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Javaheri, Shahrokh; Giannoni, Alberto; Somers, Virend K; Malhotra, Atul; Emdin, Michele; Costanzo, Maria R
doi: 10.1093/sleep/zsae307pmid: 39786443
Central sleep apnea, a rare polysomnographic finding in the general population, is prevalent in certain cardiovascular conditions including systolic and diastolic left ventricular dysfunction, atrial fibrillation, coronary artery disease, carotid artery stenosis, stroke, and use of certain cardiac-related medications. Polysomnographic findings of central sleep apnea with adverse cardiovascular impacts include nocturnal hypoxemia and arousals, which can lead to increased sympathetic activity both at night and in the daytime. Among cardiovascular diseases, central sleep apnea is most prevalent in patients with left ventricular systolic dysfunction; a large study of more than 900 treated patients has shown a dose-dependent relationship between nocturnal desaturation and mortality. Multiple small randomized controlled trials have shown mitigation of sympathetic activity when central sleep apnea is treated with nocturnal oxygen, continuous positive airway pressure, and adaptive servoventilation. However, two early randomized controlled trials with positive airway pressure devices have shown either a neutral effect on survival or excess premature mortality in the active treatment arm, compared to untreated central sleep apnea. In contrast, the results of the most recent trial using an advanced adaptive servoventilation device showed improved quality of life and no signal for mortality suggesting that treatment of central sleep apnea was at least safe. In addition to positive airway pressure devices, multiple medications have been shown to improve central sleep apnea, but no long-term trials of pharmacologic therapy have been published. Currently, phrenic nerve stimulation is approved for the treatment of central sleep apnea, and the results of a randomized controlled trial showed significant improvement in sleep metrics and quality of life.
Xia, Dong; Chen, Ying; Fu, Xiang; Liu, Hui-Yi; Sun, Mu-Yan; Wang, Fen; Zhang, Yong; Liu, Chun-Feng; Liu, Jun-Yi
doi: 10.1093/sleep/zsae297pmid: 39707678
Parkinson’s disease (PD) is a complex neurodegenerative disorder, characterized by the aggregation of α-synuclein (α-syn). Current research increasingly indicates the prevalence of sleep–wake disorders in early-stage PD, although the underlying pathogenic mechanisms remain unclear. In this study, transgenic Drosophila models were utilized to observe excessive daytime sleepiness and impaired anticipation in flies overexpressing α-syn in pan-neurons and circadian clock neurons. Additionally, deficits in projection of Pigment Dispersing Factor (PDF) neuron terminals, which are involved in Drosophila sleep and circadian rhythm, were identified. An imbalance in lipid metabolism homeostasis was detected in the brains of α-syn overexpressing mutants. Ultimately, the inhibition of Sterol Regulatory Element-Binding Protein (SREBP) activity led to an improvement in the reduced daytime sleep duration phenotype. Our results suggest that lipid pathways play a role in sleep–wake disorders triggered by α-syn mutation and aggregation, thereby providing valuable insights into potential therapeutic avenues for disrupted sleep patterns associated with PD.
Groenhout, Trent; Ponnaluri, Sumegha; Sharba, Lana; Liu, Tiecheng; Nelson, Amanda; Hambrecht-Wiedbusch, Viviane S; Vanini, Giancarlo; Pal, Dinesh
doi: 10.1093/sleep/zsae260pmid: 39504494
Azegami, Tatsuhiko; Kaneko, Hidehiro; Okada, Akira; Suzuki, Yuta; Ko, Toshiyuki; Fujiu, Katsuhito; Takeda, Norifumi; Morita, Hiroyuki; Takeda, Norihiko; Yokoo, Takashi; Yasunaga, Hideo; Nangaku, Masaomi; Hayashi, Kaori
doi: 10.1093/sleep/zsae302pmid: 39704496
Study ObjectivesSleep apnea syndrome (SAS) is potentially linked to life-threatening conditions. The decline in kidney function is involved in the development of various diseases; however, it remains unclear whether it is implicated in the onset of SAS. Therefore, this study aimed to investigate the relationship between kidney function and the incidence of SAS.MethodsThe association of estimated glomerular filtration rate (eGFR) with the incidence of SAS was assessed retrospectively using real-world administrative claims and health checkup data collected between April 2014 and November 2022. To strengthen robustness, three stratified analyses and four sensitivity analyses were conducted.ResultsWe assessed 1 589 259 individuals for the analysis. During a median (interquartile range) follow-up of 1167 (652–1699) days, 11 054 cases of SAS events were documented. Multivariable Cox regression analyses after adjusting for potential confounders, including age, sex, body mass index, hypertension, diabetes, dyslipidemia, cigarette smoking, alcohol drinking, and physical inactivity, demonstrated that the decrease in eGFR (eGFR ≥ 90, 60–89, 45–59, 30–44, and <30 mL/min/1.73 m2) was associated with a higher risk of SAS (hazard ratio [95% confidence intervals]; 1 [reference value], 1.13 [1.06–1.20], 1.22 [1.13–1.32], 1.34 [1.17–1.52], 1.82 [1.43–2.33]). In the restricted cubic spline regression model, the risk of developing SAS increased with the reduction in eGFR. The results of the sensitivity analyses were consistent with the primary findings.ConclusionOur analysis utilizing a large-scale population-based cohort concluded that reduced eGFR is associated with the risk of developing SAS in a dose-dependent manner.
