; for the Spanish Sleep Network IMPORTANCE More than 70% of patients with resistant hypertension have obstructive sleep apnea (OSA). However, there is little evidence about the effect of continuous positive airway pressure (CPAP) treatment on blood pressure in patients with resistant hypertension. OBJECTIVE To assess the effect of CPAP treatment on blood pressure values and nocturnal blood pressure patterns in patients with resistant hypertension and OSA. DESIGN, SETTING, AND PARTICIPANTS Open-label, randomized, multicenter clinical trial of parallel groups with blinded end point design conducted in 24 teaching hospitals in Spain involving 194 patients with resistant hypertension and an apnea-hypopnea index (AHI) of 15 or higher. Data were collected from June 2009 to October 2011. INTERVENTIONS CPAP or no therapy while maintaining usual blood pressure control medication. MAIN OUTCOMES AND MEASURES The primary end point was the change in 24-hour mean blood pressure after 12 weeks. Secondary end points included changes in other blood pressure values and changes in nocturnal blood pressure patterns. Both intention-to-treat (ITT) and per-protocol analyses were performed. RESULTS A total of 194 patients were randomly assigned to receive CPAP (n = 98) or no CPAP (control; n = 96). The mean AHI was 40.4 (SD, 18.9) and an average of 3.8 antihypertensive drugs were taken per patient. Baseline 24-hour mean blood pressure was 103.4 mm Hg; systolic blood pressure (SBP), 144.2 mm Hg; and diastolic blood pressure (DBP), 83 mm Hg. At baseline, 25.8% of patients displayed a dipper pattern (a decrease of at least 10% in the average nighttime blood pressure compared with the average daytime blood pressure). The percentage of patients using CPAP for 4 or more hours per day was 72.4%. When the changes in blood pressure over the study period were compared between groups by ITT, the CPAP group achieved a greater decrease in 24-hour mean blood pressure (3.1 mm Hg [95% CI, 0.6 to 5.6]; P = .02) and 24-hour DBP (3.2 mm Hg [95% CI, 1.0 to 5.4]; P = .005), but not in 24-hour SBP (3.1 mm Hg [95% CI, −0.6 to 6.7]; P = .10) compared with the control group. Moreover, the percentage of patients displaying a nocturnal blood pressure dipper pattern at the 12-week follow-up was greater in the CPAP group than in the control group (35.9% vs

Increased overnight hypoxia as a surrogate of OSA severity was associated with increased cancer incidence. This association seems to be limited to men and patients younger than 65 years of age.

In nonsleepy hypertensive patients with OSA, CPAP treatment for 1 year is associated with a small decrease in BP. This effect is evident only in patients who use CPAP for more than 5.6 hours per night. Clinical trial registered with www.clinicaltrials.gov (NCT00127348).

The aim of the present study was to assess the impact of nasal continuous positive airway pressure (nCPAP) in ischaemic stroke patients followed for 2 yrs.Stroke patients with an apnoea-hypopnoea index o20 events?h -1 were randomised to early nCPAP (n571; 3-6 days after stroke onset) or conventional treatment (n569). The Barthel Index, Canadian Scale, Rankin Scale and Short Form-36 were measured at baseline, and at 1, 3, 12 and 24 months. The percentage of patients with neurological improvement 1 month after stroke was significantly higher in the nCPAP group (Rankin scale 90.9 versus 56.3% (p,0.01); Canadian scale 88.2 versus 72.7% (p,0.05)). The mean time until the appearance of cardiovascular events was longer in the nCPAP group (14.9 versus 7.9 months; p50.044), although cardiovascular event-free survival after 24 months was similar in both groups. The cardiovascular mortality rate was 0% in the nCPAP group and 4.3% in the control group (p50.161).Early use of nCPAP seems to accelerate neurological recovery and to delay the appearance of cardiovascular events, although an improvement in patients' survival or quality of life was not shown.

Excessive daytime sleepiness (EDS) is not invariably present in patients with obstructive sleep apnoea syndrome (OSAS). The aim of the present study was to investigate polysomnographic determinants of EDS in patients with OSAS.EDS was assessed using the Epworth Sleepiness Scale (ESS) and the multiple sleep latency test (MSLT). Patients showed EDS whenever the ESS score was .10 and the MSLT score ,5 min. Absence of EDS was defined as having an ESS score of ,10 and an MSLT score of .10 min.In total, 23 male patients with EDS (mean¡SD ESS and MSLT score 17¡3 and 4¡1 min, respectively) and 17 without EDS (ESS and MSLT score 5¡2 and 16¡3 min, respectively), were studied. Both groups exhibited a similar apnoea/hypopnoea index (62¡18 versus 60¡20 events?h The mechanisms whereby some patients with OSAS complain of EDS, whereas others do not, are unclear. Some authors have related it to the abnormal sleep structure of these patients (as assessed by the number of arousals during sleep) [2,7,8], but this has not been confirmed by others [9]. Likewise, studies that investigated a potential relationship between EDS and several indices of nocturnal oxygenation also yielded controversial findings [10,11].The aim of the present study was to investigate potential mechanisms of EDS in patients with OSAS. Contrary to previous studies, however, no attempt was made to establish relationships between all of these variables in patients with varying degrees of EDS. Instead, several polysomnographic variables were compared in two groups of patients demonstrating either the absolute absence or clear presence of EDS. It was reasoned that excluding patients with intermediate levels of EDS might help to unravel the nocturnal determinants of EDS in OSAS. METHODS SubjectsConsecutive male patients (n565) who attended the sleep unit of the Respiratory Dept of Son Dureta University Hospital (Palma de Mallorca, Spain) and were found, by full polysomonography, to have an apnoea/hypopnoea index (AHI) of .20 events?h -1 were initially included in the present study. In these subjects, the presence of EDS was diagnosed by considering the results of