Obstructive sleep apnoea (OSA) is associated with high cardiovascular morbidity and mortality. Several randomised controlled trials have shown that continuous positive airway pressure (CPAP) treatment of OSA reduces blood pressure (BP). This randomised, sham-placebo controlled crossover trial assesses whether CPAP produces a similar clinically significant fall in BP in hypertensive OSA patients, but without hypersomnolence.Thirty-five, nonsleepy, hypertensive patients with OSA were treated with CPAP for 1 month, randomised first to either therapeutic or sham-placebo (subtherapeutic CPAP, about 1 cmH 2 O pressure). The second months' alternative treatment followed a 2-week washout period. BP was measured over 24 h, before and at the end of the two treatment periods: mean 24-h BP was the primary outcome variable.There was no overall significant difference in mean 24-h BP: the change in mean 24-h BP on therapeutic CPAP was -2.1 mmHg (SD 8.1), and -1.1 mmHg (SD 8.1) on subtherapeutic CPAP, with a difference of 0.7 mmHg (95% confidence interval (CI) +2.9--4.4). There was a small significant fall in Epworth Sleepiness Score, therapeutic (-1.4) versus sham (-0.3), and difference -1.2 (95% CI -2.0--0.4), but no change in objective sleepiness.In nonhypersomnolent hypertensive patients with obstructive sleep apnoea, there is no significant fall in mean 24-h blood pressure with continuous positive airway pressure, in contrast to the fall seen in hypersomnolent patients with obstructive sleep apnoea.

Sleep fragmentation and respiratory disturbance measures are used in the assessment of obstructive sleep apnea (OSA) but have proved to be disappointingly poor correlates of daytime sleepiness. This study investigates the ability of electroencephalograph (EEG) and non-EEG sleep fragmentation indices to predict both presenting sleepiness and the improvement in sleepiness with subsequent nasal continuous positive airway pressure (nCPAP) therapy (nCPAP responsive sleepiness). Forty-one patients (36 men, 5 women), ranging from nonsnorers to severe OSA (> 4% O2 dip rate, median 11.1, range 0.4 to 76.5), had polysomnography with microarousal scoring, computerized EEG analysis, autonomic arousal detection, and body movement analysis. All patients received a trial of nCPAP regardless of sleep study outcome. Spearman's correlation analysis showed significant and similar associations between all sleep fragmentation indices with both pretreatment and nCPAP responsive sleepiness. There was no deterioration in sleepiness on nCPAP in the nonsnorers. Using stepwise multiple regression analysis, the best predictor of nCPAP responsive subjective and objective sleepiness was body movement index, explaining 38% and 43% of the variance, respectively. Variability in EEG sleep depth, quantified from computerized EEG analysis, was the only other index to contribute to these models. Together these indices explained 44% and 51% of the subjective and objective response to nCPAP, respectively. These results suggest that sleep fragmentation indices are useful for identifying OSA patients with sleepiness likely to respond to nCPAP.