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PubMed2006

Inflammatory aspects of sleep apnea and their cardiovascular consequences.

Obstructive sleep apnea (OSA) is a common medical condition that occurs in a considerable percentage of the population. Substantial evidence shows that patients with OSA have an increased incidence of hypertension compared with individuals without OSA, and that OSA is a risk factor for the development of hypertension. It is established that OSA may be implicated in stroke and transient ischemic attacks. OSA is associated with coronary heart disease, heart failure, and cardiac arrhythmias. Pulmonary hypertension may be associated with OSA, especially in patients with pre-existing pulmonary disease. Although the exact cause that links OSA with cardiovascular disease is unknown, there is evidence that OSA is associated with a group of proinflammatory and prothrombotic factors that have been identified as important in the development of atherosclerosis. OSA is associated with increased daytime and nocturnal sympathetic activity. Autonomic abnormalities seen in patients with OSA include increased resting heart rate, decreased R-R interval variability, and increased blood pressure variability. Both atherosclerosis and OSA are associated with endothelial dysfunction, increased C-reactive protein, interleukin 6, fibrinogen, plasminogen activator inhibitor, and reduced fibrinolytic activity. OSA has been associated with enhanced platelet activity and aggregation. Leukocyte adhesion and accumulation on endothelial cells are common in both OSA and atherosclerosis. Clinicians should be aware that OSA may be a risk factor for the development of cardiovascular disease.

Biomarkers↗

PubMed2006

Why a polysomnogram should become part of the diagnostic evaluation of stroke and transient ischemic attack.

Neurologists need to recognize, diagnose, and treat obstructive sleep apnea (OSA) in patients with stroke or transient ischemic attack (TIA). Increasing medical evidence suggests that OSA is an independent risk factor for stroke and TIA. Stroke (or TIA) is more likely a cause, rather than a consequence, of OSA because PSG studies have shown: 1) apneas in stroke are typically obstructive, not central or Cheyne-Stokes in type; 2) apneas are just as frequent and severe in patients with either TIA or stroke; 3) OSA severity is not influenced by the acuteness or location of the stroke; 4) untreated OSA patients have more strokes, stroke morbidity, and mortality than those who are treated. OSA alone can induce hypertension, especially in younger men. A causal relationship has recently been demonstrated between OSA and hypertension. A distinctive feature of OSA-induced hypertension is loss of the normal nighttime fall in blood pressure ("nondippers"). Data from the Sleep Heart Health Study showed a dose-response association between OSA severity and the presence of hypertension 4 years later. Hypertension or ischemic heart disease usually develops in untreated patients with OSA over time without particular worsening of OSA. Studies have shown sleep itself is not a risk factor for stroke because most stroke and TIAs begin between 6 am and noon, while the individual is awake. However, OSA promptly be considered in stroke beginning during sleep because 88% of strokes that develop during sleep occur in "nondippers." Premature death in OSA patients is most often cardiovascular, but occurs while the patients are awake. The risk of myocardial infarction is increased 20-fold in untreated OSA. Treating OSA patients with continuous positive airway pressure can prevent or improve hypertension, reduce abnormal elevations of inflammatory cytokines and adhesion molecules, reduce excessive sympathetic tone, avoid increased vascular oxidative stress, reverse coagulation abnormalities, and reduce leptin levels. If all this can be achieved by a polysomnogram, then this test should become part of a neurologist's armamentarium for stroke and TIA.

Humans↗

PubMed2003

Obesity and obstructive sleep apnea.

