Adherence to positive airway pressure therapy initiated in the early subacute phase of ischemic stroke: a PRESS study follow-up.

BACKGROUND: Sleep-disordered breathing (SDB) is frequent in stroke patients and negatively affects stroke outcomes. Positive airway pressure (PAP) is the standard first-line treatment for patients with moderate-to-severe SDB. Despite a strong link between PAP adherence and therapeutic response, rates of post-stroke PAP adherence remain underexplored. Our study aimed to determine PAP adherence in patients undergoing comprehensive sleep apnea assessment and in-lab PAP titration in the early subacute phase of stroke. METHODS: In-hospital screening pulse oximetry was performed in consecutive patients with imaging-confirmed acute ischemic stroke. Subjects with desaturation index ≥ 15.3/h were selected as PAP candidates, and polysomnography was recommended. In a sleep laboratory setting, subjects underwent a diagnostic night followed by a titration night, and PAP therapy was initiated in subjects with apnea-hypopnea index ≥ 15/h. Adherence to PAP therapy was assessed at a 6-month follow-up visit. RESULTS: Of 225 consecutive patients with acute ischemic stroke, 116 were PAP candidates and 52 were able to undergo polysomnography. PAP therapy was initiated in 35 subjects. At a 6-month follow-up visit, out of 34 stroke survivors, PAP adherence (PAP use of > 4 h per night) was present in 47%. Except for the significantly lower minimal nocturnal O2 saturation determined from the polysomnography (74.6 ± 11.7% vs. 81.8 ± 5.2%, p = 0.025), no other significant difference in characteristics of the groups with PAP adherence and PAP non-adherence was found. CONCLUSIONS: Less than half of the stroke subjects remained adherent to PAP therapy at 6 months post-PAP initiation. Special attention to support adaptation and adherence to PAP treatment is needed in this group of patients.

Association of lipoprotein levels with sleep apnea: role of autonomic dysfunction.

Objectives. Although multiple mechanisms, including autonomic dysfunction, seem to link sleep-disordered breathing (SDB) with dyslipidemia in animal studies, the data in clinical studies are limited. The aim of this study was to explore the association of lipoprotein levels with SDB measures in healthy habitual snorers. We supposed that autonomic dysfunction is the linking mechanism.Methods. We enrolled 110 previously healthy subjects with complaints of habitual snoring. To assess SDB, polysomnography was performed. Blood samples for the analysis of total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein cholesterol (LDL), and triglycerides (TG) were obtained in a fasting condition after the polysomnography. Baroreflex sensitivity (BRS) was used to assess the autonomic dysfunction.Results. In stepwise multiple linear regression analysis, minimal nocturnal blood oxygen saturation (beta=-0.240, p=0.020) and neck circumference (beta=0.224, p=0.03) were the only significant contributors in model predicting TG. SDB measures were not identified as significant contributors in models predicting TC, LDL, and HDL. We failed to find any significant difference in BRS in SDB subjects when compared according to the presence or absence of hypercholesterolemia/ hypertriglyceridemia. In SDB subjects, the area under the curve in a receiver operating curve to predict hypercholesterolemia and hypertriglyceridemia by BRS was 0.468 (95% CI: 0.328-0.608) and 0.425 (95% CI: 0.304-0.546), respectively.Conclusions. Our results suggest that minimal nocturnal blood oxygen saturation is significant contributor in model predicting TG. No significant decrease in BRS was found in SDB subjects with hypercholesterolemia and hypertriglyceridemia. In SDB subjects, the role of autonomic dys-function in the development of dyslipidemia remains controversial.

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.

The Comorbidity of Focal Epilepsy and Narcolepsy Type 1 - Two Case Reports.

