Background: Obstructive sleep apnoea (OSA) is a common disease with breathing disturbances during sleep. Sulthiame (STM), a carbonic anhydrase (CA) inhibitor, was recently shown to reduce OSA in a significant proportion of patients. CA activity and hypoxia-inducible factor (HIF)-1α are two potential biomarkers reported in severe OSA and hypoxia.
View Article and Find Full Text PDFStudy Objectives: Advanced signal processing of photoplethysmographic data enables novel analyses which may improve the understanding of the pathogenesis of dysglycemia associated with sleep disorders. We aimed to identify sleep-related pulse wave characteristics in diabetic patients compared to normoglycemic individuals, independent of cardiovascular-related comorbidities.
Methods: This cross-sectional evaluation of the population-based Swedish CArdioPulmonary bioImage Study (SCAPIS) included overnight oximetry-derived pulse wave data from 3997 subjects (45 % males, age 50-64 years).
Sleep-disordered breathing, ranging from habitual snoring to severe obstructive sleep apnea, is a prevalent public health issue. Despite rising interest in sleep and awareness of sleep disorders, sleep research and diagnostic practices still rely on outdated metrics and laborious methods reducing the diagnostic capacity and preventing timely diagnosis and treatment. Consequently, a significant portion of individuals affected by sleep-disordered breathing remain undiagnosed or are misdiagnosed.
View Article and Find Full Text PDFBackground: The carbonic anhydrase inhibitor sulthiame reduces OSA severity, increases overnight oxygenation, and improves sleep quality. Insights into how sulthiame modulates OSA pathophysiologic features (endotypic traits) adds to our understanding of the breathing disorder itself, as well as the effects of carbonic anhydrases in respiratory regulation.
Research Question: How does sulthiame treatment modify endotypic traits in OSA?
Study Design And Methods: Per-protocol tertiary analysis of a randomized controlled trial with the inclusion criteria as follow: BMI, ≥ 20 to ≤ 35 kg/m; age, 18-75 years; apnea-hypopnea index (AHI) ≥ 15 events/h; Epworth sleepiness scale score, ≥ 6; as well as nonacceptance or nontolerance of positive airway pressure treatment.
Background: Emerging data suggest that determination of physiologic endotypic traits (eg, loop gain) may enable precision medicine in OSA.
Research Question: Does a single-night assessment of polysomnography-derived endotypic traits provide reliable estimates in moderate to severe OSA?
Study Design And Methods: Two consecutive in-lab polysomnography tests from a clinical trial (n = 67; male, 69%; mean ± SD age, 61 ± 10 years; apnea-hypopnea index [AHI] 53 ± 22 events/h) were used for the reliability analysis. Endotypic traits, reflecting upper airway collapsibility (ventilation at eupneic drive [V]), upper airway dilator muscle tone (ventilation at the arousal threshold [V]), loop gain (stability of ventilatory control, LG1), and arousal threshold (ArTh) were determined.
Recent evidence supports the use of pulse wave analysis during sleep for assessing functional aspects of the cardiovascular system. The current study compared the influence of pulse wave and sleep study-derived parameters on cardiovascular risk assessment. In a multi-centric study design, 358 sleep apnea patients (age 55 ± 13 years, 64% male, body mass index 30 ± 6 kg m , apnea-hypopnea index 13 [5-26] events per hr) underwent a standard overnight sleep recording.
View Article and Find Full Text PDFInsomnia has been associated with increased cardiovascular (CV) risk, which may be linked to sympathetic activation. Non-invasive overnight pulse wave analysis may be a useful tool to detect early signs of autonomic changes during sleep in insomniacs. Fifty-two participants (26 men, 37±13 years, BMI: 24±5 kg/m2, 26 insomniacs/ 26 controls) underwent overnight polysomnography with pulse oximetry and pulse wave analysis including pulse rate, vascular stiffness (pulse propagation time, PPT), and a composite cardiac risk index based on autonomic function and overnight hypoxia.
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