Abstract
Most patients with resistant hypertension (RH) have obstructive sleep apnea (OSA). We aimed to determine the impact of OSA and continuous positive airway pressure (CPAP) treatment on the leptin profile and blood pressure (BP) in patients with RH. After an initial case-control study (RH with and without OSA), we performed a randomized, single blind study in OSA + RH patients receiving either sham CPAP (3 months) followed by active CPAP (6 months) or 6 months of active CPAP. The primary outcome was the comparison of leptin levels between groups of RH patients with or without OSA. Secondary outcomes were the comparison of metabolic parameters, biomarkers of sympathetic activity, and BP indices between the two groups of RH patients with or without OSA. The same outcomes were then evaluated and compared before and after sham and effective CPAP intervention. Sixty-two patients (60 ± 10 years; 77% men) with RH (24-h daytime systolic BP (SBP)/diastolic BP: 145 ± 13/85 ± 10 mmHg, 3.7 antihypertensive drugs) were included. The 37 RH patients exhibiting OSA (60%) were predominantly men (87 vs 64% for non-OSA patients), with a greater prevalence of metabolic syndrome and higher creatininemia. Their leptin concentrations were significantly lower than in non-OSA patients [9 (6; 15) vs 17 (6; 29) ng/mL] but increased after 6 months of CPAP. Three months of effective CPAP significantly decreased night-time SBP by 6.4 mmHg and heart rate (HR) by 6.0 bpm, compared to sham CPAP. The association between OSA and RH corresponds to a specific, predominately male phenotype with a higher burden of metabolic syndrome and higher creatininemia but there was no significant difference between OSA and non-OSA patients regarding BP indices, and the number of antihypertensive drugs used. Active CPAP could be efficient at decreasing night-time BP and HR, but there was no difference between CPAP and sham CPAP groups for all metabolic and SNS markers (NCT00746902 RHOOSAS).
Highlights
Obstructive sleep apnea (OSA) syndrome is characterized by recurrent episodes of upper airway obstruction during sleep, causing intermittent hypoxia (IH) and impaired sleep continuity and quality [1]
The protocol was approved by an independent Ethics Committee (Comité de Protection des Personnes, Grenoble, France, IRB0006705) and registered on the ClinicalTrials.gov site (NCT00746902 RHOOSAS)
We found counter-intuitive lower leptin concentrations in obstructive sleep apnea (OSA) patients with Resistant hypertension (RH), that were inversely correlated with office DBP and MABP
Summary
Obstructive sleep apnea (OSA) syndrome is characterized by recurrent episodes of upper airway obstruction during sleep, causing intermittent hypoxia (IH) and impaired sleep continuity and quality [1]. OSA is recognized as an important and independent risk factor for hypertension [2], coronary heart disease [3], and stroke [4]. OSA is one of the most common causes of RH [7] and OSA patients exhibit a fivefold higher risk of suffering from RH than the general population [8]. In RH the adipokine leptin is associated with lack of BP control primarily mediated by leptin sympathoexitatory effects and renin–angiotensin–aldosterone activation [9, 10] that are seen in sleep apnea. It has been shown that uncontrolled RH patients have higher leptin and lower adiponectin levels suggesting that abnormal adipokine serum levels contribute to the difficulty in controlling BP in RH [11,12,13]
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