Sleep Apnea and Heart.
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ABSTRACT:
SUBMITTER: Kwon Y
PROVIDER: S-EPMC7375706 | biostudies-literature | 2019 Dec
REPOSITORIES: biostudies-literature
Publications
Sleep Apnea and Heart.
Kwon Younghoon Y Logan Jeongok J Pusalavidyasagar Snigdha S Kasai Takatoshi T Cheong Crystal Sj CS Lee Chi-Hang CH
Sleep medicine research 20191231 2
Scientific investigations in the past few decades have supported the important role of sleep in various domains of health. Sleep apnea is a highly prevalent yet underdiagnosed sleep disorder representing a valid cardiovascular risk factor, particularly for hypertension. While several studies have demonstrated the benefits of sleep apnea treatment on subclinical cardiovascular measures, there is a paucity of studies proving reduction of cardiovascular events and mortality. Sufficient and high-qua ...[more]
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Project description:This study examines the relationship between sleep apnea and glucose metabolism. Physiological studies have demonstrated that 5 days of exposure to intermittent hypoxia (similar to what occurs with sleep apnea) leads to significant improvements in glucose tolerance. Therefore, this study investigates the hypothesis that intermittent hypoxia may lead to upregulation of some novel peptide(s) that have a powerful glucose lowering action. Keywords: other
2003-07-16 | GSE480 | GEO
Project description:RationaleAlthough obstructive sleep apnea is associated with physiological perturbations that increase risk of hypertension and are proatherogenic, it is uncertain whether sleep apnea is associated with increased stroke risk in the general population.ObjectivesTo quantify the incidence of ischemic stroke with sleep apnea in a community-based sample of men and women across a wide range of sleep apnea.MethodsBaseline polysomnography was performed between 1995 and 1998 in a longitudinal cohort study. The primary exposure was the obstructive apnea-hypopnea index (OAHI) and outcome was incident ischemic stroke.Measurements and main resultsA total of 5,422 participants without a history of stroke at the baseline examination and untreated for sleep apnea were followed for a median of 8.7 years. One hundred ninety-three ischemic strokes were observed. In covariate-adjusted Cox proportional hazard models, a significant positive association between ischemic stroke and OAHI was observed in men (P value for linear trend: P = 0.016). Men in the highest OAHI quartile (>19) had an adjusted hazard ratio of 2.86 (95% confidence interval, 1.1-7.4). In the mild to moderate range (OAHI, 5-25), each one-unit increase in OAHI in men was estimated to increase stroke risk by 6% (95% confidence interval, 2-10%). In women, stroke was not significantly associated with OAHI quartiles, but increased risk was observed at an OAHI greater than 25.ConclusionsThe strong adjusted association between ischemic stroke and OAHI in community-dwelling men with mild to moderate sleep apnea suggests that this is an appropriate target for future stroke prevention trials.
| S-EPMC2913239 | biostudies-literature
Project description: Not available
| S-EPMC7258646 | biostudies-literature
Project description:Rationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses. Methods: Patients scheduled to undergo ventral hernia repair surgery were recruited to wear a portable home sleep monitor for two nights prior to surgery. Visceral fat biopsies were obtained intra-operatively. RNA was extracted and whole-genome expression profiling was performed. Gene Set Enrichment Analysis (GSEA) was used to identify curated gene sets that were differentially enriched in OSA subjects. Network analysis was applied to a select set of highly enriched pathways. Results: 10 patients with OSA and 8 control subjects were recruited. There were no differences in age, gender, body mass index between the two groups, but the OSA subjects had a significantly higher respiratory disturbance index (19.2 vs. 0.6, P-value 0.05) and worse hypoxemia (minimum oxygen saturation 79.7% vs. 87.8%, P-value < 0.001). GSEA identified a number of gene sets up-regulated in adipose tissue of OSA patients including the pro-inflammatory NF-M-NM-:B pathway and the proteolytic ubiquitin/proteasome module. A critical metabolic pathway, the peroxisome proliferator-activated receptor (PPAR), was down-regulated in subjects with OSA. Network analysis linked members of these modules together and identified regulatory hubs. Conclusions: OSA is associated with alterations in visceral fat gene expression. Pathway-based network analysis highlighted perturbations in several key pathways whose coordinated interactions may contribute to the metabolic dysregulation observed in this complex disorder. Total RNA from visceral fat of 18 subjects (10 OSA, 8 Control) was hybridized to 18 Affymetrix Genechip Human Gene 1.0 ST microarrays.
