Nocturnal oxygen therapy prevents progress of congestive heart failure with central sleep apnea

Abstract Background Sleep disordered breathing has been reported to be associated with congestive heart failure (CHF). Nocturnal oxygen has been shown to abolish apnea. The aim of this study is to examine whether nocturnal oxygen reduces sympathetic nerve activity, and prevents progress of CHF. Methods 93 patients with left ventricular ejection fractions< 60%, were examined with overnight saturation monitoring for an oxygen desaturation index. Subjects with oxygen desaturation of 4% ≥ 4/h were examined with polysomnography. Apnea–hypopnea index (AHI) was calculated as the total number of episodes of apnea and hypopnea per hour of sleep. We started nocturnal oxygen for the patients with AHI ≥ 20. Urinary and plasma catecholamines concentrations, serum brain natriuretic peptide, human atrial natriuretic peptide, and endothelial nitric oxide synthase levels were measured before and after starting oxygen. Results Compared among the three groups, CHF with central sleep apnea (CHF-CSA) group had significantly higher 24-h urinary adrenaline (CHF-CSA: 4.411 ± 2.940 μmol/day, CHF with obstructive sleep apnea (CHF-OSA): 2.686 ± 1.084 μmol/day, CHF without apnea (CHF-N): 3.178 ± 1.778 μmol/day, P < 0.05). Oxygen therapy significantly decreased AHI and 4 serum BNP levels (from 91.75 ± 80.35 pg/ml to 52.75 ± 45.70 pg/ml, mean change = 33.85 pg/ml, P = 0.0208). Serum eNOS levels were lower in CHF-CSA group and CHF-OSA group than in CHF-N group (CHF-CSA: 15.89 ± 10.75 pg/ml, CHF-OSA: 7.46 ± 3.91 pg/ml, CHF-N: 27.33 ± 14.83 pg/ml, P < 0.05). Conclusions Nocturnal oxygen may prevent progress of CHF with central sleep apnea.