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1 Institute of Medicine and Pneumology, University of Palermo, and 2 Institute of Biomedicine and Molecular Immunology (IBIM), National Research Council (CNR), Palermo 3 Clinica Medica, Milano-Bicocca University, 4 Cardiology II, S. Luca Hospital, Istituto Auxologico Italiano, 5 Centro di Bioingegneria, Fondazione Don C. Gnocchi, Milan, Italy.
CORRESPONDENCE: M. R. Bonsignore, Institute of Medicine and Pneumology, University of Palermo, Via Trabucco, 180, Palermo, Italy. Fax: 39 0916802165. E-mail: marisa{at}ibim.cnr.it
Keywords: Baroreceptors, blood pressure, hypoxia, positive intrathoracic pressure, sleep
Received: April 13, 2004
Accepted September 28, 2005
Baroreflex control of heart rate during sleep (baroreflex sensitivity; BRS) has been shown to be depressed in obstructive sleep apnoea (OSA), and improved after treatment with continuous positive airway pressure (CPAP). Whether CPAP also acutely affects BRS during sleep in uncomplicated severe OSA is still debatable.
Blood pressure was monitored during nocturnal polysomnography in 18 patients at baseline and during first-time CPAP application. Spontaneous BRS was analysed by the sequence method, and estimated as the mean sequence slope.
CPAP did not acutely affect mean blood pressure or heart rate but decreased cardiovascular variability during sleep. Mean BRS increased slightly during CPAP application (from 6.5±2.4 to 7.5±2.9 ms·mmHg–1), mostly in response to decreasing blood pressure. The change in BRS did not correlate with changes in arterial oxygen saturation or apnoea/hypopnoea index.
The small change in baroreflex control of heart rate during sleep at first application of continuous positive airway pressure in severe obstructive sleep apnoea was unrelated to the acute resolution of nocturnal hypoxaemia, and might reflect autonomic adjustments to positive intrathoracic pressure, and/or improved sleep architecture. The small increase in baroreflex control of heart rate during sleep may be of clinical relevance as it was accompanied by reduced cardiovascular variability, which is acknowledged as an independent cardiovascular risk factor.
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