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Results for “Sleep Apnea, Obstructive”

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PubMed2005

The effect of continuous positive airway pressure on glucose control in diabetic patients with severe obstructive sleep apnea.

Obstructive sleep apnea (OSA) is independently associated with glucose intolerance and insulin resistance, and recent studies have shown that continuous positive airway pressure (CPAP) improves insulin sensitivity. The objective of this study was to describe the change in glycosylated hemoglobin (HbA1c) after treatment with CPAP in patients with type 2 diabetes mellitus and OSA. To test this hypothesis, we performed a retrospective analysis of 38 patients seen in the sleep clinic of an urban public teaching hospital. All patients had OSA and type 2 diabetes mellitus, and their diabetic medication regimen had remained unchanged during the period of CPAP therapy. Sixty-one percent were men, body mass index was 42+/-9.5 kg/m(2), and the Apnea-Hypopnea Index was 53+/-36 per hour. HbA1c before therapy with CPAP was 7.8+/-1.4% and decreased to 7.3+/-1.3% after 134+/-119 days of therapy (p<0.001). Treatment with CPAP leads to a clinically significant drop in HbA1c in patients with type 2 diabetes mellitus and severe OSA.

Blood Glucose↗

PubMed2006

Nasal pressure recordings to detect obstructive sleep apnea.

Obstructive sleep apnea (OSA) is a common disease. Given the costs of in-laboratory polysomnography (PSG), alternative ambulatory methods for accurate diagnosis are desirable. The objective of this study was to evaluate the performance of a simple device (SleepCheck) to identify patients with sleep apnea. A total of 30 consecutive patients with suspected OSA syndrome referred to the sleep clinic were prospectively evaluated with standard PSG and SleepCheck simultaneously during an in-laboratory, supervised full-night diagnostic study. The PSG apnea and hypopnea index (AHI) was evaluated according to standard criteria, and SleepCheck assessed the respiratory disturbance index (RDI) based on nasal cannula pressure fluctuations. Compared to the full-night PSG, SleepCheck systematically overscored respiratory events (the mean difference between SleepCheck RDI and PSG AHI was 27.4+/-13.3 events per hour). This overscoring was in part related to normal physiologic decreases in flow during rapid eye movement sleep or after an arousal. However, there was reasonable correlation between AHI and RDI (r=0.805). Receiver operating characteristic curves with threshold values of AHI of 10 and 20/h demonstrated areas under the curves (AUCs) of 0.915 and 0.910, respectively. Optimum combinations of sensitivity and specificity for these thresholds were calculated as 86.4/75.0 and 88.9/81.0, respectively. Overall, the SleepCheck substantially overscored apneas and hypopneas in patients with suspected OSA. However, after correction of the bias, the SleepCheck had reasonable accuracy with an AUC, sensitivity, and specificity similar to other ambulatory type 4 devices currently available.

Adult↗

PubMed2006

Evidence for activation of nuclear factor kappaB in obstructive sleep apnea.

Obstructive sleep apnea (OSA) is a risk factor for atherosclerosis, and atherosclerosis evolves from activation of the inflammatory cascade. We propose that activation of the nuclear factor kappaB (NF-kappaB), a key transcription factor in the inflammatory cascade, occurs in OSA. Nine age-matched, nonsmoking, and non-hypertensive men with OSA symptoms and seven similar healthy subjects were recruited for standard polysomnography followed by the collection of blood samples for monocyte nuclear p65 concentrations (OSA and healthy groups). In the OSA group, p65 and of monocyte production of tumor necrosis factor alpha (TNF-alpha) were measured at the same time and after the next night of continuous positive airway pressure (CPAP). p65 Concentrations in the OSA group were significantly higher than in the control group [median, 0.037 ng/microl (interquartile range, 0.034 to 0.051) vs 0.019 ng/microl (interquartile range, 0.013 to 0.032); p = 0.008], and in the OSA group were significantly correlated with apnea-hypopnea index and time spent below an oxygen saturation of 90% (r = 0.77 and 0.88, respectively) after adjustment for age and BMI. One night of CPAP resulted in a reduction in p65 [to 0.020 ng/mul (interquartile range, 0.010 to 0.036), p = 0.04] and levels of TNF-alpha production in cultured monocytes [16.26 (interquartile range, 7.75 to 24.85) to 7.59 ng/ml (interquartile range, 5.19 to 12.95), p = 0.01]. NF-kappaB activation occurs with sleep-disordered breathing. Such activation of NF-kappaB may contribute to the pathogenesis of atherosclerosis in OSA patients.

