Non-Invasive Positive Pressure Ventilation Use-Practice Recommendations of the Slovak Society of Pulmonology and Phthisiology.

Non-invasive positive pressure ventilation (NIPPV) is increasingly used as a treatment method for patients with respiratory failure. The first recommendations for the use of NIPPV in Slovakia were developed by the Slovak Society of Pulmonology and Phthisiology in 2007 and were partially revised in 2015. New scientific evidence prompted the present update, which is based on widely accepted international guidelines and was adapted to address local needs. Important features of the present update include a classification of acute indications for NIPPV into three categories based on the level of supporting evidence, namely 1. definite indications for in-hospital use of NIPPV; 2. possible indications for in-hospital use of NIPPV; and 3. disorders and states in which in-hospital use of NIPPV is not recommended. The current update also reflects the importance of comorbid sleep-related breathing disorders and other chronic respiratory conditions, as well as the use and limitations of continuous positive airway pressure therapy. Since oxygen therapy is often administered along with NIPPV, guidance on the safe use of oxygen in NIPPV-treated patients has also been included. Also, the present update extends the range of its users, addressing the needs of specialists in pediatric respiratory medicine as a novelty.

The impact of sleep apnea syndrome on the altered lipid metabolism and the redox balance.

BACKGROUND: Obstructive sleep apnea (OSA) is a disorder with a significant risk for cardiovascular diseases. Dyslipidemia and redox imbalance belong to potential mechanisms linking OSA with the development of vascular diseases. The main aim of this study was the evaluation of the presence of lipid abnormalities in OSA patients, focusing on small dense low-density lipoprotein (LDL) and high-density lipoprotein (HDL) subfractions and determination of the redox imbalance by evaluating the marker of oxidative damage to plasma lipids - lipoperoxides. METHODS: The study included 15 male subjects with polysomnographically confirmed OSA and 16 male healthy controls. Plasma levels of total cholesterol, LDL and HDL and their subfractions, triacylglycerols and lipoperoxides were determined in all study individuals. Plasma LDL and HDL subfractions were separated by the Lipoprint system which is a polyacrylamide gel electrophoresis. Lipoperoxide levels were determined spectrophotometrically. RESULTS: OSA patients had significantly higher triacylglycerols, total cholesterol and LDL-cholesterol compared to healthy controls. HDL cholesterol was not significantly different. Of the LDL and HDL subfractions, OSA patients had significantly lower levels of atheroprotective LDL1 and large HDL subfractions and significantly higher levels of atherogenic small dense LDL3-7 and HDL8-10 subfractions. Lipoperoxide levels in patients with OSA were significantly elevated compared to healthy individuals. CONCLUSION: The lipoprotein pro-atherogenic phenotype was found in individuals with OSA characterized by increased levels of atherogenic lipoprotein subfractions and reduced levels of atheroprotective subfractions. In addition, a plasma redox imbalance was found in patients with OSA compared to controls by detecting higher oxidative damage to lipids. Abnormalities in lipoprotein levels in patients with OSA, as well as the redox imbalance, could lead to an acceleration of the atherosclerotic process in predisposed individuals and thus represent a significant risk factor for vasular diseases.

Obstructive sleep apnea and hypertension: the role of gut microbiome.

Obstructive sleep apnea is common disorder affecting approximately one quarter of the common population. Prevalence is even higher in a population with increased vascular risk. Obstructive sleep apnea is a significant risk factor for hypertension, with approximately 50% of obstructive sleep apnea patients suffering hypertension. While the relationship between sleep apnea and hypertension has been firmly established, mechanisms linking these disorders are still poorly understood. Importance of sympathetic nervous system and renin-angiotensin-aldosterone system hyperactivity as well as endothelial dysfunction is suspected. There is increasing evidence supporting gut dysbiosis as one of the underlying mechanisms. Current article describes possible mechanisms linking obstructive sleep apnea with the development of hypertension. The role of gut microbiota in this process is discussed more closely.

Short-term effects of continuous positive airway pressure on oxidative stress in severe sleep apnea.

