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, R2 0.019), and between changes in PAC and changes in office DBP (P < 0.020, R2 0.083)
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.