The aim of this study is to remind the possibility of co-occurrence of epilepsy and narcolepsy. In the first case report, narcolepsy type 1 was diagnosed in 29-year-old female. After one year of the treatment with modafinil a new episodes of automatic behavior appeared. Patient was reevaluated and the diagnosis of focal epilepsy with partial complex seizures was established. Patient was treated with modafinil and lamotrigine and became seizure-free. In the second case report a 21-year-old female was referred with a typical history of narcolepsy type 1, but also with atypical episodes of gazing and automatic behavior with amnesia for these episodes. Narcolepsy type 1 and focal epilepsy was diagnosed. Some clinical symptoms of narcolepsy (cataplexy, automatic behavior, episodes of sleep attacks) need to be carefully analyzed by EEG and video-EEG not to overlook the epilepsy.

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.

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.

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.

Association of lipoprotein subfractions with endothelial function and arterial stiffness in acute ischemic stroke.

Hypercholesterolemia represents a risk factor for the development of atherosclerosis. Lipoprotein research has recently been focused on the phenomenon of atherogenic and non-atherogenic lipoproteins. The aim of this study was to explore the association of lipoprotein subfractions with a measure for endothelial function (represented by reactive hyperemia index [RHI]) and arterial stiffness (represented by augmentation index [AI]) in patients with acute ischemic stroke. We enrolled 51 patients with acute ischemic stroke. Blood samples were obtained within 24 h after the stroke onset in a fasting condition. Electrophoresis method on polyacrylamide gel was used for the analysis of plasma lipoproteins. RHI and AI was measured by peripheral arterial tonometry (EndoPAT2000 device). We failed to find any significant correlation between RHI and baseline characteristics of the population. Significant correlation was found between AI and age, hypertension, low density lipoprotein cholesterol (LDL) 1, LDL 3-7, score for anti-atherogenic risk and atherogenic profile. Age (beta = .362, p = .006) and LDL1 (beta = -0.283, p = .031) were the only independent variables significantly associated with AI in regression analysis. Significantly higher AI was found in an atherogenic lipoprotein profile compared to a non-atherogenic profile population (median 25% vs. median 11.5%, p = .043). In conclusion, our results suggest significant inverse correlation between levels of LDL 1 subfraction and measures of AI in patients with acute ischemic stroke. Significantly higher values of AI were observed in the population with an atherogenic lipoprotein profile.

Sleep-disordered breathing and excessive daytime sleepiness in patients with epilepsy - a polysomnographic study.

OBJECTIVES: Epilepsy and sleep-disordered breathing (SDB) are relatively common disorders. SDB induces repetitive arousals and sleep fragmentation and may cause symptomatic epileptic seizures or hypoxic encephalopathy. Epileptic seizures change sleep architecture with increase of light sleep and reduction of REM sleep, which may lead to central apneas. The aim of this study was to evaluate the relationship between SDB and daytime sleepiness in patients with epilepsy, who underwent polysomnography (PSG) due to problems with breathing during sleep or due to excessive daytime sleepiness. METHODS: We enrolled 40 patients with epilepsy. Type, etiology of epilepsy and actual antiepileptic therapy was recorded. All of them underwent overnight PSG. Excessive daytime sleepiness (EDS) was assessed by Epworth Sleepiness Scale (ESS). RESULTS: SDB (apnea-hypopnea index [AHI]<5) was present in 25 patients, 15 patients had no SDB (AHI≥5). EDS was present in 16 patients (40%). ESS significantly correlated with presence of symptomatic epilepsy (r=0.385, p=0.014), presence of SDB (r=0.524, p=0.001), AHI (r=0.416, p=0.003) and duration of REM sleep (r=-0.476, p=0.002). The presence of SDB (beta=0.447, p=0.002) and duration of REM sleep (beta=-0.308, p=0.029) were the only independent variables significantly associated with ESS in regression analysis. CONCLUSION: SDB has negative influence on quality of sleep and daytime vigility in patients with epilepsy. Sleep fragmentation with the reduction of the REM sleep seems to be the most important mechanism leading to EDS. We suppose that PSG could be beneficial in all patients with epilepsy and EDS.

Causes of Excessive Daytime Sleepiness in Patients with Acute Stroke--A Polysomnographic Study.