Adult↗

PubMed2003

Functional magnetic resonance imaging responses to expiratory loading in obstructive sleep apnea.

Obstructive sleep apnea (OSA) is characterized by diminished upper airway muscle phasic and tonic activation during sleep, but enhanced activity during waking. We evaluated neural mechanisms underlying these patterns with functional magnetic resonance imaging procedures during baseline and expiratory loading conditions in nine medication-free OSA and 16 control subjects. Both groups developed similar expiratory loading pressures, but appropriate autonomic responses did not emerge in OSA cases. Reduced neural signals emerged in OSA cases within the frontal cortex, anterior cingulate, cerebellar dentate nucleus, dorsal pons, anterior insula and lentiform nuclei. Signal increases in OSA over control subjects developed in the dorsal midbrain, hippocampus, quadrangular cerebellar lobule, ventral midbrain and ventral pons. Fastigial nuclei and the amygdala showed substantially increased variability in OSA subjects. No group differences were found in the thalamus. OSA patients show aberrant responses in multiple brain areas and inappropriate cardiovascular responses to expiratory loading, perhaps as a consequence of previously-demonstrated limbic, cerebellar and motor area gray matter loss.

Adult↗

PubMed2003

Genomic approaches to understanding obstructive sleep apnea.

Obstructive sleep apnea (OSA) is an increasingly recognized, common chronic disease in the developed nations and is a complex disease that has high social and economic costs. OSA and its associated 'intermediate' phenotypes-craniofacial structure, body fat distribution and metabolism, and neurological control of the upper airway muscles and of sleep and circadian rhythm-are under a substantial degree of genetic control. Investigating the genetic aetiology of OSA offers a means of better understanding its pathogenesis, with the goal of improving preventive strategies, diagnostic tools and therapies. Molecular studies of OSA itself are in their infancy, but considerable effort and expense has already been expended in attempts to detect genetic loci contributing to OSA-associated intermediate phenotypes, such as obesity. However, many of the fundamental questions relating to the genetic epidemiology of OSA and associated factors remain unanswered. This chapter reviews the current state of knowledge of the genetics of OSA, with a focus on genomic approaches to understanding sleep disorders.

Animals↗

PubMed2006

Phenotypic characteristics associated with hypertension in patients with obstructive sleep apnea.

Obstructive sleep apnea (OSA) causes secondary hypertension. However, the reasons why the prevalence of hypertension among OSA patients varies widely (35-70%) are not clear. We sought to investigate the phenotypic characteristics of patients with and without hypertension among OSA patients who were matched for disease severity. We studied 152 OSA patients (76 normotensive and 76 hypertensive) diagnosed by polysomnography. Detailed phenotypic characteristics, including laboratorial analysis, were determined in all patients. Univariate analysis followed by multiple logistic regression analysis was used to identify variables that were independently associated with hypertension. The apnea-hypopnea index in normotensive and hypertensive patients was similar (48+/-26 and 48+/-26 events/h, respectively) as well as minimum arterial oxygen saturation (76+/-10 and 75+/-10%, respectively) and total sleep time with oxyhaemoglobin saturation <90% (25+/-25 and 28+/-26%, respectively). Hypertensive patients were older (57+/-11 vs 47+/-12 years; P<0.001), had a higher body mass index (BMI; 34+/-7 vs 30+/-5 kg/m(2); P<0.001), had a higher frequency of women (37 vs 8%; P<0.001), had a higher incidence of diabetes (25 vs 6%; P=0.002) and a higher family history of hypertension (75 vs 42%; P=0.01) than did the normotensive patients. Multiple logistic regression analysis indicated that age (P=0.004), familial history of hypertension (P=0.004), BMI (P=0.04) and female sex (P=0.03) were the independent variables associated with hypertension. We concluded that increasing age and BMI, familial history of hypertension as well as female gender are phenotypic characteristics associated with hypertension among OSA patients with similar disease severity.

