Study objectives: Obstructive sleep apnea (OSA) and atrial fibrillation (AF) are highly prevalent conditions sharing multiple risk factors including obesity. Adipokines secreted from adipose tissue could modify pathways affecting atrial remodeling. We evaluated if adipokines are i) elevated in patients with paroxysmal AF and OSA, ii) affected by positive airway pressure (CPAP) or catheter ablation.
Methods: The study comprised 143 patients with paroxysmal AF and moderate to severe OSA (apnea-hypopnea index ≥15), of which 99 participated in a randomized controlled trial and were randomized to CPAP (n = 51) or standard care (n = 48). In addition, healthy controls (HC, n = 22), and patients with AF and no or mild OSA (n = 19) were included. Levels of the adipokines NAMPT, meteorin-like (METRNL), adiponectin, chemerin and resistin were analyzed at baseline, 6- and 12-months follow-up.
Results: Patients with paroxysmal AF and OSA had higher levels of leptin (mean difference [95 % CI], p, eta squared); (1.8 [1.2-2.8] ng/mL, p = 0.005, η2p = 0.055), chemerin (1.3 [1.1-1.5] ng/mL, p < 0.001, η2p = 0.077), and METRNL (1.1 [1.0-1.2] ng/mL, p = 0.044, η2p = 0.044) compared to HC. Accounting for multiple testing leptin and chemerin remained higher in patients. Adipokine levels were not affected by CPAP therapy and were not associated with AF burden, recurrence after catheter ablation or OSA severity.
Conclusions: We observed i) higher levels of leptin, chemerin and METRNL in paroxysmal AF, but were not related to OSA severity or AF activity, ii) Adipokine levels were not modified by CPAP or catheter ablation. The lack of association does not identify these adipokines as prominent targets linking OSA and AF.
Keywords: Adipokines; Adiposity; Continuous positive airway pressure; Obstructive sleep apnea; Paroxysmal atrial fibrillation; Pulmonary ventilation function.
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