Augmented Resting Sympathetic Activity in Awake Patients With Obstructive Sleep Apnea

Carlson, Jan; Hedner, Jan; Elam, Mikael; Ejnell, Hasse; Sellgren, Johan; Wallin, B. Gunnar

doi:10.1378/chest.103.6.1763

Cited by 608 publications

(403 citation statements)

References 21 publications

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“…Regardless of the method used, essentially all studies have reported that OSA is associated with increased sympathetic activity. 20,22,24,25 Furthermore, unlike the situation in normal subjects, blood pressure 26 and sympathetic activity remain high during sleep in OSA patients. These findings highlight the challenges of using autonomic signals to detect sleep stages in OSA patients.…”

Section: Light/deep Sleep Detectionmentioning

confidence: 98%

Sleep Staging Based on Autonomic Signals: A Multi-Center Validation Study

Hedner

White

Malhotra

et al. 2011

Journal of Clinical Sleep Medicine

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119

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Study Objectives: One of the most important caveats of ambulatory devices is the inability to record and stage sleep. We assessed an algorithm determining 4 different stages: wake, light sleep, deep sleep, and REM sleep using signals derived from the portable monitor Watch-PAT100 (PAT recorder). Methods: Participants (38 normal subjects and 189 patients with obstructive sleep apnea [OSA]) underwent simultaneous overnight recordings with polysomnography (PSG) and the PAT recorder in a study originally designed to assess the accuracy of the PAT recorder in diagnosing OSA. Light/deep sleep and REM sleep from the PAT recorder recording were automatically scored based on features extracted from time series of peripheral arterial tone amplitudes and inter pulse periods. The PSG scored sleep stages 1 and 2 were classified as light sleep for epoch-by-epoch comparisons. Results:The overall agreement in detecting light/deep and REM sleep were 88.6% ± 5.9% and 88.7% ± 5.5%, respectively. There was a good agreement between PSG and the PAT recorder in quantifying sleep efficiency (78.4% ± 9.9% vs. 78.8% ± 13.4%), REM latency (237 ± 148 vs. 225 ± 159 epochs), and REM percentage (14.4% ± 6.5% vs. 19.3% ± 8.7%). OSA severity did not affect the sensitivity and specificity of the algorithm. The Cohen κ coefficient for detecting all sleep stages: sleep from wake, REM from NREM sleep, and deep from light sleep were 0.48, 0.55, 0.59, and 0.46, respectively. Conclusions: Analysis of autonomic signals from the PAT recorder can detect sleep stages with moderate agreement to more standard techniques in normal subjects and OSA patients. This novel algorithm may provide insights on sleep and sleep architecture when applying the PAT recorder for OSA diagnosis.

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Section: Light/deep Sleep Detectionmentioning

confidence: 98%

Sleep Staging Based on Autonomic Signals: A Multi-Center Validation Study

Hedner

White

Malhotra

et al. 2011

Journal of Clinical Sleep Medicine

Self Cite

119

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“…The first included eleven obese OSA patients 28 who were not fully matched to the healthy control subjects for age or BMI. NPY in the OSA patients was not increased and the authors explained their negative results by the low sympathetic nerve activity (SNA) of the patients they included, as NPY is a marker of sympathetic activation.…”

Section: Neuropeptides and Impaired Glucose Tolerancementioning

confidence: 99%

Lack of Association Between Impaired Glucose Tolerance and Appetite Regulating Hormones in Patients with Obstructive Sleep Apnea