Adult↗

PubMed2000

Complications and consequences of obstructive sleep apnea.

Obstructive sleep apnea (OSA) has many consequences. There is an independent association between OSA and hypertension. The Sleep Heart Health Study reported that hypertension prevalence increased as sleep disordered breathing severity increased. The Nurses' Health Study noted an age-adjusted relative risk of cardiovascular events of 1.46 for occasional snorers and 2.02 for regular snorers, and a risk of stroke of 1.60 for occasional snorers and 1.88 for regular snorers. Sleep apnea is also associated with pulmonary hypertension, neurocognitive effects, depressed quality of life, motor vehicle accidents, awakening headache, childhood growth interruption, pregnancy-induced hypertension, fetal growth retardation, and disruption of the patients' bed-partners' sleep quality. Further research will examine the possibility of causality, pathophysiologic mechanisms, and outcomes of therapeutic interventions for OSA on the many consequences of OSA.

Cardiovascular Diseases↗

PubMed2004

Circulating free nitrotyrosine in obstructive sleep apnea.

Obstructive sleep apnea (OSA) has been increasingly linked to cardiovascular disease, endothelial dysfunction, and oxidative stress, generated by repetitive nocturnal hypoxemia and reperfusion. Circulating free nitrotyrosine has been reported as a novel biomarker of nitric oxide (NO)-induced oxidative/nitrosative stress. Nitrosative stress has been implicated as a possible mechanism for development of cardiovascular diseases. We tested the hypothesis that repetitive severe hypoxemia resulting from OSA would increase NO-mediated oxidative stress. We studied 10 men with newly diagnosed moderate to severe OSA who were free of other diseases, had never been treated for OSA, and were taking no medications. Nitrotyrosine measurements, performed by liquid chromatography-tandem mass spectrometry, were made before and after untreated apneic sleep. We compared free nitrotyrosine levels in these patients with those obtained at similar times in 10 healthy male control subjects without OSA, with similar age and body mass index. Evening baseline nitrotyrosine levels were similar before sleep in the control and OSA groups [0.16 +/- 0.01 and 0.15 +/- 0.01 ng/ml, respectively, P = not significant (NS)]. Neither normal nor disturbed apneic sleep led to significant changes of plasma nitrotyrosine (morning levels: control group 0.14 +/- 0.01 ng/ml; OSA group 0.15 +/- 0.01 ng/ml, P = NS). OSA was not accompanied by increased circulating free nitrotyrosine either at baseline or after sleep. This observation suggests that repetitive hypoxemia during OSA does not result in increased NO-mediated oxidative/nitrosative stress in otherwise healthy subjects with OSA.

Adult↗

PubMed2005

Respiratory control stability and upper airway collapsibility in men and women with obstructive sleep apnea.

Obstructive sleep apnea (OSA) is two to three times more common in men as in women. The mechanisms leading to this difference are currently unclear but could include gender differences in respiratory stability [loop gain (LG)] or upper airway collapsibility [pharyngeal critical closing pressure (Pcrit)]. The aim of this study was to compare LG and Pcrit between men and women with OSA to determine whether the factors contributing to apnea are similar between genders. The first group of 11 men and 11 women were matched for OSA severity (mean +/- SE apnea-hypopnea index = 43.8 +/- 6.1 and 44.1 +/- 6.6 events/h). The second group of 12 men and 12 women were matched for body mass index (BMI; 31.6 +/- 1.9 and 31.3 +/- 1.8 kg/m2, respectively). All measurements were made during stable supine non-rapid eye movement sleep. LG was determined using a proportional assist ventilator. Pcrit was measured by progressively dropping the continuous positive airway pressure level for three to five breaths until airway collapse. Apnea-hypopnea index-matched women had a higher BMI than men (38.0 +/- 2.4 vs. 30.0 +/- 1.9 kg/m2; P = 0.03), but LG and Pcrit were similar between men and women (LG: 0.37 +/- 0.02 and 0.37 +/- 0.02, respectively, P = 0.92; Pcrit: 0.35 +/- 0.62 and -0.18 +/- 0.87, respectively, P = 0.63). In the BMI-matched subgroup, women had less severe OSA during non-rapid eye movement sleep (30.9 +/- 7.4 vs. 52.5 +/- 8.1 events/h; P = 0.04) and lower Pcrit (-2.01 +/- 0.62 vs. 1.16 +/- 0.83 cmH2O; P = 0.005). However, LG was not significantly different between genders (0.38 +/- 0.02 vs. 0.33 +/- 0.03; P = 0.14). These results suggest that women may be protected from developing OSA by having a less collapsible upper airway for any given degree of obesity.

