To date, there is no standard approach to manage and to improve central sleep apnea (CSA). The most applicable therapeutic approaches are positive airway pressure therapy (PAP), bi-level PAP therapy (BIPAP), supplemental O2 and servo ventilation, or a combination of two approaches. Given the high prevalence of heart disease (HF) and/or concomitants of other diseases and opioid use worldwide; it seemingly requires evaluation of patients' conditions in response to each abovementioned approach to select the most effective approach.

A 58-yr-old man with primary alveolar hypoventilation, central sleep apnea, and secondary polycythemia failed to improve when treated with respiratory stimulant medications, including oxtriphylline, acetazolamide, and medroxyprogesterone. In contrast, after institution of treatment with low-flow nocturnal oxygen, there was a marked decrease in the number and duration of sleep apneas, and an increase in the level of ventilation during sleep. These changes were sustained during 5 months of nocturnal oxygen therapy. The improvement produced by oxygen may have been due to the fact that the patient had no demonstrable ventilatory response to hypoxia during wakefulness, and therefore may have developed hypoxic brainstem depression during sleep. The findings suggest that oxygen therapy during sleep may be beneficial in patients with primary alveolar hypoventilation and central sleep apnea who demonstrate no ventilatory response to hypoxia during wakefulness.

Increasing evidence suggests overlap in mechanisms of obstructive and central sleep apnea. Our objective was to compare the patient characteristics and polysomnographic findings of children with concurrent obstructive and central sleep apnea (obstructive sleep apnea + central sleep apnea [OSA + CSA]), to those with OSA only.

Treatment-emergent central sleep apnea (TECSA) is the appearance of central apneas and hypopneas after significant resolution of the obstructive events has been attained using positive airway pressure (PAP) therapy. The aim of the study was to determine the prevalence of TECSA and to understand what factors are associated with its development.

This study aimed to investigate the effects of continuous positive airway pressure (CPAP) on the electroencephalographic (EEG) characteristics of patients with primary central sleep apnea syndrome (CSAS). Nine patients with primary CSAS were enrolled in this study. The raw sleep EEG data were analyzed based on two main factors: fractal dimension (FD) and zero-crossing rate of detrended FD. Additionally, conventional EEG spectral analysis in the delta, theta, alpha, and beta bands was conducted using a fast Fourier transform. The FD in patients with primary CSAS who underwent CPAP treatment was significantly decreased during nonrapid eye movement (NREM) sleep but increased during rapid eye movement (REM) sleep (p < 0.05). Regarding the EEG spectral analysis, the alpha power increased, while the delta/alpha ratio decreased during REM sleep in patients with CSAS (p < 0.05). In conclusion, CPAP treatment can reduce FD in NREM sleep and increase FD during REM sleep in patients with primary CSAS. FD may be used as a new biomarker of EEG stability and improvement in brain function after CPAP treatment for primary CSAS.

Treatment-emergent central sleep apnea (TECSA) is observed in some patients when they are treated with positive airway pressure (PAP) after significant resolution of the preexisting obstructive events in patients with obstructive sleep apnea. The objective of this study was to systematically review the literature for studies describing the natural history of TECSA.

Nocturnal hypoxemic burden is established as a robust prognostic metric of sleep-disordered breathing (SDB) to predict mortality and treating hypoxemic burden may improve prognosis. The aim of this study was to evaluate improvements in nocturnal hypoxemic burden using transvenous phrenic nerve stimulation (TPNS) to treat patients with central sleep apnea (CSA). The remedē System Pivotal Trial population was examined for nocturnal hypoxemic burden. The minutes of sleep with oxygen saturation < 90% significantly improved in Treatment compared with control (p < .001), with the median improving from 33 min at baseline to 14 min at 6 months. Statistically significant improvements were also observed for average oxygen saturation and lowest oxygen saturation. Hypoxemic burden has been demonstrated to be more predictive for mortality than apnea-hypopnea index (AHI) and should be considered a key metric for therapies used to treat CSA. Transvenous phrenic nerve stimulation is capable of delivering meaningful improvements in nocturnal hypoxemic burden. There is increasing interest in endpoints other than apnea-hypopnea index in sleep-disordered breathing. Nocturnal hypoxemia burden may be more predictive for mortality than apnea-hypopnea index in patients with poor cardiac function. Transvenous phrenic nerve stimulation is capable of improving nocturnal hypoxemic burden. Graphical Abstract.