Patterson¹,

Twigg²,

Vazir³

et al. 2011

Journal of Clinical Sleep Medicine

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Study Objectives: Understanding the etiologic mechanisms underlying impaired glucose tolerance in obstructive sleep apnea (OSA) would assist development of therapies against this comorbidity. We hypothesized that in patients with OSA impaired glucose tolerance (IGT) would be associated with elevated levels of hormones associated with appetite regulation (leptin, ghrelin, neuropeptide Y [NPY] and peptide tyrosine-tyrosine [PYY]). Method: We studied 68 OSA patients (mean AHI 22 events/h) and 37 age and weight matched healthy controls recruited by advertisement. All participants received a standardized evening meal, attended polysomnography and an oral glucose tolerance test (OGTT) on waking. Hormones were measured in blood taken before sleep (22:30) and at the start of the OGTT. Results: Impaired glucose tolerance was present in 54% of patients and 32% of controls (p = 0.05). The only differences between groups was that leptin was signifi cantly higher at 22:30 in OSA patients compared to controls (9.6 ng/L vs 7.9 ng/L, p = 0.05). OSA patients had marginally elevated plasma NPY levels at 22:30 (56.6 [52, 67] S C I E N T I F I C I N v E S T I G A T I O N SU ntreated obstructive sleep apnea (OSA) is associated with insulin resistance, 1,2 and some studies suggest that treatment with CPAP improves glucose control, 3,4 although this was not found in a randomized controlled trial of diabetics with sleep apnea. 5 The observation that established type 2 diabetics cannot improve glucose control when their OSA is treated with CPAP, emphasizes the importance of understanding the pathophysiology of insulin resistance associated with OSA.One mechanism linking OSA with impaired glucose tolerance could be sympathetic nerve activity which is a recognized phenomenon in OSA 6 ; indeed it has previously been hypothesized that this process is responsible for the elevated leptin levels seen in newly diagnosed OSA patients. 7 Consistent with this sibutramine, a serotonin and noradrenaline reuptake inhibitor, was able to improve insulin resistance in OSA independent of visceral fat. 8 Moreover two studies raise the hypothesis that hormones involved in appetite regulation could contribute to impaired glucose tolerance. Broglio et al. 9 demonstrated that ghrelin administered to healthy subjects simultaneously with glucose, resulted in a transient decrease of insulin concentration that was coupled with signifi cant increase in glucose levels. In addition it has been reported that IR is associated with increased plasma leptin concentration independent of the body fat. 10 Consistent with this hypothesis, previous studies have reported that OSA is independently associated with neuroendocrine dysregulation; in fact OSA has been reported to be bRIEF SUMMARY Current knowledge/Study Rationale: Impaired glucose tolerance is a common and important co-morbidity of obstructive sleep apnea yet its pathogenesis, beyond the shared etiology of obesity is unknown. Here we tested the hypothesis that OSA might induce increases of appetite regulating h...

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“…In type 2 diabetic patients, euglycemic-hyperinsulinemic clamp studies similarly show evidence of improved insulin sensitivity with CPAP (90), with evidence as well of improvement in postprandial glycemia in those using CPAP Ͼ4 h/night, with progressive improvement in A1C in these persons over a 5-month period of treatment (91) and evidence of improved glycemic patterns with continuous glucose monitoring studies. The mechanisms of adverse effect of OSA appear to involve sympathetic activation, with increased muscle sympathetic activity in persons with OSA with and without hypertension and with increased circulating norepinephrine levels (92), with sympathetic nerve activity and blood pressure increased during periods of nocturnal wakefulness, responding to CPAP treatment (93). Experimental sleep deprivation is associated with increased serum cortisol levels on the following evening (83), another potential mechanism of adverse metabolic effect, with CPAP reversing the hypercortisolemia (94).…”

Section: Nonalcoholic Fatty Liver Diseasementioning

confidence: 99%

Third Annual World Congress on the Insulin Resistance Syndrome

Bloomgarden

2006

Diabetes Care

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Augmented Resting Sympathetic Activity in Awake Patients With Obstructive Sleep Apnea

Cited by 608 publications

References 21 publications

Sleep Staging Based on Autonomic Signals: A Multi-Center Validation Study

Sleep Staging Based on Autonomic Signals: A Multi-Center Validation Study

Lack of Association Between Impaired Glucose Tolerance and Appetite Regulating Hormones in Patients with Obstructive Sleep Apnea

Third Annual World Congress on the Insulin Resistance Syndrome

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