Cardiac autonomic function in older adults with sleep-disordered breathing.

We searched for possible associations between various measures of severity of sleep-disordered breathing (SDB) and indices of cardiac autonomic function in older subjects (>60 years). Twenty four overnight unattended home-based polysomnograms obtained from the Sleep Heart Health Study were analyzed using spectral analysis. For each subject, six autonomic indices reflecting heart rate variability were quantitatively determined during wakefulness, REM sleep and non-REM sleep. Each individual autonomic marker was regressed against each of 4 measures of SDB, including the respiratory disturbance index (RDI), respiratory oscillation index, cumulative oxygen desaturation, and arousal index. In general, we found no correlation between any of these measures of SDB severity and each of the autonomic indices. However, mean heart rate was found to decrease as RDI increased. As well, the ratio of low-frequency to high-frequency power (LHR) decreased with increasing RDI. Contrary to previous reports, our preliminary findings suggest that sympathetic activity decreases with increasing severity of SDB. This paradoxical association between SDB and cardiac autonomic function may be the result of natural compensatory mechanisms at work, allowing some subjects with SDB to be protected from systemic hypertension or other cardiovascular diseases.

Elucidating nonlinear baroreflex and respiratory contributions to heart rate variability in obstructive sleep apnea syndrome.

Using a Volterra-Wiener model and the Laguerre expansion technique, we estimated in a previous study the parameters that characterize linear and the second order effects of respiration ("RSA") and arterial blood pressure ("ABR") on heart rate. RSA and ABR gains were significantly lower in Obstructive Sleep Apnea (OSA) patients than in normal subjects. During sleep, ABR gain increased in normals but remained unchanged in OSA. In the present work, we investigated the physiological interpretation of the nonlinear components of the described model of heart rate variability, by means of simulation on the computed linear and nonlinear kernels. Our results indicate that the 2ndorder kernels reflect specific characteristics of the RSA and ABR mechanisms, such as a RSA frequency response dependence upon tidal volume, saturation in the ABR-Blood Pressure relation, and respiratory modulation of ABR.

Closed-loop minimal model analysis of the cardiovascular response to transient arousal from sleep in healthy humans.

In a previous work we reported discrepancies in the cardiovascular response to arousal from NREM sleep between OSAS patients and healthy controls. The long lasting cardiac sympathetic increase observed in normals was not present in the OSAS group, whereas the peripheral vasculature reaction was similar between the two groups. Analysis of REM arousal revealed that there was a similar temporary cardiac sympathetic impairment in the control group. In this work we have implemented a model-based time domain system identification method to assess the mechanisms involved in this reaction to arousal from both NREM and REM sleep in a group of healthy subjects. The use of time-varying techniques has enabled us to characterize the arousal reaction by analyzing the change in shape of the impulse responses of the system. The mechanisms regulating respiration and vascular effects on heart rate (respiratory sinus arrhythmia or RSA and arterial baroreflex or ABR, respectively) were the most affected by NREM arousal, likely as a result of the return of the wakefulness stimulus. The effect observed on the cardiac influence on the vasculature (circulatory dynamics, CID) was attributed to a change in the dominant mechanism prevailing in its dynamics.