A large number of heart failure patients face sleep-disordered breathing, which seriously affects sleep quality. Repeated hypoxia during sleep can excite sympathetic nerves and damage vascular endothelial function, further aggravating the degree of heart failure. During the ESC 2022 conference, Professor Thomas Douglas Bradley from the University of Toronto, Canada shared the results of the ADVENT-HF study and discussed the treatment of heart failure with sleep apnea. This issue specially invited him to give a detailed introduction to related issues.
International Circulation: Sleep-disordered breathing is closely related to heart failure. What are its incidence and risk factors?
Professor Thomas Douglas Bradley: The incidence of obstructive and central sleep apnea is approximately 40%~50% in patients with heart failure. Of those, about 60% are obstructive, and about 40% are central. So it is very common.
There are different risk factors for the different types. For obstructive sleep apnea (OSA), obesity is very important. Older age group is very important. And predominantly seen in men. In terms of central sleep apnea (CSA), it is seen in older patients mainly with ischemic cardiomyopathy who have lower ejection fractions and higher left ventricular filling pressures. In both cases, fluid retention also contributes to it. Heart failure is a disease of fluid retention, and when you lie down at night, the fluid from your legs moves up to your chest and into your neck. Depending upon where it ends up, if it is mainly in your neck, it will aggravate obstructive sleep apnea; if is mainly in your lungs, it will aggravate central sleep apnea. So those are the main risk factors.
International Circulation: What are the characteristics of objective sleep characteristics in patients with heart failure with different ejection fractions?
Professor Thomas Douglas Bradley: We have only studied people with low ejection fractions, so-called HFrEF (heart failure with reduced ejection fraction), so I can’t really say very much about those with normal ejection fraction. For the reduced ones, we know that even if you don’t have sleep apnea, if you have heart failure, you sleep one hour less than the otherwise healthy population. So patients with heart failure sleep less, only 5-6 hours per night, rather than 6 or 7. Because they have sleep apnea, their sleep is very disrupted, because they have to wake up in order to breath. If they have 500 episodes of apnea, they have to wake up 500 times. As a consequence, they generally don’t have much deep slow-wave sleep, or very little rapid eye movement sleep. Their sleep is fragmented and poor quality and short.
International Circulation: At this conference, you shared a study on the treatment of heart failure with sleep apnea. Would you please share the main findings?
Professor Thomas Douglas Bradley: The main result was that in the 731 patients treated, those randomized to get the ASV (adaptive servo ventilation) device, which is triggered by peak respiratory flow, had no significant difference in the composite endpoint of all-cause mortality, cardiovascular hospitalizations, new onset atrial fibrillation, and ICD discharges. There was no significant difference. If we divided them into those with predominantly OSA and CSA, there was no significant difference between those groups either. In terms of overall mortality, there was no significant difference in the overall group and in the OSA group. In the group with central sleep apnea, there was a trend toward lower mortality in those treated with the peak flow ASV device, however, the difference wasn’t significant. The risk reduction was about 22%, but the p value was 0.34, so it was not significant.
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