PURPOSE: Obstructive sleep apnea (OSA) is associated with oxidative stress that is involved in the pathogenesis of cardiovascular and metabolic complications. The concentrations of salivary markers of oxidative stress in patients with OSA increase considerably during the night. The dynamics is not affected by continuous positive airway pressure (CPAP) in mild to moderate OSA. The aim of this study was to analyze the short-term effects of CPAP on salivary oxidative stress markers in patients with severe OSA. METHODS: Salivary samples were collected from 24 patients with apnea-hypopnea index higher than 30 during the first (diagnostic) night, who were treated by CPAP during the second (therapeutic) night. RESULTS: The salivary markers of oxidative stress (TBARS, AGEs, and AOPP) were higher in the morning after the diagnostic night when compared to the evening concentrations (p < 0.01 for TBARS and p < 0.05 for AGEs and AOPP). Treatment by CPAP significantly decreased the morning concentrations of TBARS, AOPP (p < 0.01 for both), and AGEs (p < 0.05). Also, TBARS and AGEs positively correlated with apnea-hypopnea index (r = 0.48 and 0.49, respectively; p < 0.05). Antioxidant statuss was not affected. CONCLUSION: Severe OSA is associated with increased levels of saliva markers for lipid peroxidation, protein oxidative damage, and carbonyl damage. Even short-term CPAP partially prevents oxidative and carbonyl stress during the night and this can be monitored non-invasively using saliva.

Obstructive sleep apnea and dyslipidemia.

Obstructive sleep apnea is a sleep disorder characterized by repetitive partial or complete upper airway obstruction that lead to hemodynamic changes, arousals from sleep and intermittent hypoxia. Obstructive sleep apnea activates multiple pathways that lead to vascular disease. The vascular risk imposed by obstructive sleep apnea may be mediated through the metabolic consequences of sleep-disordered breathing. There is increasing evidence that obstructive sleep apnea is independently associated with dyslipidemia, a well known vascular risk factor. However, the role of obstructive sleep apnea in causality of dyslipidemia remains to be established. Current article focuses on possible mechanisms linking obstructive sleep apnea with the development of dyslipidemia. Possible role of obstructive sleep apnea as a therapeutic target to improve dyslipidemia is also discussed. Key words: dyslipidemia - obstructive sleep apnea.

EU questionnaire to screen for obstructive sleep apnoea validated in Slovakia.

OBJECTIVE: Obstructive sleep apnoea syndrome (OSAS) associated with daytime sleepiness (DS) contributes to a higher incidence of motor vehicle accidents. Validation of fitness to drive in driving license applicants, with special concern regarding OSAS accompanied by excessive DS, became mandatory under new EU legislation in January 2016. The aim of the study was to translate and validate the recommended questionnaire to screen for OSAS (Q-OSAS) in the Slovak population. No data on any Q-OSAS validation has previously been published. METHODS: The translated Q-OSAS was administered to 311 Slovak patients prior to a planned overnight polysomnography. The diagnostic accuracy of the Q-OSAS in OSAS with an apnoea-hypopnoea index of 15 or more/h of sleep was evaluated by calculating the area under the ROC curve. RESULTS: The sensitivity and specificity of the cut-off at 10 points for the Q-OSAS was 57% and 67%, respectively, with an increase of sensitivity and a decrease of specificity with a lowering of the cut-off values. Excluding the Epworth Sleepiness Scale (ESS) score from the final statistics yielded the best sensitivity (77%), specificity (50%), and an area under the ROC curve (0.637) for the cut-off value of 8 points (an equivalent of 10 points with the full version of the Q-OSAS). CONCLUSION: The Q-OSAS is an appropriate screening tool to facilitate the screening of subjects potentially at risk from moderate and severe OSAS. A modified two-step interpretation of the Q-OSAS in Slovakia yielded the best sensitivity, and in the future could promote evaluation of sleepiness in sleep and wake disorders other than OSAS for fitness to drive.

Carotid intima-media thickness is not associated with homocysteine and vitamin D levels in obstructive sleep apnea.

Obstructive sleep apnea syndrome (OSA) is associated with increased vascular morbidity. Accelerated atherosclerosis might be one of the most important mechanisms linking OSA with the development of vascular disorders. Homocysteine (HCY) and vitamin D has been associated with atherogenesis. The aim of this study was to assess a possible association between the levels of HCY and vitamin D and the carotid intima-media thickness (cIMT), which is a known marker for subclinical atherosclerosis in patients with OSA. We prospectively enrolled 110 patients with the history of snoring, who underwent standard overnight polysomnography. Clinical characteristics of the population were recorded on admission and blood samples were obtained in the fasting condition following morning. Extracranial cIMT measurements were performed according to the standardized scanning protocol. A significant correlation was found between cIMT and apnea-hypopnea index (r = .276, p = .006), age (r = .486, p < .001), diabetes mellitus (r = .377, p < .001), coronary artery disease (r = .274, p = .006) and history of stroke (r = .251, p = .012). We failed to find any significant correlation between cIMT and the levels of HCY (r = .036, p = .724) or vitamin D (r = .027, p = .800). In conclusion, our data suggest that the association of cIMT with the severity of OSA can be influenced by multiple metabolic consequences of OSA including traditional and non-traditional risk factors. HCY and vitamin D do not seem to play a superior role in this process.

