Luigi Taranto Montemurro1, John S Floras2, Philip J Millar2, Takatoshi Kasai3, Joseph M Gabriel3, Jonas Spaak4, Fernando Morgadinho S Coelho5, T Douglas Bradley6. 1. Sleep Research Laboratory of the Toronto Rehabilitation Institute, Toronto, ON, Canada. Electronic address: taranto.luigi@gmail.com. 2. Department of Medicine of the University Health Network and Mount Sinai Hospital, Toronto, ON, Canada. 3. Sleep Research Laboratory of the Toronto Rehabilitation Institute, Toronto, ON, Canada. 4. Department of Medicine of the University Health Network and Mount Sinai Hospital, Toronto, ON, Canada; Department of Clinical Sciences, Danderyd University Hospital, Karolinska Institutet, Danderyd, Sweden. 5. Department of Medicine, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, ON, Canada. 6. Sleep Research Laboratory of the Toronto Rehabilitation Institute, Toronto, ON, Canada; Department of Medicine of the University Health Network and Mount Sinai Hospital, Toronto, ON, Canada.
Abstract
BACKGROUND: Patients with heart failure (HF) and obstructive sleep apnea (OSA) are less sleepy than patients with OSA but without HF. Furthermore, unlike the non-HF population, in the HF population, the degree of daytime sleepiness is not related to the apnea-hypopnea index (AHI). The sympathetic nervous system plays a critical role in alertness. HF and OSA both increase sympathetic nervous system activity (SNA) during wakefulness. We hypothesized that in patients with HF and OSA, the degree of subjective daytime sleepiness would be inversely related to SNA. METHODS: Daytime muscle SNA (MSNA) was recorded in patients with HF and OSA. Subjective daytime sleepiness was assessed by the Epworth Sleepiness Scale (ESS). RESULTS: We studied 27 patients with HF and OSA and divided them into two groups based on the median ESS score: a less sleepy group, with an ESS score < 6 (n = 13), and a sleepier group, with an ESS score ≥ 6 (n = 14). The less sleepy group had higher MSNA than did the sleepier group (82.5 ± 9.9 bursts/100 cardiac cycles vs 69.3 ± 18.6 bursts/100 cardiac cycles; P = .037) and a longer sleep-onset latency (33 ± 29 min vs 14 ± 13 min; P = .039). The ESS score was inversely related to MSNA (r = -0.63; P < .001) but not to the AHI, arousal index, or indices of oxygen desaturation. CONCLUSIONS: In patients with HF and OSA, the degree of subjective daytime sleepiness is inversely related to MSNA. This relationship is likely mediated via central adrenergic alerting mechanisms. These findings help to explain the previously reported lack of daytime hypersomnolence in patients with HF and OSA.
BACKGROUND:Patients with heart failure (HF) and obstructive sleep apnea (OSA) are less sleepy than patients with OSA but without HF. Furthermore, unlike the non-HF population, in the HF population, the degree of daytime sleepiness is not related to the apnea-hypopnea index (AHI). The sympathetic nervous system plays a critical role in alertness. HF and OSA both increase sympathetic nervous system activity (SNA) during wakefulness. We hypothesized that in patients with HF and OSA, the degree of subjective daytime sleepiness would be inversely related to SNA. METHODS: Daytime muscle SNA (MSNA) was recorded in patients with HF and OSA. Subjective daytime sleepiness was assessed by the Epworth Sleepiness Scale (ESS). RESULTS: We studied 27 patients with HF and OSA and divided them into two groups based on the median ESS score: a less sleepy group, with an ESS score < 6 (n = 13), and a sleepier group, with an ESS score ≥ 6 (n = 14). The less sleepy group had higher MSNA than did the sleepier group (82.5 ± 9.9 bursts/100 cardiac cycles vs 69.3 ± 18.6 bursts/100 cardiac cycles; P = .037) and a longer sleep-onset latency (33 ± 29 min vs 14 ± 13 min; P = .039). The ESS score was inversely related to MSNA (r = -0.63; P < .001) but not to the AHI, arousal index, or indices of oxygen desaturation. CONCLUSIONS: In patients with HF and OSA, the degree of subjective daytime sleepiness is inversely related to MSNA. This relationship is likely mediated via central adrenergic alerting mechanisms. These findings help to explain the previously reported lack of daytime hypersomnolence in patients with HF and OSA.
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