Positive airway pressure (PAP) therapy for central sleep apnea (CSA) is often poorly tolerated, ineffective, or contraindicated. Transvenous phrenic nerve stimulation (TPNS) offers an alternative, although its impact on previously PAP-treated patients with CSA has not been examined.

Polysomnography is the gold standard for detection of central sleep apnea in patients with stable heart failure. However, this procedure is costly, time consuming, and a burden to the patient and therefore unsuitable as a screening method. An electronic health (eHealth) app to measure overnight oximetry may be an acceptable screening alternative, as it can be automatically analyzed and is less burdensome to patients.

This study addressed the following question: "Is it possible to highlight the link between obstructive sleep apnea (OSA) and central serous chorioretinopathy (CSC) through common biopsychosocial pathogenetic pathways?". The study was conducted through electronic searches of the PubMed, Web of Science, and Scopus databases. All relevant selected human research studies published from January 2003 to December 2020 were included. The scientific literature search was performed through repeated use of the words "OSA" and/or "acute/chronic CSC" paired with "biomedical/biopsychosocial illness model", "psychopathology", "stress", "personality characteristics", "functional diseases", "comorbidity", and "quality of life" in different combinations. Our literature search identified 213 reports, of which 54 articles were ultimately reviewed in this paper. Taken together, the results indicate that there is a cross-link between OSA and CSC that can be classified among biopsychological disorders in which various major biological variables integrate with psychological-functional and sociological variables; many of these variables appear in both diseases. This concept can have important implications for improving patients' quality of life, thus providing the necessary strategies to cope with challenging life events even through nonpharmacological approaches.

Background: Although sleep respiratory disorders are known as a relevant source of cardiovascular risk, there is a substantial lack of trials aimed to evaluate the eventual occurrence of associations between sleep apnea (SA) and valvular heart diseases (VHD). Methods: We recruited 411 patients referring to our sleep disorder unit, among which 371 had SA. Ninety-three subjects with SA also suffered from VHD. Physical examination, echocardiography, nocturnal cardio-respiratory monitoring, and laboratory tests were performed in each patient. Patient subgroups were comparatively evaluated through cross-sectional analysis. Results: A statistically significant increase in the prevalence of VHD was detected in relation to high apnea hypopnea index (AHI) values (p = 0.011). Obstructive sleep apnea occurrence was higher in SA patients without VHD (p < 0.0001). Conversely, central and mixed sleep apneas were more frequent among SA patients with VHD (p = 0.0003 and p = 0.002, respectively). We observed a direct correlation between AHI and BMI values (p < 0.0001), as well as between AHI and serum uric acid levels (p < 0.0001), high sensitivity C-reactive protein (p < 0.0001), and indexed left ventricular end-diastolic volume (p < 0.015), respectively. BMI and VHD resulted to be the main predictors of AHI values (p < 0.0001). Conclusions: Our study suggests that a significant association can occur between SA and VHD. It is clinically relevant that when compared to SA patients without VHD, higher frequencies of central and mixed apneas were found in subjects with SA and VHD. Moreover, after elevated BMI, VHD represented the second predictor of AHI values.

This SERVE-HF (Treatment of Predominant Central Sleep Apnea by Adaptive Servo Ventilation in Patients With Heart Failure) sub study analysis evaluated polysomnography (PSG) data in patients with heart failure with reduced ejection fraction (HFrEF) and predominant central sleep apnea (CSA) randomised to guideline-based medical therapy, with or without adaptive servo ventilation (ASV). Patients underwent full overnight PSG at baseline and at 12 months. All PSG recordings were analysed by a core laboratory. Only data for patients with baseline and 3- or 12-month values were included. The sub study included 312 patients; the number with available PSG data differed for each variable (94-103 in the control group, 77-99 in the ASV group). After 12 months, baseline-adjusted respiratory measures were significantly better in the ASV group versus control. Although some between-group differences in sleep measures were seen at 12 months (e.g., better sleep efficiency in the ASV group), these were unlikely to be clinically significant. The number of periodic leg movements during sleep (PLMS) increased in the ASV group (p = 0.039). At 12 months, the respiratory arousal index was significantly lower in the ASV versus control group (p < 0.001), whilst the PLMS-related arousal index was significantly higher in the ASV group (p = 0.04 versus control). ASV attenuated the respiratory variables characterising sleep apnea in patients with HFrEF and predominant CSA in SERVE-HF. Sleep quality improvements during ASV therapy were small and unlikely to be clinically significant. The increase in PLMS and PLMS-related arousals during ASV warrants further investigation, particularly relating to their potential association with increased cardiovascular risk.

