4.5 Article

Effects of continuous positive airway pressure treatment on aldosterone excretion in patients with obstructive sleep apnoea and resistant hypertension: a randomized controlled trial

Journal

JOURNAL OF HYPERTENSION
Volume 35, Issue 4, Pages 837-844

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/HJH.0000000000001254

Keywords

continuous positive airway pressure; obstructive sleep apnoea; randomized controlled trial; resistant hypertension; urinary aldosterone excretion

Funding

  1. Conselho Brasileiro de Desenvolvimento Cientifico e Tecnologico (CNPq)
  2. Fundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro (FAPERJ)

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Objective: Aldosterone excess has been equally associated with resistant hypertension (RHT) and obstructive sleep apnoea (OSA). We conducted a randomized controlled study to assess the effect of continuous positive airway pressure (CPAP) treatment on 24-h urinary aldosterone excretion in patients with RHT and moderate/severe OSA. Methods: A total of 117 patients were randomized (57 CPAP and 60 control groups). Aldosterone excretion was determined by 24 h urine (24h-UAldo) collected at randomization and after 6 months of follow-up. Twentyfour hour UAldo differences were assessed by general linear model with the allocation group (CPAP or control) as a fixed factor adjusted for their respective baseline values. Both intention-to-treat and per-protocol (45 patients with optimal adherence to CPAP) analyses were performed. Results: Baseline 24h-UAldo was higher in severe OSA than in moderate OSA patients. After CPAP treatment, there was a borderline significant reduction in 24h-UAldo [mean difference: -2.5mg/24 h; 95% confidence interval (95% CI): -5.3 to +0.3 mu g/24 h; P = 0.07] in intention-totreat analysis, whereas in the per-protocol analysis, the CPAP group had a greater reduction in 24h-UAldo than the control group (mean difference: -3.3 mu g/24 h; 95% CI: -6.1 to -0.4 mu g/24 h; P = 0.027). This effect occurred solely in patients with uncontrolled ambulatory BPs, and was more pronounced in those with the nondipping pattern, not using spironolactone, less obese, and with lowest sleep SaO(2) levels. Conclusion: Only optimal CPAP treatment reduced aldosterone excretion in patients with uncontrolled RHT, while on intention-to-treat the effect was borderline. Although nondefinitive, our results suggest that CPAP treatment might improve cardiovascular outcomes by reducing aldosterone excess in resistant hypertensive individuals with OSA.

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