BACKGROUND: Sleep disorders are common in stroke patients. Sleep-disordered breathing (SDB), which is present in up to 72% of stroke patients, is the most frequent cause of excessive daytime sleepiness (EDS) in common population. The aim of this study was to assess the frequency of EDS in stroke patients and to analyze the impact of SDB, stroke severity, and location of stroke on EDS in the acute phase of stroke. METHODS: We enrolled 102 patients with the clinical diagnosis of acute stroke. Baseline clinical characteristics were recorded on admission. An Epworth sleepiness scale score higher than 9 was considered as EDS. To detect SDB, we performed standard overnight polysomnography within 4 ± 2 days after the stroke onset. RESULTS: EDS was present in 21 patients (20.6%). In a population with EDS, we found a significantly higher number of obstructive apneic pauses, central apneic pauses, as well as significantly higher values of respiratory disturbance index (RDI), RDI during nonrapid eye movement sleep, desaturation index, and significant decrease of REM sleep duration. RDI (odds ratio [OR], 1.031; 95% confidence interval [CI], 1.007-1.056; P = .01) and duration of REM sleep (OR, .922; 95% CI, .853-.997; P = .042) were the only independent variables significantly associated with EDS in a binary multivariate regression model. CONCLUSION: SDB is a common, significant, and treatable cause of EDS in acute stroke patients. We suppose that examination in sleep laboratories is reasonable in all stroke patients with EDS, although the impact of SDB therapy on EDS and overall outcome in acute stroke remains unknown.

Characteristics of Sleep-Disordered Breathing in Etiologic Subtypes of Minor-to-Moderate Acute Ischemic Stroke.

BACKGROUND: Sleep-disordered breathing (SDB) is frequent in stroke patients. A strong association has been suggested between SDB and atrial fibrillation (AF). In this study, we evaluated the characteristics of SDB in etiologic subtypes of acute ischemic stroke. We also investigated the relationship between SDB and AF in acute ischemic stroke. METHODS: We prospectively enrolled 72 patients with minor-to-moderate acute ischemic stroke. Clinical and laboratory characteristics of population were recorded on admission. SDB was assessed using standard polysomnography within 7 days after stroke onset. RESULTS: Apnea-hypopnea index (AHI) in small-vessel strokes was significantly lower than that in large-artery atherosclerosis strokes (P = .031), cardioembolic strokes (P = .011), and strokes of other or unknown etiology (.008). Desaturation index (DI) in small-vessel strokes was significantly lower than that in cardioembolic strokes and in large-artery strokes (P = .008, P = .035). Arousal index (AI) in large-artery strokes was significantly higher than that in small-vessel strokes (P = .013), cardioembolic strokes (P = .007), and strokes of other or unknown etiology (.027). In a multivariate regression model were age (odds ratio [OR], 1.083; 95% confidence interval [CI], 1.022-1.148; P = .007) and DI (OR, 1.037; 95% CI, 1.004-1.071; P = .026) the only significant variables independently associated with AF. CONCLUSIONS: We observed higher AHI, DI, and AI in large-artery strokes that may relate to more severe neurologic deficit in this subgroup. Age and DI were the only independent variables significantly associated with AF in acute ischemic stroke. Higher AHI and DI in cardioembolic strokes may thus mirror more frequent premorbid presence of SDB in patients with AF.

Is nocturnal epilepsy cause of disturbed quality of sleep and elevated daytime sleepiness?