There is a very high prevalence of OSA in obese individuals and a high prevalence of obesity in patients with OSA. The pathophysiology of OSA is intimately linked to obesity. Anatomic and functional considerations of the pharyngeal airway, the CNS, central obesity, and leptin likely interact in the development of OSA in obese individuals. OSA may itself predispose individuals to worsening obesity because of sleep deprivation, daytime somnolence, and disrupted metabolism. The diagnosis of OSA requires the clinician's awareness of its potential to cause a spectrum of acute and chronic neurocognitive, psychiatric, and nonspecific symptoms in patients who may be unaware that their sleep is disturbed. Symptoms and examination findings help predict which obese individuals have OSA, and polysomnography is the gold standard by which to make the diagnosis and assess the effects of treatment. Numerous disease states are associated with both OSA and obesity, and it is becoming clear that the relationships are mediated by complex interrelated mechanisms. Common diseases and disease mechanisms in OSA and obesity suggest that conditions related to obesity may be better managed if patients, particularly those who are morbidly obese, are evaluated and treated for previously undiagnosed OSA. OSA is cured in only specific cases with craniofacial or upper airway surgery, and the general application of UVP is not efficacious. OSA also can be cured with sufficient lifestyle-mediated or surgical weight loss; however, in the absence of long-term weight maintenance, OSA returns with weight gain. Although not curative, nasal CPAP is the initial treatment of choice for most patients because of its noninvasive approach and technical efficacy. It is limited, however, by patient acceptance and long-term compliance. Advances in mask comfort and use of humidified air should increase its acceptance. Future management strategies include newer generations of positive airway devices that automatically titrate pressures (which are not yet recommended by expert organizations) and multidisciplinary approaches to managing the care of patients with OSA.

Blood Coagulation Disorders↗

PubMed2001

Arousals and obstructive sleep apnea syndrome in children.

OBJECTIVE: Observations of children with obstructive sleep apnea syndrome (OSAS) show a restless sleep. But there is no significant disturbance of sleep macrostructure as in adult OSAS patients. It will be proved, whether the analysis of arousals permits a comprehensive characterization of this respiratory related sleep disturbance. Considering the problems in EEG-arousals detection in dependence of age and maturation we will compare the results of analysis of EEG- and movement arousals to find out a more practicable way for arousal analysis in childhood. METHODS: Twenty OSAS pediatric patients (aged 3.1-14.3 years, median 7.5 years) and 20 age matched children with no OSAS (aged 3.3-13.9 years, median 7.9 years) were examined polysomnographically. Clinically confirmed OSAS patients with an apnea/hypopnea index (AHI) > or = 5/h TST (total sleep time) were examined during 1 whole night before treatment (diagnostic night - baseline) and after/under receiving therapy. Various polygraphic parameters to describe the macrostructure of sleep (sleep efficiency, NREM 1-4, REM) and the microstructure of sleep (EEG- and movement arousals) were analyzed. Furthermore the AHI, heart rate and oxygen saturation were evaluated. RESULTS: Patients with clinically and polysomnographically confirmed OSAS had significantly more EEG (median 21.0/interquartile range 9.31 /h TST) and movement arousals (20.4/13.1 /h TST) before therapy than after/under therapy (EEG: 9.9/6.3 /h TST; movement: 9.2/3.8/h TST). The frequency of arousals was comparable in OSAS children after/under treatment and controls (EEG: 9.0/4.2/h TST; movement 9.3/3.4/h TST). In the 3 groups there was no significant correlation between AHI and number of EEG-arousals and movement arousals. AHI was significantly higher in OSAS children in comparison to controls and treated OSAS. In contrast to adults, sleep efficiency and macrostructure of sleep were not different in controls and OSAS children with or without treatment. Also, oxygen saturation and heart rate, had the same values in controls, OSAS children and OSAS children after/under treatment. CONCLUSIONS: OSAS in children is characterized by a restless sleep, i.e. by an enhanced number of movement and EEG-arousals. The microstructure of sleep but not the macrostructure is changed. There is a high coincidence between EEG arousals and movement arousals. The evaluation of arousals especially the analysis of movement arousals is helpful to estimate treatment effect in OSAS patients.

Adolescent↗

PubMed2006

[Long term change in quality of life after adenotonsillectomy for pediatric obstructive sleep disorders].