2012-09-01 | E-GEOD-38792 | biostudies-arrayexpress
Project description:Rationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses. Methods: Patients scheduled to undergo ventral hernia repair surgery were recruited to wear a portable home sleep monitor for two nights prior to surgery. Visceral fat biopsies were obtained intra-operatively. RNA was extracted and whole-genome expression profiling was performed. Gene Set Enrichment Analysis (GSEA) was used to identify curated gene sets that were differentially enriched in OSA subjects. Network analysis was applied to a select set of highly enriched pathways. Results: 10 patients with OSA and 8 control subjects were recruited. There were no differences in age, gender, body mass index between the two groups, but the OSA subjects had a significantly higher respiratory disturbance index (19.2 vs. 0.6, P-value 0.05) and worse hypoxemia (minimum oxygen saturation 79.7% vs. 87.8%, P-value < 0.001). GSEA identified a number of gene sets up-regulated in adipose tissue of OSA patients including the pro-inflammatory NF-κB pathway and the proteolytic ubiquitin/proteasome module. A critical metabolic pathway, the peroxisome proliferator-activated receptor (PPAR), was down-regulated in subjects with OSA. Network analysis linked members of these modules together and identified regulatory hubs. Conclusions: OSA is associated with alterations in visceral fat gene expression. Pathway-based network analysis highlighted perturbations in several key pathways whose coordinated interactions may contribute to the metabolic dysregulation observed in this complex disorder.
2012-09-01 | GSE38792 | GEO
Project description:Study objectivesTo evaluate home sleep apnea testing (HSAT) using a type 3 portable monitor to help diagnose sleep-disordered breathing (SDB) and identify respiratory events including obstructive sleep apnea, central sleep apnea, and Cheyne-Stokes respiration in adults with stable chronic heart failure.MethodsEighty-four adults with chronic heart failure (86.9% males, age [mean ± standard deviation] 58.7 ± 16.3 years, body mass index 29.4 ± 13.0 kg/m², left ventricular ejection fraction 40.3% ± 11.5%) performed unattended HSAT followed by an in-laboratory polysomnography (PSG) with simultaneous portable monitor recording.ResultsThe apnea-hypopnea index was 22.0 ± 17.0 events/h according to HSAT, 26.8 ± 20.5 events/h on an in-laboratory portable monitor, and 23.8 ± 21.3 events/h using PSG (P = .373). A Bland-Altman analysis of the apnea-hypopnea index using HSAT vs PSG showed a mean difference (95% confidence interval) of -2.4 (-4.9 to 0.1) events/h and limits of agreement (±2 standard deviations) of -24.1 to 19.2 events/h. HSAT underestimated the apnea-hypopnea index to a greater extent at a higher apnea-hypopnea index (rho = -.358; P < .001). Similar levels of agreement from HSAT vs PSG were observed when comparing the obstructive apnea index, central apnea index, and percentage of time in a Cheyne-Stokes respiration pattern. When we used an apnea-hypopnea index ≥ 5 events/h to diagnose SDB, HSAT had 86.7% sensitivity, 76.5% specificity, 92.9% positive predictive value, and 61.9% negative predictive value compared to PSG. Detection of Cheyne-Stokes respiration using HSAT showed 94.6% sensitivity, 91.1% specificity, 88.6% positive predictive value, and 97.6% negative predictive value compared to PSG.ConclusionsHSAT with a type 3 portable monitor can help diagnose SDB and identify obstructive sleep apnea, central sleep apnea, and Cheyne-Stokes respiration events in adults with chronic heart failure.
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Project description:Heart failure (HF) affects 23 million people worldwide and results in 300000 annual deaths. It is associated with many comorbidities, such as obstructive sleep apnea (OSA), and risk factors for both conditions overlap. Eleven percent of HF patients have OSA and 7.7% of OSA patients have left ventricular ejection fraction <50% with arrhythmias being a significant comorbidity in HF and OSA patients. Forty percent of HF patients develop atrial fibrillation (AF) and 30%-50% of deaths from cardiac causes in HF patients are from sudden cardiac death. OSA is prevalent in 32%-49% of patients with AF and there is a dose-dependent relationship between OSA severity and resistance to anti-arrhythmic therapies. HF and OSA lead to various downstream arrhythmogenic mechanisms, including metabolic derangement, remodeling, inflammation, and autonomic imbalance. (1) Metabolic derangement and production of reactive oxidative species increase late Na+ currents, decrease outward K+ currents and downregulate connexin-43 and cell-cell coupling. (2) remodeling also features downregulated K+ currents in addition to decreased Na+/K+ ATPase currents, altered Ca2+ homeostasis, and increased density of If current. (3) Chronic inflammation leads to downregulation of both Nav1.5 channels and K+ channels, altered Ca2+ homeostasis and reduced cellular coupling from alterations of connexin expression. (4) Autonomic imbalance causes arrhythmias by evoking triggered activity through increased Ca2+ transients and reduction of excitation wavefront wavelength. Thus, consideration of these multiple pathophysiological pathways (1-4) will enable the development of novel therapeutic strategies that can be targeted against arrhythmias in the context of complex disease, such as the comorbidities of HF and OSA.
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