Is there a familial association between obstructive sleep apnoea/hypopnoea and the sudden infant death syndrome?

Background: One postulated cause of the sudden infant death syndrome (SIDS) is upper airway obstruction during sleep. Several studies have suggested that SIDS may be more common in families with obstructive sleep apnoea/hypopnoea syndrome (OSAHS), but were limited by uncertainty as to whether the deaths were due to SIDS. We have tested the hypothesis that parents of true SIDS cases have an increased frequency of apnoeas and hypopnoeas during sleep. Methods: The parents of 269 rigorously determined SIDS cases were invited for single night polysomnography and daytime ventilatory control measurement. Results: Parents of 198 cases were identified but 152 did not respond or declined. Fifty five parents of 34 cases were studied and matched for age, height, and weight to 55 subjects from general practice registers. There was no difference in breathing during sleep between the parents of SIDS cases (median (IQR) 5.9 (3.2, 10.7) apnoeas+hypopnoeas/h) and controls (6.7 (4.0, 12.2) apnoeas+hypopnoeas/h; p = 0.47), but the SIDS parents had lower minimum nocturnal oxygen saturation (median (IQR) 92 (89, 93)%) than controls (92 (90, 94)%; p = 0.048). There were no major differences in control of breathing when awake between SIDS parents and controls. Conclusions: These results provide no evidence to support an association between SIDS and OSAHS. However, the minor impairment of oxygenation during sleep in SIDS parents requires further study

Auto-titrating continuous positive airway pressure therapy in patients with chronic heart failure and obstructive sleep apnoea: a randomized placebo-controlled trial

Aims Obstructive sleep apnoea (OSA) is highly prevalent in patients with chronic heart failure (CHF) and may contribute to CHF progression. We aimed to determine whether treatment of OSA with continuous positive airway pressure (CPAP) would improve subjective and objective measures of heart failure severity in patients with CHF and OSA. Methods and results Twenty-six patients with stable symptomatic CHF and OSA were randomized to nocturnal auto-titrating CPAP or sham CPAP for 6 weeks each in crossover design. Study co-primary endpoints were changes in peak VO2 and 6 min walk distance. Secondary endpoints were changes in left ventricular ejection fraction, VE/VCO2 slope, plasma neurohormonal markers, and quality-of-life measures. Twenty-three patients completed the study protocol. Mean CPAP and sham CPAP usage were 3.5 ± 2.5 and 3.3 ± 2.2 h/night, respectively (P = 0.31). CPAP treatment was associated with improvements in daytime sleepiness (Epworth Sleepiness Score 7 ± 4 vs. 8 ± 5, P = 0.04) but not in other quality-of-life measures. There were no changes in other study endpoints. Conclusion In patients with CHF and OSA, auto-titrating CPAP improves daytime sleepiness but not other subjective or objective measures of CHF severity. These data suggest that the potential therapeutic benefits of CPAP in CHF are achieved by alleviation of OSA rather than by improvement in cardiac function