BACKGROUND: To study short-term and long-term changes in quality of life (QOL) in children before and after adenotonsillectomy (T and A) for obstructive sleep disorders (OSDs). MATERIALS AND METHODS: Prospective study of 20 children underwent T and A for OSDs at the University hospital of Ulm/Germany. Caregivers were asked to complete the Brouillette-Score (BS) and OSA-18 survey, validated instruments for detecting symptoms and QOL change in children with OSDs, at the initial office visit prior to surgery (BS/1 and OSA-18/1) within 7.5 +/- 1.14 weeks after surgery (BS/2 and OSA-18/2), and 14.8 +/- 1.98 months after surgery (BS/3 and OSA-18/3). The BS comprises 3 items including: difficulty breathing during sleep, apnea observed by the caregivers and snoring. The OSA-18 survey comprises 18 items in 5 domains of sleep disturbance, physical suffering, emotional distress, daytime problems, and caregiver concerns. Scores from the preoperative and postoperative surveys were compared using the paired T-test and SPEARMAN-RANK test. RESULTS: 13 children were male (65 %). The mean age at the time of inclusion in the study was 6.2 +/- 1.63 years, mean preoperative body mass index (BMI) was 17.4 +/- 1.24 kg/m(2). Brouillette-Score: The mean Brouillette-Score before T and A (2.72) was significantly higher ( P = or < .001) than in the short-term (- 2.19) and in the long-term. (- 3.54). OSA-18 SURVEY: The mean total score for OSA-18/1 (83.4) was significantly higher ( P = or < .001) than the mean total score for OSA-18/2 (29.8) and OSA-18/3 (25.6). The overall correlation between BS and OSA-18 was R = .887 ( P = or < .001). CONCLUSION: Children with suspicious OSDs demonstrate significant short term and long-term improvement in the Brouillette-Score and OSA-18 survey. Caregivers perceive a long-term improvement for a minimum of one year in QOL after T and A for OSDs, although these improvements are not uniform across all domains of the OSA-18 survey. Use of the Brouillette-Score and the OSA-18 survey should decrease the need for polysomnographic monitoring and facilitate selection of children for T and A, whereas the OSA-18 questionnaire permits the more differentiated finding.

Adenoidectomy↗

PubMed1995

Impact of self-reported sleep-breathing disturbances on psychosocial performance in the Swedish Obese Subjects (SOS) Study.

Patients with severe obesity commonly have obstructive sleep apnea (OSA). In order to determine the impact of OSA on psychosocial morbidity in severe obesity, subjects enrolled in the Swedish Obese Subjects (SOS) Study were classified into two subgroups based on questionnaire data: one group with a high likelihood and one with a low likelihood of OSA. These groups were contrasted and multivariable analysis was used to examine whether OSA had independent effects on divorce rate, sick leave, work performance, income and self-estimated general health after adjustment for obesity, fat distribution, alcohol, smoking, medications and coexisting medical conditions. A high likelihood of OSA was identified in 338 men and 155 women, compared with 216 men and 481 women who had a low likelihood of OSA. Men with OSA were identical in age to men without OSA and had slightly higher levels of visceral fat (p = 0.01), but were similar in most psychosocial variables except self-perceived general health. Women with OSA were identical in age and visceral fat mass to women without OSA, but were characterized by a higher rate of impaired work performance, sick leave and divorce. When frequent sleepiness was used as an additional discriminator between OSA and non-OSA groups, marked differences in psychosocial morbidity were observed. Multivariable analysis revealed either OSA or frequent sleepiness or both to be independent predictors of amount of sick leave, worse self-rated general health, impaired work performance and divorce rate. Therefore OSA, measured by self report, is an important independent predictor of psychosocial morbidity in subjects with severe obesity.

Body Mass Index↗

PubMed2006

Prevalence of obstructive sleep apnoea in men with type 2 diabetes.