OBJECTIVES: Authors evaluated quality of sleep and daytime vigilance in patients with nocturnal epilepsy and compared it to those with daytime epilepsy. BACKGROUND: Nocturnal seizures are an important type of epilepsy. They can result in morbidity due to disruption of sleep architecture. Daytime sleepiness, as a serious consequence of nocturnal seizures, has negative influence on quality of life in patients with epilepsy. METHODS: Authors examined 100 patients with epilepsy. The occurrence of epileptic seizures in circadian rhythm, type of epilepsy and epileptic seizures, as well as aetiology of epilepsy were evaluated. Patients were divided in two groups, 17 patients with nocturnal epilepsy and 83 patients with epileptic seizures not related to sleep. All of them underwent overnight video-EEG-polysomnography and they filled in the Epworth Sleepiness Scale questionnaire (ESS) as well as The Pittsburgh Sleep Quality Index questionnaire (PSQI). RESULTS: Overnight video-EEG-polysomnography detected significant changes in the sleep architecture in patients with nocturnal epilepsy. Significant decrease of N3 stage of NREM sleep (14.31%±8.07 in the group of nocturnal epilepsy vs. 20.12%±9.24 in the group of daytime epilepsy, p=0.01). Concurrently, significantly poorer sleep quality according to PSQI (18.52±7.51 in the group of nocturnal epilepsy vs. 6.21±3.62 in the group of daytime epilepsy, p=0.01) and tendency to increased daytime sleepiness according to ESS was revealed in these patients. CONCLUSION: Remarkable changes in sleep architecture associated with poor quality of sleep and increased daytime sleepiness were detected in patients with nocturnal epilepsy. In conclusion, we emphasize the importance of sleep history taking in patients with epilepsy and their further evaluation in sleep laboratory.

Predictors of impaired endothelial function in obstructive sleep apnea syndrome.

OBJECTIVES: Obstructive sleep apnea syndrome (OSA) is associated with increased cardiovascular morbidity and mortality. Endothelial dysfunction (ED), accelerated atherosclerosis and autonomic dysfunction might be the key players responsible for development of vascular diseases in patients with OSA. In a population with suspected OSA and low burden of cardiovascular risk factors, we therefore aimed to investigate the association between potential cardiovascular risk factors including OSA-specific indices, ED and autonomic activity. METHODS: ED was investigated using reperfusion hyperaemia index (RHI). OSA was assessed using standard polysomnography, autonomic activity was assessed using baroreflex sensitivity (BRS). RESULTS: We enrolled 31 patients (42.1±11.7 years) with OSA. Significant inverse correlation was found between RHI and apnea-hypopnea index (AHI) (r=-0.550, p=0.001) and between RHI desaturation index (r=-0.533, p=0.002). Positive correlation was found between RHI and minimal nocturnal oxygen saturation (r=0.394, p=0.028). In a multiple regression model AHI was the only significant variable to predict RHI (ß=-0.522, p=0.003). We found no correlation between RHI and BRS. RHI in the population with severe OSA (AHI above 30) was significantly lower than RHI in the rest of the population (p=0.012). CONCLUSION: AHI was the only significant independent predictor of impaired endothelial function as expressed by RHI. RHI showed no association with BRS in patients with OSA.

The Interplay of Dyslipidemia, Oxidative Stress, and Clinical Outcomes in Acute Ischemic Stroke Patients with and without Coronary Artery Disease.

We assessed lipid and lipoprotein profiles, along with oxidative stress (OS) parameters, in patients within the crucial 24 h period following an acute ischemic stroke (AIS), comparing those with and without coronary artery disease (CAD). We aimed to correlate these measures with clinical condition scales (NIHSS, mRS) post-AIS. This study included 27 AIS patients without CAD (AIS group) and 37 AIS patients with CAD (CAD-AIS group). Using polyacrylamide gel electrophoresis (Lipoprint system), we determined plasma LDL and HDL subfractions. Spectrophotometric methods were used to assess plasma antioxidant capacity, lipoperoxides, homocysteine (HC) levels, paraoxonase1, and catalase activities. We also measured urine isoprostanes and the activities of antioxidant enzymes (SOD, GPx) with commercial kits. CAD-AIS patients had notably higher HC levels, while there were no significant differences in lipoprotein subfractions and OS parameters between both groups. In the AIS group, mRS scores showed negative correlations with catalase, GPx activities, and total cholesterol. In the CAD-AIS group, atherogenic lipoproteins (IDLC, LDL2, LDL3-7) exhibited a significant positive correlation with mRS. This study underscores the role of dyslipidemia and OS in the development of AIS and CAD. It emphasizes the complex connections between specific biomarkers and post-stroke clinical outcomes. Our results suggest a significant impact of CAD treatment on lipid profile but not on homocysteine levels. The traditional narrative associating high cholesterol as the ultimate risk factor for cardiovascular diseases needs to be challenged, at least with respect to neurological outcomes. These insights may guide more targeted therapeutic approaches.

