads to a significant improvement of cardiovascular variability, little is known of the possibility of achieving the same results with other therapeutic approaches. The aim of our study was to investigate the responses of autonomic indexes of neural cardiac control to another type of OSA treatment based on an oral jawpositioning appliance. Methods: In 10 otherwise healthy subjects with OSA (OSA؉) and in 10 subjects without OSA (OSA؊) we measured heart rate, BP, and indices of autonomic cardiac regulation derived from time-domain and spectral analysis of R-R interval (RRI), before and after 3 months of treatment with the oral device. High-frequency (HF) power of RRI was taken as an index of parasympathetic cardiac modulation, and the ratio between low-frequency (LF) and HF RRI powers as an indirect marker of the balance between sympathetic and parasympathetic cardiac modulation. Results: At baseline, in comparison with OSA؊ subjects, OSA؉ subjects displayed a significantly lower RRI variance (p < 0.02) and reduced HF RRI powers (p < 0.001). After 3 months of treatment with the oral device, the OSA؉ group showed a marked reduction in apnea-hypopnea index (p < 0.001), a lengthening in RRI and a significant increase in its variance (p < 0,02), an increased HF RRI power (from 134 ؎ 26 to 502 ؎ 48 ms 2 , p < 0.001), and a reduction in LF/HF RRI power ratio (from 3.11 ؎ 0.8 to 1.5 ؎ 0.5). As a result of these changes, after the 3-month treatment there were no more significant differences between the two groups in these parameters. In both OSA؉ and OSA؊ groups, body weight, heart rate, and BP did not change over time. Conclusions: Three months of treatment with a specific oral jaw-positioning appliance improves cardiac autonomic modulation in otherwise healthy patients with OSA of mild degree.

Abstract-Salt-sensitive hypertensive subjects, as defined by conventional categorical classification, exhibit alterations of autonomic cardiovascular control. The aim of our study was to explore whether, in hypertensive subjects, the degree of autonomic dysfunction and the level of salt sensitivity are correlated even when the latter is only mildly elevated and displays under-threshold values. Salt sensitivity of 34 essential hypertensive subjects was assessed on a continuous basis by the salt sensitivity index after low-and high-sodium diet. Beat-by-beat finger blood pressure was recorded after each diet period. Autonomic cardiovascular control was evaluated by spectral analysis of blood pressure and pulse interval and by assessment of spontaneous baroreflex sensitivity (sequence technique). Salt sensitivity and baroreflex sensitivity showed a negative relationship during low and high sodium intake, starting from low values of the salt sensitivity index. All spectral indexes of pulse interval, except the ratio between low-and high-frequency powers, were inversely related to salt sensitivity index after high sodium intake. In subjects with lower salt sensitivity, baroreflex sensitivity and pulse interval power in the high-frequency band were higher after high sodium intake than after low sodium intake. In contrast, subjects with a higher salt sensitivity index showed lower values of baroreflex sensitivity and pulse interval power in the high-frequency band, uninfluenced by salt intake. Our results provide the first demonstration of an impairment of parasympathetic cardiac control in parallel with the increase in the degree of salt sensitivity, also in subjects who were not ranked as salt-sensitive by the conventional categorical classification. Key Words: autonomic nervous system Ⅲ heart rate Ⅲ baroreflex Ⅲ blood pressure Ⅲ sodium, dietary T he higher rate of cardiovascular events occurring in salt-sensitive subjects, either normotensive or hypertensive, has led to the suggestion that a salt sensitivity condition might represent an independent cardiovascular risk factor. 1,2 An enhanced sympathetic cardiovascular drive has been suggested to play a role in determining the increased cardiovascular risk associated with salt sensitivity. In fact, an impaired sympathetic inhibition has been described during high sodium intake in salt-sensitive hypertensive humans, 3 and a deranged reflex cardiovascular control has been proposed as one of the responsible mechanisms. 4,5 Usually, salt sensitivity is considered a categorical parameter, with salt-sensitive individuals being defined as those with a difference in mean arterial pressure (MAP) between low-and high-sodium diet Ͼ10%, and salt-resistant subjects those in whom MAP does not increase or shows an increase Ͻ5% under sodium loading. 6 -8 However, adoption of this categorical approach does not allow exploring whether an impairment of cardiovascular autonomic regulation may occur also in subjects with salt-related blood pressure (BP) changes smaller than those defining...