BACKGROUND: A study was undertaken to establish the prevalence of obstructive sleep apnoea (OSA) in men with type 2 diabetes. METHODS: Men with type 2 diabetes from local hospital and selected primary care practitioner databases received questionnaires about snoring, apnoeas, and daytime sleepiness based on the Berlin questionnaire. Selected respondents had overnight oximetry to establish whether they had OSA. Comparisons of oximetry were made with those from a previous general population study. HbA1c results were collected. RESULTS: 1682 men were sent questionnaires, 56% of whom replied. 57% scored as "high" and 39% as "low" risk for OSA; 4% were already known to have OSA. Oximetry was performed in 240 respondents from both risk groups: 31% of the "high" and 13% of the "low" risk group had significant OSA (more than 10 >4% Sao(2) dips/hour or Sao(2) tracing consistent with OSA). These results were verified by detailed sleep studies. Extrapolation of the oximetry data to the questionnaire respondent population suggests that 23% had OSA. Comparison of the oximetry results with men from a previous general population study (using only more than 10 >4% Sao(2) dips/hour to define OSA) showed the prevalence of OSA is significantly higher in this diabetes population (17% v 6%, p<0.001). Multiple linear regression revealed BMI and diabetes as significant independent predictors of OSA. Following correction for BMI (which explained 13% of the variance in OSA), diabetes explained a further 8% of the variance (p<0.001). There was a low correlation between OSA severity and HbA1c in the subgroup recruited from the hospital database (r = 0.2, p = 0.006) which remained significant after allowing for obesity (p = 0.03). CONCLUSIONS: OSA is highly prevalent in men with type 2 diabetes; most are undiagnosed. Diabetes itself may be a significant independent contributor to the risk of OSA.

Adolescent↗

PubMed2004

Obstructive sleep apnea: MR imaging volume segmentation analysis.

PURPOSE: To retrospectively determine airway wall motion with volume segmentation of transverse cine magnetic resonance (MR) images in children with obstructive sleep apnea (OSA). MATERIALS AND METHODS: Transverse fast gradient-echo cine MR images of the hypopharynx were obtained at 1.5 T in 31 children with OSA (eight girls, 23 boys; mean age, 11.3 years) and 21 children free of airway symptoms who underwent MR imaging for other clinical indications (11 girls, 10 boys; mean age, 3.5 years). Volume segmentation with a k-means clustering algorithm was applied to transverse cine MR images to quantify airway volumes at each time. Airway wall motion for each child was described with standard deviation and range. Coefficient of variance and normalized range, which are independent of airway size, were used to compare groups (Kruskal-Wallis test). RESULTS: Plots of airway volume over time demonstrated large fluctuations during respiration in children with OSA and minimal fluctuations in controls; findings were consistent with airway distention and airway collapse in OSA. Average airway transverse volume was larger in the group with OSA than in the control group (OSA group, 2.52 mL; control group, 0.936 mL; P <.001). Mean standard deviation (OSA group, 0.840 mL; control group, 0.17 mL; P <.001) and mean range of airway cross section (OSA group, 3.552 mL; control group, 0.864 mL; P <.001) were larger in the group with OSA. Coefficient of variance (OSA group, 0.32; control group, 0.17; P <.001) and normalized range (OSA group, 1.42; control group, 0.96; P <.001) indicate statistically significant difference in airway dynamics in children with OSA. CONCLUSION: Volume segmentation of transverse cine MR images of the hypopharynx aids in quantification of increased airway wall motion in children with OSA. Transverse MR imaging demonstrates both airway distention and collapse in children with OSA.

Child↗

PubMed2006

Metabolic risk factors for vascular disease in obstructive sleep apnea: a matched controlled study.

RATIONALE: Obstructive sleep apnea (OSA) is reported to have a metabolic profile predisposing to cardiovascular disease. However, previous case-control studies have not adequately controlled for confounders. OBJECTIVES: To determine whether OSA is associated with increased insulin resistance and related metabolic risk factors. METHODS: We performed a matched case-control study (n = 42) examining putative metabolic risks among men with OSA attending a sleep clinic (apnea-hypopnea index [AHI] > 15] compared with no OSA (AHI < 5). Participants were matched for age +/- 5 yr, body mass index +/- 10%, and current smoking status. They were free of diabetes, clinically demonstrable cardiovascular disease, marked hypertension, and dyslipidemia. MEASUREMENTS AND MAIN RESULTS: Mean +/- SD AHI was higher in patients with OSA (40 +/- 27) than in control subjects (3 +/- 1.3, p = 0.02), and median (interquartile range) nocturnal oxygen saturation was lower (OSA, 83 [76-88]; control, 91 [90-93]%; p < 0.001). Patients with OSA had a higher median (interquartile range) homeostasis model assessment score for insulin resistance (OSA, 1.7 [0.8-4.1]; control, 1.0 [0.7-1.8] mU.mmol/L(2); p = 0.02), total cholesterol (OSA, 5.6 [4.8-6.2]; control, 4.8 [4.3-5.4] mmol/L; p = 0.049), and low-density-lipoprotein cholesterol (OSA, 3.8 [2.9-4.2]; control, 3.1 [2.6-3.6] mmol/L; p = 0.04). Patients with OSA had higher 24-h and nocturnal (12-h) urinary norepinephrine excretion and plasma leptin levels, and lower insulin-like growth factor (IGF)-1 levels (all, p < or = 0.02). Multiple linear regression, adjusting for central obesity, age, and alcohol consumption, confirmed an independent association between OSA and metabolic risks (all, p < 0.05), with a trend for IGF-1 (p = 0.053). CONCLUSIONS: In a sleep clinic population, men with OSA and no identifiable cardiovascular disease have increased insulin resistance and other metabolic changes that act to increase the risk of vascular disease, compared with age- and body mass index-matched attendees without OSA.