Components of the renin-angiotensin system (RAS) situated within the carotid body or central nervous system may promote hypoxia-induced chemoreceptor reflex sensitization or central sleep apnea (CSA). We determined if losartan, an angiotensin-II type-I receptor (AT1R) antagonist, would attenuate chemoreceptor reflex sensitivity before or after 8 h of nocturnal hypoxia, and consequently CSA severity. In a double-blind, randomized, placebo-controlled, crossover protocol, 14 men (age: 25 ± 2 years; BMI: 24.6 ± 1.1 kg/m2; means ± SEM) ingested 3 doses of either losartan (50 mg) or placebo every 8 h. Chemoreceptor reflex sensitivity was assessed during hypoxic and hyperoxic hypercapnic ventilatory response (HCVR) tests and during six-20s hypoxic apneas before and after 8 h of sleep in normobaric hypoxia (F I O2 = 0.135). Loop gain was assessed from a ventilatory control model fitted to the ventilatory pattern of CSA recorded during polysomnography. Prior to nocturnal hypoxia, losartan had no effect on either the hyperoxic (losartan: 3.6 ± 1.1, placebo: 4.0 ± 0.6 l/min/mmHg; P = 0.9) or hypoxic HCVR (losartan: 5.3 ± 1.4, placebo: 5.7 ± 0.68 l/min/mmHg; P = 1.0). Likewise, losartan did not influence either the hyperoxic (losartan: 4.2 ± 1.3, placebo: 3.8 ± 1.1 l/min/mmHg; P = 0.5) or hypoxic HCVR (losartan: 6.6 ± 1.8, placebo: 6.3 ± 1.5 l/min/mmHg; P = 0.9) after nocturnal hypoxia. Cardiorespiratory responses to apnea and participants' apnea hypopnea indexes during placebo and losartan were similar (73 ± 15 vs. 75 ± 14 events/h; P = 0.9). Loop gain, which correlated with CSA severity (r = 0.94, P < 0.001), was similar between treatments. In summary, in young healthy men, hypoxia-induced CSA severity is strongly associated with loop gain, but the AT1R does not modulate chemoreceptor reflex sensitivity before or after 8 h of nocturnal hypoxia.

Obstructive sleep apnea syndrome (OSAS) is a disorder with high prevalence among adults and is an independent risk factor for various diseases, especially those affecting the central nervous system (CNS). Continuous positive airway pressure (CPAP) is usually the optimal choice of treatment for OSAS. Alzheimer's disease (AD) is a neurodegenerative disease affecting a large proportion of the elderly population. The purpose of this study was to collect information concerning the two pathological entities and investigate the effectiveness of CPAP in the treatment of AD.

Recently we reported an association between pediatric obstructive sleep apnea syndrome (OSAS) and Group A streptococcus (GAS) sub-acute chronic tonsil colonization. We showed that GAS may contribute to tonsil hyperplasia via a streptolysin O (SLO)-dependent cysteinyl leukotrienes (CysLTs) production, which can trigger T and B cell proliferation. In the present study, we characterized the GAS strains isolated from pediatric OSAS patients in comparison with a panel of age and sex matched GAS strains unrelated to OSAS, but isolated in the same area and during the same period ranging from 2009 to 2013. We found that slaA gene, previously reported to be associated to CysLTs production pathway, was significantly associated to GAS OSAS strains. Moreover, the most numerous group (32%) of the GAS OSAS strains belonged to M75 type, and 6 out of 7 of these strains harbored the slaA gene. Multilocus Sequence Typing (MLST) experiments demonstrated that the clone emm75/ST49/ smeZ, slaA was associated to OSAS cases. In conclusion, we found an association between slaA gene and the GAS OSAS strains, and we showed that the clone emm75/ST49 harboring genes smeZ and slaA was exclusively isolated from patients affected by OSAS, thus suggesting that this genotype might be associated to the pathogenesis of OSAS, although further studies are needed to elucidate the possible role of SlaA in tonsil hypertrophy development.