No Difference in Sleep Desaturations Severity between Patients with Wake-Up and Non-Wake-Up Stroke: A PRESS Study Results.

BACKGROUND: Wake-up stroke (WUS) is a certain type of ischemic stroke in which a patient wakes up with a new neurological deficit due to cerebral ischemia. Sleep-disordered breathing is an independent risk factor for stroke, but the role of nocturnal oxygen desaturation in the pathophysiology of WUS is still insufficiently explored. According to several studies, patients with WUS have a significantly more severe sleep apnea syndrome and lower mean blood oxygen saturation. This study aimed to assess the severity of nocturnal desaturations in acute WUS and non-WUS patients using nocturnal pulse oximetry. MATERIAL AND METHODS: The cohort of 225 consecutive patients with neuroimaging-verified acute cerebral ischemia was prospectively enrolled. For further analyses, 213 subjects with known WUS/non-WUS status were selected (111 males and 102 females, average age 70.4 ±12.9, median baseline NIHSS = 5, median baseline mRS = 3). Patients were divided into the WUS group (n = 45) and the non-WUS group (n = 168). Overnight pulse oximetry was performed within 7 days of the stroke onset and data of both of the studied groups were compared. RESULTS: We found oxygen desaturation index (ODI) in the WUS group was 14.5 vs. 16.6 (p = 0.728) in the non-WUS group, basal O2 saturation was 92.2% vs. 92.5% (p = 0.475), average low O2 saturation was 90.3% vs. 89.6% (p = 0.375), minimal O2 saturation was 79.5% vs. 80.6% (p = 0.563), and time with O2 saturation <90% (T90) was 4.4% vs. 4.7% (p = 0.729). CONCLUSIONS: In the studied sample, monitored respiratory parameters including ODI, basal O2 saturation, average low O2 saturation, minimal O2 saturation, and T90 did not significantly differ between groups of WUS and non-WUS patients.

Lipoprotein Subfractions Associated with Endothelial Function in Previously Healthy Subjects with Newly Diagnosed Sleep Apnea-A Pilot Study.

BACKGROUND: Obstructive sleep apnea (OSA) activates several pathophysiological mechanisms which can lead to the development of vascular diseases. Endothelial dysfunction (ED) is an initial step in the development of atherosclerosis. The association between ED and OSA has been described in several studies, even in previously healthy subjects. High-density lipoproteins (HDL) were generally considered to be atheroprotective, and low-density lipoprotein (LDL) to be an atherogenic component of lipoproteins. However, recent findings suggest a pro-atherogenic role of small HDL subfractions (8-10) and LDL subfractions (3-7). This study aimed to evaluate the relationship between endothelial function and lipid subfractions in previously healthy OSA subjects. MATERIAL AND METHODS: We prospectively enrolled 205 subjects with sleep monitoring. Plasma levels of triacylglycerols, total cholesterol, LDL, HDL, and their subfractions were assessed. Endothelial function was determined using peripheral arterial tonometry, and reperfusion hyperemia index (RHI) was assessed. RESULTS: Plasma levels of small and intermediate HDL subfractions have statistically significant pro-atherogenic correlations with endothelial function (p = 0.015 and p = 0.019). In other lipoprotein levels, no other significant correlation was found with RHI. In stepwise multiple linear regression analysis, small HDL (beta = -0.507, p = 0.032) was the only significant contributor in the model predicting RHI. CONCLUSIONS: In our studied sample, a pro-atherogenic role of small HDL subfractions in previously healthy subjects with moderate-to-severe OSA was proven.

Vasovagal (neurocardiogenic) syncope in the clinical practice.