Body Mass Index↗

PubMed2005

Impact of obstructive sleep apnoea on left ventricular mass and global function.

Obstructive sleep apnoea syndrome (OSAS) might be a cause of heart failure. The present study aimed to assess left ventricular mass and myocardial performance index (MPI) in OSAS patients. A total of 67 subjects without any cardiac or pulmonary disease, referred for evaluation of OSAS, had overnight polysomnography and echocardiography. According to apnoea-hypopnoea index (AHI), subjects were classified into three groups: mild OSAS (AHI: 5-14; n = 16), moderate OSAS (AHI: 15-29; n = 18), and severe OSAS (AHI: > or = 30; n = 33). Thickness of interventricular septum (IVS) and posterior wall (LVPW) were measured by M-mode, along with left ventricular mass (LVM) and LVM index (LVMI). Left ventricular MPI was calculated as (isovolumic contraction time+isovolumic relaxation time)/aortic ejection time by Döppler echocardiography. There were no differences in age or body mass index among the groups, but blood pressures were higher in severe OSAS compared with moderate and mild OSAS. In severe OSAS, thickness of IVS (11.2+/-1.1 mm), LVPW (11.4+/-0.9 mm), LVM (298.8+/-83.1 g) and LVMI (144.7+/-39.8 g x m(-2)) were higher than in moderate OSAS (10.9+/-1.3 mm; 10.8+/-0.9 mm; 287.3+/-74.6 g; 126.5+/-41.2 g x m(-2), respectively) and mild OSAS (9.9+/-0.9 mm; 9.8+/-0.8 mm; 225.6+/-84.3 g; 100.5+/-42.3 g x m(-2), respectively). In severe OSAS, MPI (0.64+/-0.14) was significantly higher than in mild OSAS (0.50+/-0.09), but not significantly higher than moderate OSAS (0.60+/-0.10). In conclusion, severe and moderate obstructive sleep apnoea syndrome patients had higher left ventricular mass and left ventricular mass index, and also left ventricular global dysfunction.

Adult↗

PubMed1998

Sleep architecture in a canine model of obstructive sleep apnea.

Obstructive sleep apnea (OSA) causes recurrent sleep disruption that is thought to contribute to excessive daytime sleepiness in patients with this disorder. The purpose of this study was to determine the specific effects of OSA on overall sleep architecture in a canine model of OSA. The advantage of this model is that sleep during long-term OSA can be compared to both normal sleep before OSA and recovery sleep after OSA. Studies were performed in four dogs in which sleep-wake state was monitored continuously by a computer that received telemetered EEG and EMG signals. Whenever sleep was detected, the computer sent a signal to close a valve through which the dog breathed; when the dog awoke the occlusion was released. In each dog, data were analyzed from 4 consecutive nights in three phases: a control phase before induction of OSA, a phase during long-term OSA (mean = 85 days, apnea index = 59/hour), and a recovery phase after cessation of OSA. During recovery there was a significant increase in the amount of rapid-eye-movement (REM) sleep compared to the OSA phase (p < 0.01), as well as significant increases in sleep efficiency and decreases in wakefulness (p < 0.01), similar to that reported in OSA patients. The REM rebound during recovery, however, could not be attributed to overall REM deprivation since the amount of REM sleep during the OSA phase was not different from the control phase (p = 0.708). This finding suggests that REM rebound during recovery from OSA is not the result of an overall REM sleep deficit per se. Rather, repeated sleep disruption due to the effects of repetitive apneas and hypoxia may lead to an increased REM sleep drive that manifests itself as a REM sleep rebound during recovery sleep after OSA.