In obstructive sleep apnea (OSA), there are brief episodes of partial or total upper airway obstruction during sleep, which leads to apnea or hypopneas. Much attention is required to understand OSA's effects on the human body, owing to how common but under-diagnosed this disorder remains. Though the role of OSA in cardiovascular (CV) disease is commonly discussed, it remains unclear how it induces changes in the human body. The intermittent and recurrent hypoxia occurring at the cellular level in this condition is critical for the dramatic changes observed. Vascular endothelial cell (VEC) injury and other mechanisms seen in OSA lead to changes in the CV system. OSA can take a toll on a person's overall functioning, especially with so much importance in today's time on preventing and treating cardiac-related deaths. A total of 31 published articles were included from the PubMed database for our literature review. Most of the studies showed a strong association of OSA with hypertension, especially resistant hypertension. Findings were consistent with OSA's independent role in causing CV diseases, included heart failure, coronary artery disease (cardiac ischemia), arrhythmias, and ischemic stroke. Continuous Positive Airway Pressure (CPAP) is one of the reliable and beneficial treatments for OSA patients. OSA is a treatable and modifiable risk factor for cardiac events and related deaths. The primary purpose of our review article was to address any existing gaps between OSA and its effect on the human body with particular emphasis on cardiovascular changes.

Children with Down syndrome (DS) are at high risk for developing obstructive sleep apnea (OSA) compared to children without DS. The negative impact of OSA on health, behavior, and cognitive development in children with DS highlights the importance of timely and effective treatment. Due to the higher prevalence of craniofacial and airway abnormalities, obesity, and hypotonia in patients with DS, residual OSA can still occur after exhausting first-line options. While treatment commonly includes adenotonsillectomy (AT) and continuous positive airway pressure (CPAP) therapy, additional therapy such as medical management and/or adjuvant surgical procedures need to be considered in refractory OSA. Given the significant comorbidities secondary to untreated OSA in children with DS, such as cardiovascular and neurobehavioral consequences, more robust randomized trials in this patient population are needed to produce treatment guidelines separate from those for the general pediatric population of otherwise healthy children with OSA. Further studies are also needed to look at desensitization and optimization of CPAP use in patients with DS and OSA.

Obstructive sleep apnea is characterized by a reduced airflow through the upper airways during sleep. Two forms of obstructive sleep apnea are described: the central form and the obstructive form. The obstructive form is related to many factors, such as the craniofacial morphology.

Obstructive sleep apnea (OSA) has been associated to cardiovascular risk factors. However, the association between OSA and cardiovascular disease is still controversial. The objective of the present study was to verify the association between OSA and myocardial infarction (MI). This is a systematic review of the literature performed through electronic data sources MEDLINE/PubMed, PubMed Central, Web of Science and BVS -Biblioteca Virtual em Saúde (Virtual Health Library). The descriptors used were: 'obstructive sleep apnea' AND 'polysomnography' AND 'myocardial infarction' AND 'adults NOT 'treatment.' The present work analysed three prospective studies, selected from 142 articles. The studies followed a total sample of 5,067 OSA patients, mostly composed by male participants. All patients underwent night polysomnography, and all studies found an association between OSA and fatal and non-fatal cardiovascular outcomes. Thus, we were able to observe that 644 (12.7%) of the 5,067 patients suffered MI or stroke, or required a revascularization procedure, and 25.6% of these cardiovascular events were fatal. MI was responsible for 29.5% of all 644 analysed outcomes. There is an association between OSA and MI, in male patients, and apnea and hypopnea index (AHI) are the most reliable markers.

Obstructive sleep apnea syndrome (OSAS) is characterized by intermittent hypoxia (IH) during sleep due to recurrent upper airway obstruction. The derived oxidative stress (OS) leads to complications that do not only concern the sleep-wake rhythm but also systemic dysfunctions. The aim of this narrative literature review is to investigate molecular alterations, diagnostic markers, and potential medical therapies for OSAS. We analyzed the literature and synthesized the evidence collected. IH increases oxygen free radicals (ROS) and reduces antioxidant capacities. OS and metabolic alterations lead OSAS patients to undergo endothelial dysfunction, osteoporosis, systemic inflammation, increased cardiovascular risk, pulmonary remodeling, and neurological alterations. We treated molecular alterations known to date as useful for understanding the pathogenetic mechanisms and for their potential application as diagnostic markers. The most promising pharmacological therapies are those based on N-acetylcysteine (NAC), Vitamin C, Leptin, Dronabinol, or Atomoxetine + Oxybutynin, but all require further experimentation. CPAP remains the approved therapy capable of reversing most of the known molecular alterations; future drugs may be useful in treating the remaining dysfunctions.