Adaptive support ventilation as an effective treatment option for central sleep apnea in an older adult with heart failure with preserved ejection fraction: a case report

Background Adaptive support ventilation (ASV) is a proposed treatment option for central sleep apnea (CSA). Although the effectiveness of ASV remains unclear, some studies have reported promising results regarding the use of ASV in patients with heart failure with preserved ejection fraction (HfpEF). To illustrate the importance of suspecting and diagnosing sleep-disordered breathing (SDB) in older adults unable to recognize symptoms, we discuss a case in which ASV was effective in a patient with CSA and HfpEF, based on changes in the Holter electrocardiogram (ECG). Case presentation. An 82-year-old man presented to our hospital with vomiting on April 19, 2021. Approximately 10 years before admission, he was diagnosed with type 1 diabetes mellitus and recently required full support from his wife for daily activities due to cognitive dysfunction. Two days before admission, his wife was unable to administer insulin due to excessively high glucose levels, which were displayed as “high” on the patient’s glucose meter; therefore, we diagnosed the patient with diabetic ketoacidosis. After recovery, we initiated intensive insulin therapy for glycemic control. However, the patient exhibited excessive daytime sleepiness, and numerous premature ventricular contractions were observed on his ECG monitor despite the absence of hypoglycemia. As we suspected sleep-disordered breathing (SDB), we performed portable polysomnography (PSG), which revealed CSA. PSG revealed a central type of apnea and hypopnea due to an apnea–hypopnea index of 37.6, which was > 5. Moreover, the patient had daytime sleepiness; thus, we diagnosed him with CSA. We performed ASV and observed its effect using portable PSG and Holter ECG. His episodes of apnea and hypopnea were resolved, and an apparent improvement was confirmed through Holter ECG. Conclusion Medical staff should carefully monitor adult adults for signs of or risk factors for SDB to prevent serious complications. Future studies on ASV should focus on older patients with arrhythmia, as the prevalence of CSA may be underreported in this population and determine the effectiveness of ASV in patients with HfpEF, especially in older adults.

Association between sleep disordered breathing in early pregnancy and glucose metabolism

Study Objectives To examine the association between maternal sleep disordered breathing (SDB) and glucose metabolism in early gestation. Methods Women with body mass index (BMI) ≥27 kg/m2 and singleton pregnancies underwent in-home sleep study (HSAT) and homeostatic model assessment (HOMA) in early pregnancy. Insulin resistance (HOMA-IR) and β-cell function (HOMA %B) were derived. Exclusion criteria included pregestational diabetes, use of continuous positive airway pressure and chronic steroid therapy. We performed linear regression analyses to evaluate the association between continuous measures of SDB (respiratory event index (REI), and oxygen desaturation index (ODI)) and glucose metabolism parameters (HOMA-IR and HOMA %B). Analyses were adjusted for a set of a priori selected variables which included gestational age, maternal age, BMI, ethnicity, race, and parity. Results One hundred and ninety-two pregnant women with median (interquartile range) BMI of 35.14 (8.30) kg/m2 underwent HSAT and HOMA assessment at 11.14 (3) and 15.35 (4.14) gestational weeks, respectively. REI and ODI, as continuous values, were associated with HOMA-IR after adjusting for covariates. OSA (obstructive sleep apnea) diagnosis (REI > 5 events per hour) was not associated with HOMA-IR after adjusting for BMI (p ≥ 0.05). None of the parameters were associated with HOMA %B (p > 0.07). Conclusions SDB and insulin resistance are associated in early pregnancy, with a dose response association between respiratory event index severity and insulin resistance. Further studies are needed to establish if pregnant women with overweight and obesity may benefit from early SDB screening to improve glucose metabolic outcome. Clinical trials: NCT02412696, Positive Airway Pressure, Sleep Apnea, and the Placenta (PAP-SAP) https://clinicaltrials.gov/ct2/show/NCT02412696?term=Bourjeily&draw=2&rank=2 and NCT02917876, Predictors of De-novo Development of Obstructive Sleep Apnea in Pregnancy (Predictors) https://clinicaltrials.gov/ct2/show/NCT02917876?term=Bourjeily&draw=2&rank=1

Poor sleep quality is negatively associated with low cognitive performance in general population independent of self-reported sleep disordered breathing

Background Sleep disordered breathing (SDB) plays a significant role in both sleep quality and cognition and whether it has an impact on the relationship between above two factors remains to be clear. The study aimed to explore the association between sleep quality and cognitive performance in general population by considering influence of sleep disordered breathing (SDB). Methods In this cross-sectional study, we enrolled subjects aged ≥ 18 years using a multi-stage random sampling method. Cognitive status was assessed using Mini Mental State Examination (MMSE) questionnaire, sleep quality using Pittsburgh Sleep Quality Index (PSQI) and SDB was assessed using No-SAS scale, respectively. Multi-variable logistic regression was applied to examine the association of sleep quality and cognitive performance. Subgroup analyses were performed in different age groups, and in those with and without SDB. Results Finally, 30,872 participants aged 47.5 ± 13.8 years with 53.5% women were enrolled, of whom 32.4% had poor sleep quality and 18.6% had low cognitive performance. Compared with good sleepers, subjects with poor sleep quality exhibited significantly higher presence of low cognitive performance (23.7% vs 16.2%, P < 0.001). Poor sleepers revealed 1.26 (95%CI: 1.16,1.36), 1.26 (1.08,1.46) and 1.25 (1.14,1.37) fold odds for low cognitive performance in general population and in subjects with and without self-reported SDB respectively. Stratified by age and SDB, the association was observed in young and middle-aged group without SDB (OR = 1.44, 95%CI: 1.30,1.59) and in the elderly group with SDB (OR = 1.30, 95%CI: 1.07,1.58). Conclusions Sleep quality is in a negative association with cognitive performance in general population independent of SDB, implying improvement of sleep disturbances is a potential objective of intervention strategies for cognitive protection at population level.

Sleep Disordered Breathing, Obesity and Atrial Fibrillation: A Mendelian Randomisation Study

It remains unclear whether the association between obstructive sleep apnoea (OSA), a form of sleep-disordered breathing (SDB), and atrial fibrillation (AF) is causal or mediated by shared co-morbidities such as obesity. Existing observational studies are conflicting and limited by confounding and reverse causality. We performed Mendelian randomisation (MR) to investigate the causal relationships between SDB, body mass index (BMI) and AF. Single-nucleotide polymorphisms associated with SDB (n = 29) and BMI (n = 453) were selected as instrumental variables to investigate the effects of SDB and BMI on AF, using genetic association data on 55,114 AF cases and 482,295 controls. Primary analysis was conducted using inverse-variance weighted MR. Higher genetically predicted SDB and BMI were associated with increased risk of AF (OR per log OR increase in snoring liability 2.09 (95% CI 1.10–3.98), p = 0.03; OR per 1-SD increase in BMI 1.33 (95% CI 1.24–1.42), p < 0.001). The association between SDB and AF was not observed in sensitivity analyses, whilst associations between BMI and AF remained consistent. Similarly, in multivariable MR, SDB was not associated with AF after adjusting for BMI (OR 0.68 (95% CI 0.42–1.10), p = 0.12). Higher BMI remained associated with increased risk of AF after adjusting for OSA (OR 1.40 (95% CI 1.30–1.51), p < 0.001). Elevated BMI appears causal for AF, independent of SDB. Our data suggest that the association between SDB, in general, and AF is attributable to mediation or confounding from obesity, though we cannot exclude that more severe SDB phenotypes (i.e., OSA) are causal for AF.