Yang, Yuting; Thackray, Alice E; Shen, Tonghui; Alotaibi, Tareq F; Alanazi, Turki M; Clifford, Tom; Hartescu, Iuliana; King, James A; Roberts, Matthew J; Willis, Scott A; Lolli, Lorenzo; Atkinson, Greg; Stensel, David J
doi: 10.1093/sleep/zsae250pmid: 39446630
Study ObjectivesUsing the necessary replicate-crossover design, we investigated whether there is interindividual variability in home-assessed sleep in response to acute exercise.MethodsEighteen healthy men (mean [SD]: 26[6] years) completed two identical control (8 hour laboratory rest, 08:45–16:45) and two identical exercise (7 hour laboratory rest; 1 hour laboratory treadmill run [62(7)% peak oxygen uptake], 15:15–16:15) trials in randomized sequences. Wrist-worn actigraphy (MotionWatch 8) measured home-based sleep (total sleep time, actual wake time, sleep latency, and sleep efficiency) two nights before (nights 1 and 2) and three nights after (nights 3–5) the exercise/control day. Pearson’s correlation coefficients quantified the consistency of individual differences between the replicates of control-adjusted exercise responses to explore: (1) immediate (night 3 minus night 2); (2) delayed (night 5 minus night 2); and (3) overall (average post-intervention minus average pre-intervention) exercise-related effects. Within-participant linear mixed models and a random-effects between-participant meta-analysis estimated participant-by-trial response heterogeneity.ResultsFor all comparisons and sleep outcomes, the between-replicate correlations were nonsignificant, ranging from trivial to moderate (r range = −0.44 to 0.41, p ≥ .065). Participant-by-trial interactions were trivial. Individual differences SDs were small, prone to uncertainty around the estimates indicated by wide 95% confidence intervals, and did not provide support for true individual response heterogeneity. Meta-analyses of the between-participant, replicate-averaged condition effect revealed that, again, heterogeneity (τ) was negligible for most sleep outcomes.ConclusionsControl-adjusted sleep in response to acute exercise was inconsistent when measured on repeated occasions. Interindividual differences in sleep in response to exercise were small compared with the natural (trial-to-trial) within-subject variability in sleep outcomes.Clinical trials informationhttps://clinicaltrials.gov/study/NCT05022498. Registration number: NCT05022498.
Huang, Xiaoyu; Zhang, Zhengjiao; Lan, Xiaoxin; Song, Xuefeng; Dong, Yanzhao; Jia, Siqi; Yuan, Haibo
doi: 10.1093/sleep/zsae269pmid: 39570770
Study ObjectivesObstructive sleep apnea (OSA) is associated with an increasing risk of cognitive impairment, but traditional hypoxic indicators can not accurately identify cognitive impairment. This study aimed to assess a new indicator, hypoxic burden, in cognitive impairment in OSA.MethodsA total of 116 patients with OSA were enrolled in this study. Daytime sleepiness and cognition were assessed using the Epworth Sleepiness Scales and Montreal Cognitive Assessment (MoCA), respectively. All participants underwent polysomnography (PSG). The hypoxic burden was derived from PSG and calculated according to a specific algorithm. All the participants were divided into two groups. Seventy-seven were OSA with mild cognitive impairment (OSA + MCI), and 39 were OSA without mild cognitive impairment (OSA-MCI). The relationship between hypoxic burden and cognitive impairment was analyzed by establishing a series of logistic regression models.ResultsHypoxic burden was higher in OSA + MCI group compared with OSA-MCI group, while there was no significance found for the apnea-hypopnea index between the two groups. After adjusting for various confounders, patients with OSA who had a higher total hypoxic burden and rapid eye movement-hypoxic burden in the fourth quartile were found to have an increased risk of MCI compared to those in the first quartile. The adjusted ORs were 7.69 (95% CI, 1.15 to 51.55) and 8.87 (95% CI, 1.22 to 64.34), respectively. However, There was no significant association between the other traditional hypoxic parameters and cognitive function after adjusting for various confounders.ConclusionsCompared to the conventional hypoxic parameter, a higher hypoxic burden is associated with cognition and may be an important indicator for assessing MCI in OSA.
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