This controlled trial assessed the effect of continuous positive airway pressure (CPAP) on blood pressure (BP) in patients with obstructive sleep apnea (OSA) and resistant hypertension (RH). We evaluated 96 patients with resistant hypertension, defined as clinic BP at least 140/90 mmHg despite treatment with at least three drugs at adequate doses, including a diuretic. Patients underwent a polysomnography and a 24-h ambulatory BP monitoring (ABPM). They were classified as consulting room or ABPM-confirmed resistant hypertension, according to 24-h BP lower or higher than 125/80 mmHg. Patients with an apnea-hypopnea index at least 15 events/h (n = 75) were randomized to receive either CPAP added to conventional treatment (n = 38) or conventional medical treatment alone (n = 37). ABPM was repeated at 3 months. The main outcome was the change in systolic and diastolic BP. Sixty-four patients completed the follow-up. Patients with ABPM-confirmed resistant hypertension treated with CPAP (n = 20), unlike those treated with conventional treatment (n = 21), showed a decrease in 24-h diastolic BP (-4.9 ± 6.4 vs. 0.1 ± 7.3 mmHg, P = 0.027). Patients who used CPAP > 5.8 h showed a greater reduction in daytime diastolic BP {-6.12 mmHg [confidence interval (CI) -1.45; -10.82], P = 0.004}, 24-h diastolic BP (-6.98 mmHg [CI -1.86; -12.1], P = 0.009) and 24-h systolic BP (-9.71 mmHg [CI -0.20; -19.22], P = 0.046). The number of patients with a dipping pattern significantly increased in the CPAP group (51.7% vs. 24.1%, P = 0.008). In patients with resistant hypertension and OSA, CPAP treatment for 3 months achieves reductions in 24-h BP. This effect is seen in patients with ABPM-confirmed resistant hypertension who use CPAP more than 5.8 h.

Obstructive sleep apnea syndrome (OSAS) is a process that is associated with the development of arterial hypertension, the main risk factor for aortic dissection and during obstructive episodes of the upper airways with marked increases in transmural pressure of the aorta wall. The aim of this work was to study the association between aortic dissection and OSAS. Nineteen consecutive patients with thoracic aorta dissection and 19 hypertensive patients of similar age, sex, and body mass index were studied by clinical questionnaire and polysomnography. Snoring and nonrefreshing sleep were common in both groups. Thirteen patients (68%) from each group showed an apnea–hypopnea index of more than 5 per hour. However, patients with aortic dissection presented a higher apnea–hypopnea index (28 [30.3] versus 11.1 [10.4], p = 0.032). Seven patients with dissection presented an apnea–hypopnea index of more than 30 versus 1 patient in the control group (p = 0.042). Patients with thoracic aorta dissection presented a high prevalence of previously undiagnosed and frequently severe OSAS. Further studies, including this diagnosis as a prognostic variable in the follow-up of patients with aortic dissection, are required. Our results suggest that in patients with aortic dissection and symptoms consistent with OSAS, a sleep study should be considered in their clinical management.

The high prevalence of obstructive sleep apnea in patients with resistant hypertension could be mediated by an activation of the renin-angiotensin-aldosterone system. This study assessed the impact of continuous positive airway pressure (CPAP) treatment on plasma aldosterone concentration (PAC). One hundred and twenty-four patients with resistant hypertension were assessed, and those who fulfilled inclusion criteria (n = 116) underwent full night polysomnography, 24-h ambulatory blood pressure monitoring, and PAC measurement. Patients with an apnea-hypopnea index above 15 (n = 102) were randomized to CPAP (n = 50) or to conventional treatment (n = 52) for 3 months. Seventy-eight patients completed the follow-up (36 CPAP, 42 conventional treatment); 58 had true resistant hypertension (74.3%), whereas 20 had white-coat resistant hypertension (25.6%). Most patients were men (70.7%), age 58.3 ± 9.4 years, and the mean apnea-hypopnea index was 50.1 ± 21.6. In patients with true resistant hypertension, CPAP achieved a significant decrease in most 24-h BP measurements and a nonsignificant decrease in PAC (25 ± 8.7 vs. 22.7 ± 9 ng/dl; P < 0.182). In patients with white-coat resistant hypertension, CPAP achieved a significant decrease in PAC (26.1 ± 11.2 vs. 18.9 ± 10.1 ng/dl; P < 0.041) and in night-time DBP. After adjustment, a weak but significant association was found between cumulative time spent with SaO2 below 90% (CT90%) and baseline PAC (P < 0.047, R 0.019), and between changes in PAC and changes in office DBP (P < 0.020, R 0.083) CONCLUSIONS:: Night-time hypoxemia and changes in DBP showed an association with baseline and changes in PAC, respectively. CPAP achieved a significant reduction in PAC only in patients with white-coat resistant hypertension, although the CPAP effect on BP was highest in patients with true resistant hypertension.