Adult↗

PubMed2006

Effects of nasal continuous positive airway pressure and oxygen supplementation on norepinephrine kinetics and cardiovascular responses in obstructive sleep apnea.

Obstructive sleep apnea (OSA) is characterized by noradrenergic activation. Nasal continuous positive airway pressure (CPAP) is the treatment of choice and has been shown to effectively reduce elevated norepinephrine (NE) levels. This study examined whether the reduction in NE after CPAP is due to an increase in NE clearance and/or a decrease of NE release rate. Fifty CPAP-naive OSA patients with an apnea-hypopnea index >15 were studied. NE clearance and release rates, circulating NE levels, urinary NE excretion, and blood pressure and heart rate were determined before and after 14 days of CPAP, placebo CPAP (CPAP administered at ineffective pressure), or oxygen supplementation. CPAP led to a significant increase in NE clearance (P < or = 0.01), as well as decreases in plasma NE levels (P < or = 0.018) and daytime (P < 0.001) and nighttime (P < 0.05) NE excretion. NE release rate was unchanged with treatment. Systolic (P < or = 0.013) and diastolic (P < or = 0.026) blood pressure and heart rate (P < or = 0.014) were decreased in response to CPAP but not in response to oxygen or placebo CPAP treatment. Posttreatment systolic blood pressure was best predicted by pretreatment systolic blood pressure and posttreatment NE clearance and release rate (P < 0.01). The findings indicate that one of the mechanisms through which CPAP reduces NE levels is through an increase in the clearance of NE from the circulation.

Adult↗

PubMed2003

A decision rule for diagnostic testing in obstructive sleep apnea.

Obstructive sleep apnea (OSA) is traditionally diagnosed using overnight polysomnography. Decision rules may provide an alternative to polysomnography. A consecutive series of patients referred to a tertiary sleep center underwent prospective evaluation with the upper airway physical examination protocol, followed by determination of the respiratory disturbance index using a portable monitor. Seventy-five patients were evaluated with the upper airway physical examination protocol. Historic predictors included age, snoring, witnessed apneas, and hypertension. Physical examination-based predictors included body mass index, neck circumference, mandibular protrusion, thyro-rami distance, sterno-mental distance, sterno-mental displacement, thyro-mental displacement, cricomental space, pharyngeal grade, Sampsoon-Young classification, and over-bite. A decision rule was developed using three predictors: a cricomental space of 1.5 cm or less, a pharyngeal grade of more than II, and the presence of overbite. In patients with all three predictors (17%), the decision rule had a positive predictive value of 95% (95% confidence interval [CI], 75-100%) and a negative predictive value of 49% (95% CI, 35-63%). A cricomental space of more than 1.5 cm (27% of patients) excluded OSA (negative predictive value of 100%, 95% CI, 75-100%). Comparable performance was obtained in a validation sample of 50 patients referred for diagnostic testing. This decision rule provides a simple, reliable, and accurate method of identifying a subset patients with, and perhaps more importantly, without OSA.

Adult↗

PubMed2002

Brain morphology associated with obstructive sleep apnea.

Obstructive sleep apnea (OSA) is characterized by repeated occurrences of hypoxic, hypercapnic, and transient blood pressure elevation episodes that may damage or alter neural structures. Underdeveloped structures or pre-existing damage in brain areas may also contribute to the genesis of the syndrome. Brain morphology in 21 patients with OSA and in 21 control subjects was assessed using high-resolution T1-weighted magnetic resonance imaging. Three-dimensional brain images were obtained with voxels of approximately 1 mm3. Images were spatially normalized and segmented into gray matter, white matter, and cerebrospinal fluid. For each segment, regional volumetric differences were determined relative to age, handedness, and group (patients with OSA versus control subjects), using voxel-based morphometry, with OSA effects weighted by disease severity. A significant age effect on total gray matter was found in control subjects but not in patients with OSA. Diminished regional and often unilateral gray matter loss was apparent in multiple sites of the brain in patients with OSA, including the frontal and parietal cortex, temporal lobe, anterior cingulate, hippocampus, and cerebellum. Unilateral loss in well-perfused structures suggests onset of neural deficits early in the OSA syndrome. The gray matter loss occurs within sites involved in motor regulation of the upper airway as well as in areas contributing to cognitive function.