Salivary markers of oxidative stress in patients with obstructive sleep apnea treated with continuous positive airway pressure.

PURPOSE: Obstructive sleep apnea syndrome (OSAS) is characterized by elevated oxidative stress. Measurement of oxidative stress in saliva seems to be promising in long-term treatment monitoring of OSAS patients. In this study, our aim was to investigate whether short-term continuous positive airway pressure (CPAP) treatment would influence oxidative stress in saliva. METHODS: Patients with diagnosed OSAS (16 women, 28 men) underwent polysomnography during the first night and CPAP treatment during the second night. Saliva samples were taken in the evening and morning on both days. Markers of oxidative stress and antioxidant status were analyzed in saliva. RESULTS: Evening concentrations of the salivary thiobarbituric acid reacting substances (p < 0.001), advanced glycation end-products (p < 0.001), and advanced oxidation protein products (p < 0.01) were significantly lower than morning values during the diagnostic night. However, salivary concentrations of none of the oxidative stress markers were significantly influenced by the CPAP treatment. No changes in salivary antioxidant status after CPAP therapy were found. CONCLUSION: Salivary markers of oxidative stress and antioxidant status do not change significantly after one night treatment with CPAP. On the contrary, after 1 month with CPAP therapy, reduced markers of oxidative stress were reported. Therefore, the future studies should be focused on finding the optimal sampling frequency to clarify the potential of saliva for the monitoring of OSAS treatment.

Antioxidant vitamins prevent oxidative and carbonyl stress in an animal model of obstructive sleep apnea.

PURPOSE: The aim of our study was to analyze the effects of an antioxidant treatment on markers of oxidative and carbonyl stress in a rat model of obstructive sleep apnea. METHODS: Wistar rats were randomized into six groups-according to gender and intervention-sham, intermittent hypoxia, and intermittent hypoxia with treatment by vitamins C and E. Rats underwent tracheostomy. The tracheal cannula was closed for 12 s every minute for 1 h to simulate obstructive sleep apnea-related intermittent hypoxia. In the treatment group, rats received vitamin C and E 24 h prior to surgery. RESULTS: The intervention had a significant effect on advanced oxidation protein products (p = 0.008) and advanced glycation end products-specific fluorescence (p = 0.006) but no effect on malondialdehyde. Oxidation and glycation protein products were higher in intermittent hypoxia groups than in sham and in treated groups. CONCLUSIONS: Antioxidants alleviate oxidative and carbonyl stress in an experimental model of obstructive sleep apnea. Future studies will show whether such treatment has any clinical value regarding cardiovascular complications of sleep apnea syndrome, preferably in patients with low compliance to continuous positive airway pressure.

Oxidative and carbonyl stress in patients with obstructive sleep apnea treated with continuous positive airway pressure.

PURPOSE: The pathogenesis of cardiovascular complications of obstructive sleep apnea syndrome (OSAS) can be explained by oxidative and carbonyl stress due to oxygenation and reoxygenation injury during sleep. This hypothesis has yet to be proved experimentally, although several clinical observations have found increased oxidative damage in plasma. Continuous positive airway pressure (CPAP) improves symptoms and prognosis of patients with OSAS. METHODS: Patients with confirmed SAS (n = 89) underwent polysomnography and received CPAP treatment. Plasma and saliva samples were taken before CPAP therapy as well as after 1 and 6 months of CPAP treatment. Selected markers of oxidative and carbonyl stress were measured in plasma and saliva, and their dynamics was statistically analyzed. RESULTS: Plasma levels of thiobarbituric acid reacting substances-a marker of lipoperoxidation-and advanced glycation end products (AGEs)-a marker of carbonyl stress-were decreased by the CPAP therapy. The decrease of AGEs and fructosamine was also found in saliva. Interestingly, no gender differences and no changes of antioxidant status measured as total antioxidant capacity and ferrous reducing ability were found in either of the samples. CONCLUSION: Previous findings of lowered plasma markers of oxidative stress were confirmed. Plasma AGEs were lowered by CPAP therapy. This is the first study analyzing markers of oxidative and carbonyl stress in saliva. Non-invasive sampling of saliva makes it a very interesting source of information for repeated monitoring of therapy success. Salivary AGEs and fructosamine as markers of carbonyl stress were decreased by the CPAP therapy and might therefore have potential informative value for clinical observations, as well as for the understanding of the pathogenesis of OSAS complications.