OBJECTIVES: Vasovagal syncope (VVS) is the most common type of syncope with the incidence of 21-43%. The aim of this study was to explain difficulties of correct diagnosis of VVS. DESIGN AND METHODS: Our group comprises 70 patients (24 men, 46 women) at the age of 15-71 years, in whom VVS was verified by the head-up tilt test (HUT-test). We evaluated the type of VVS, admission diagnoses present in the patients, interictal EEG findings and the presence of convulsions during the syncopal states. For statistical processing of the results we used binomial tests for two independent proportions, Fisher-Freeman-Haltons exact test and Cramér's V index. RESULTS: Out of 70 VVS 35 were vasodepressoric, 19 cardioinhibitive and 16 intermediate. Admission diagnoses present in the patients were: disorders of consciousness of an unknown etiology - 42.9% cases; supposable epilepsy and epilepsy - 30% cases and syncope - 27.1% cases. Interictal EEG was normal in 51.4% cases, nonepileptiform abnormality was present in 48.6% cases. Statistical comparison among particular types of VVS revealed a significant difference in distribution and medial strong association between the type of VVS and the EEG finding (Cramér V=0.35) and also between the type of VVS and the occurrence of convulsions (Cramér V= 0.40). CONCLUSION: The results of our study evidently suggest that interdisciplinary cooperation in accurate diagnostics in this field of medicine is needed and that HUT-test has to be in standard diagnostic algorithm in patients with failures of consciousness of an unknown cause.

Psychotic Episode and Schizophrenia in Slovakian Narcolepsy Database.

Narcolepsy type 1 (NT1), a central disorder of hypersomnolence, is associated with mood, anxiety or hyperactivity mental disorders. Association with psychotic episode or schizophrenia is rare and could be the source of diagnostic and therapeutic difficulties. Their frequency in the national narcolepsy database has not been systematically studied. The aim of the presented study was to calculate the frequency of NT1 patients diagnosed with psychosis and/or schizophrenia, to identify clinical characteristics of these cases, and to look for narcoleptic and psychotic symptoms during re-evaluation years later. We identified three (4%) cases diagnosed with a psychotic episode in the course of NT1. They were diagnosed with NT1 by age ≤18 years. In the re-evaluation (mean follow-up 9.8 years), we identified one case with a dual diagnosis of NT1 and schizophrenia; two cases were diagnosed with a solitary psychotic episode in the course of NT1. NT1 patients diagnosed in the age ≤18 years are at higher risk of psychotic episode, and this may be related to higher vulnerability during the ongoing neurodevelopmental period. Comorbid schizophrenia with NT1 in the Slovakian Narcolepsy Database was within the prevalence expected in the general population. The solitary psychotic episode in the course of NT1 did not reduce the possibility of subsequent symptomatic treatment afterwards.

Cognition in Patients with Sleep-Disordered Breathing: Can Obstructive and Central Apneic Pauses Play a Different Role in Cognitive Impairment?

BACKGROUND: There are increasing data linking sleep apnea with cognitive impairment. We aimed to clarify the relationship between sleep-disordered breathing (SDB) and cognition. Detailed attention was assigned to the potential role of central versus obstructive apneic pauses in cognitive impairment. METHODS: Patients with suspected SDB were prospectively enrolled, and a complex sleep study was performed that included overnight polysomnography. A revised version of Addenbrooke's Cognitive Examination (ACE-R) was used to assess cognition, evaluating overall cognition and individual subdomains. RESULTS: A total number of 101 participants were included in the study. In multivariate binary logistic regression analysis, obstructive apnea index ([OAI], 95% CI: 1.009-1.057, p = 0.008) was the only significant contributor to the model predicting attention deficit. The proportion of N1 stage of NREM sleep was the only significant contributor to the model predicting impaired verbal fluency (95% CI: 1.004-1.081, p = 0.029). No significant differences in sleep-related indices were observed in the remaining ACE-R subdomains. CONCLUSION: Except for verbal fluency and attention, we failed to find any significant association of sleep-related indices with the impairment in different cognitive subdomains. Our data suggest that impairment observed in verbal fluency is associated with a higher proportion of shallow NREM sleep, and attention deficit is associated with higher OAI. Obstructive respiratory episodes seem to play a more important role in cognitive impairment when compared to central ones.