FIG. 15:  In a randomized trial of OSA treatment in patients with heart failure, treatment would be aimed at the usual goals to improve symptoms of daytime sleepiness, morning headaches, severe fatigue, etc.  This Figure shows results from an epidemiologic study in patients referred to the Heart Failure Clinic of Mount Sinai Hospital in Toronto versus patients enrolled in the prospective Wisconsin Sleep Cohort Study, who served as a control group.^[7]  The groups were stratified into groups with no sleep apnea (apnea/hypopnea index [AHI] <5), mild sleep apnea (AHI 5–15), or moderate-to-severe apnea (AHI ³15). 

As shown, at any level of sleep apnea the group with heart failure had a significantly lower Epworth sleepiness score (ESS).  No matter how severe the sleep apnea, the average patient with heart failure generally does not complain of being sleepy.  This represents a significant paradox, because although these patients with heart failure have less sleepiness, they sleep less.  From the lower part of the Figure, it is clear that the heart failure patients in this study had an average of 1.5 hours less sleep, at any level of sleep apnea, than the group without sleep apnea.  That indicates that patients with heart failure do not have the typical symptoms of sleep apnea, despite the fact that they are sleeping far less. 

The reason for this seems to be excessive sympathetic nervous system activity, which counteracts the soporific effects of sleep fragmentation.  The upper graph shows that the ESS in patients with heart failure is inversely proportional to sympathetic nerve burst frequency.  The reason for this is probably that sympathetic activity is also an alerting signal as part of the “fight or flight” response.  If the sympathetic nervous system is activated all the time, the person tends to be alert; that is our hypothesis.