Adult↗

PubMed2002

Left ventricular hypertrophy and abnormal ventricular geometry in children and adolescents with obstructive sleep apnea.

Obstructive sleep apnea (OSA) has been shown to be an independent risk factor for cardiovascular disease in adults. However, there are severe limitations in the extent to which the cardiovascular consequences of OSA are being studied in children. To investigate the echocardiographic changes in children with OSA, right and left ventricular (RV, LV) dimensions and LV mass index and geometry were measured in 28 children with OSA and 19 children with primary snoring (PS). The study showed that LV mass index and relative wall thickness were greater in the OSA group compared with those with PS (p = 0.012 and p < 0.0001, respectively). An apnea-hypopnea index of more than 10 per hour was significantly associated with RV dimension above the 95th percentile (odds ratios, 6.7; 95% confidence interval, 1.4-32) and LV mass index above the 95th percentile (odds ratios, 11.2; confidence interval, 1.9-64). Abnormality of LV geometry was present in 15% of children with PS compared with 39% of children with OSA. We conclude that OSA in children is associated with increased LV mass.

Adolescent↗

PubMed2003

The surgical treatment of obstructive sleep apnea.

Obstructive sleep apnea is a highly prevalent disorder that significantly increases mortality when it is moderate to severe. Continuous positive airway pressure (CPAP) provides excellent relief to sleep apnea in the majority of patients. Unfortunately, many patients cannot tolerate CPAP and seek surgical alternatives. The reported surgical success rates range between 25 and 100% with most studies achieving a 50-70% success rate. The severity of the sleep apnea, as well as the patient's physical features influence the surgical success rate. Patients with mild sleep apnea should be treated if systematic. Treatment should be encouraged for patients with moderate to severe sleep apnea because of the decrease in life expectancy and other associated morbidities. Current surgical procedures include uvulopalatopharyngoplasty, genioglossus advancement, radiofrequency ablation to the base of tongue, tongue suspension, maxillomandibular advancement, and tracheostomy.

Follow-Up Studies↗

PubMed2003

Can nasal continuous positive airway pressure decrease clinic blood pressure in patients with obstructive sleep apnea?

Obstructive sleep apnea (OSA) is commonly associated with systemic hypertension and now recognized as an independent risk factor for daytime hypertension. We aimed to study the short- and long-term effect of nasal continuous positive airway pressure (CPAP) in hypertensive and normotensive patients with OSA. Forty-six patients with moderated to severe OSA were treated with nasal CPAP and followed after one year of treatment. Clinic blood pressure, heart rate, and body weight were taken before and followed up for one year after beginning nasal CPAP. In this study 25 patients with OSA were found to have hypertension (54.3%). The hypertensive group showed a significant reduction in clinic blood pressure after nasal CPAP, whereas the normotensive group showed no changes. The subgroup of hypertensive patients with OSA who had no anti-hypertensive medication revealed a decrease in clinic blood pressure comparable to those with anti-hypertensive drugs. The heart rate was not significantly changed in any patients. There was no significant correlation between the decrease in body weight and the reduction in blood pressure. These results suggest that nasal CPAP alone might have a substantial blood pressure lowering effect in hypertensive patients with OSA. This effect could decrease the morbidity and mortality related to cardiovascular complications in patients with OSA.

Adult↗

PubMed2005

Oral appliance therapy for obstructive sleep apnea.

Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive, complete or partial closure of the upper airway during sleep, resulting in sleep fragmentation and oxygen desaturation. The disorder causes significant morbidity, particularly in terms of impairment of daytime functioning and the impact this has on quality of life. There is also evidence that links OSA to long-term cardiovascular morbidity, including hypertension, myocardial infarction, and stroke, and increased risk of motor vehicle accidents. There is clear evidence that effective treatment of OSA provides major benefit to patients. Nasal continuous positive airway pressure (CPAP) is the current treatment of choice, but its cumbersome nature makes tolerance and compliance less than optimal. This gives rise to the need for other alternatives that are equally effective, but more tolerable. There is growing interest in the use of oral appliances to treat snoring and OSA. The rationale is that advancement of the mandible and tongue impacts positively on upper airway caliber and function. There are many such types of appliances, and they have potential advantages over CPAP in that they are unobtrusive, make no noise, do not need a power source, and are potentially less costly. There is a growing evidence base to support the use of oral appliances in the management of OSA. Recent evidence from randomized controlled trials indicates that oral appliance therapy is effective in controlling OSA in up to 50% of patients, including some patients with more severe forms of OSA. This is associated with a significant improvement in symptoms, including snoring and daytime sleepiness. This evidence is strong for short term, and emerging for long-term treatment of OSA with oral appliances. Whilst direct comparisons with CPAP indicate the superiority of CPAP overall, similar outcomes between the two treatments appear to be achieved in a substantial subgroup of patients. Patient acceptance has, in general, been in favor of oral appliances. Notwithstanding the expanding role of oral appliance therapy, there are a number of limitations that are yet to be overcome. Key issues include the inability to reliably predict treatment outcome, the apparent need for an acclimatization period to attain maximal efficacy of treatment, uncertainty about selection of the appropriate 'dosage' of mandibular advancement required to control OSA in the individual patient, uncertainty about the influence of appliance design on treatment outcome and adverse effects, adherence to treatment, and potential long-term complications of therapy. These issues require resolution before oral appliance therapy can surpass CPAP as first-line treatment for OSA.

Continuous Positive Airway Pressure↗

PubMed2006

Airway inflammation in patients affected by obstructive sleep apnea.

Obstructive sleep apnea (OSA) is characterised by repetitive episodes of upper airway occlusion during sleep. OSA has been shown to be associated with a variable degree of nasal inflammation, uvula mucosal congestion and airway hyperreactivity. The upper airway inflammation, whose clinical importance is uncertain, is characterised by leukocytes infiltration and interstitial oedema. In addition, recent data has shown the presence of neutrophilic inflammation in the lower airways. The current opinion is that airway inflammation is caused by the local, repeated mechanical trauma related to the intermittent airway occlusion typical of the disease. Another potential mechanism involves the intermittent nocturnal hypoxemia that through the phenomenon of the ischemia-reperfusion injury may induce the production of oxygen free radicals and therefore cause local and systemic inflammation. Finally, a state of low-grade systemic inflammation may be related to obesity per se with the pro-inflammatory mediators synthesised in the visceral adipose cells. Several authors stress the role of circulating and local inflammatory mediators, such as pro-inflammatory cytokines, exhaled nitric oxide, pentane and 8-isoprostane as the determinants of inflammation in OSA.

Breath Tests↗

PubMed2006

Cardiovascular diseases in obstructive sleep apnea.

Obstructive sleep apnea (OSA) affects approximately 5% of women and 15% of men in the middle-aged adults, and associated with adverse health outcomes. Cardiovascular disturbances are the most serious complications of OSA. These complications include heart failure, left/right ventricular dysfunction, acute myocardial infarction, arrhythmias, stroke, systemic and pulmonary hypertension. All these cardiovascular complications increase morbidity and mortality of OSA. Several epidemiologic studies have demonstrated that sleep related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic activity, and altered baroreflex control during sleep. Arterial hypertension, obesity, diabetes mellitus and coronary artery disease (CAD) which are independent predictors of left ventricular dysfunction, often have co-existence with OSA. Especially severe OSA patients having diastolic dysfunction might have an increased risk of heart failure, since diastolic dysfunction might be combined with systolic dysfunction. Early recognition and appropriate therapy of ventricular dysfunction is advisable to prevent further progression to heart failure and death. Patients with acute myocardial infarction, especially if they had apneas and hypoxemia without evident heart failure should be evaluated for sleep disorders. So, patients with CAD should be evaluated for OSA and vice versa. Early recognition and treatment of OSA may improve cardiovascular functions. Continuous positive airway pressure (CPAP) applied by nasal mask, is still the gold standard method for treatment of the disease and prevention of complications.

Cardiovascular Diseases↗