Animals↗

PubMed2003

Doppler measurement of blood flow velocities in extraocular orbital vessels in patients with obstructive sleep apnea syndrome.

PURPOSE: We used color Doppler sonography to determine blood flow velocities in the extraocular orbital vessels of patients with obstructive sleep apnea syndrome (OSAS) and compared the results with those of healthy control subjects without OSAS. METHODS: Patients with OSAS were classified according to the apnea-hypopnea index (AHI) as having mild OSAS (AHI < 20) or severe OSAS (AHI > or = 20). The peak systolic velocity (PSV), end-diastolic velocity (EDV), and resistance index were measured in the ophthalmic artery (OA), central retinal artery (CRA), lateral short posterior ciliary artery, and medial short posterior ciliary artery using color Doppler sonography. Only 1 eye was measured in each study participant, and right and left eyes were chosen randomly. The blood flow velocities of patients with OSAS and those of control subjects were compared with the Kruskal-Wallis test and Wilcoxon's rank-sum test. RESULTS: The study comprised 30 patients (15 with mild and 15 with severe OSAS) and 20 healthy control subjects. Blood flow velocities were higher in most measured vessels in patients with OSAS than they were in the control subjects. Among patients with mild OSAS, the PSVs and EDVs in the posterior ciliary arteries were statistically significantly higher than those of the control group (p < 0.05), but those in the OA and CRA did not differ significantly between the mild OSAS group and the control group (p > 0.05). However, as the severity of OSAS increased, the PSVs and EDVs of the OA and CRA were also affected (p < 0.05). CONCLUSIONS: Color Doppler sonographic measurements of blood flow parameters in the orbital vessels may differ significantly between patients with OSAS and those without the syndrome. Therefore, OSAS should be considered in addition to other conditions when interpreting the results of color Doppler sonography of the extraocular orbital vessels if the clinical history points toward such a diagnosis.

Adult↗

PubMed2001

Higher prevalence of smoking in patients diagnosed as having obstructive sleep apnea.

Nightly nicotine withdrawal as well as other respiratory and pulmonary effects of smoking may result in sleep-disordered breathing, especially obstructive sleep apnea (OSA). We hypothesize that there is higher prevalence of smoking in patients with OSA. We also hypothesize that smoking is an independent risk factor for OSA. The aim of this study is to determine whether there is a higher prevalence of smoking in patients with OSA compared with patients who do not have OSA. To investigate this, we randomly selected a group of 108 patients who were diagnosed as having OSA, defined by an apnea-hypopnea index (AHI) of greater than 10 events per hour. We compared their smoking history with another randomly selected group of 106 patients without OSA, defined by an AHI of less than five events per hour. The prevalence of smoking in patients with OSA was found to be 35%, whereas it was only 18% in patients without OSA. Logistic regression analyses were performed to investigate the effects of smoking while adjusting for age, gender, body mass index (BMI), and number of alcoholic drinks per week. While holding fixed the BMI, gender, age, and number of alcoholic drinks per week, current smokers were found to be 2.5 times more likely to have OSA than former smokers and nonsmokers combined (odds ratio = 2.5, CI 1.3-4.7, p = 0.0049), and 2.8 times more likely to have OSA than former smokers alone (odds ratio = 2.8, CI = 1.4-5.4, p = 0.0028). Adjusted for BMI, gender, age, and number of alcoholic drinks per week, former smokers were not more likely than never smokers to have OSA (odds ratio = 1.2, CI = 0.55-2.7, p = 0.64). We conclude that cigarette smoke may be an independent risk factor for OSA in this referral population.

Body Mass Index↗

PubMed1999

Snoring, obstructive sleep apnea, and surgery.

Snoring and OSA syndrome are prevalent and important causes of sleep disturbance. Snoring, historically considered to be only a habitual annoyance, has significant physical and social consequences. OSA is now considered to be a major public health concern with significant morbidity and mortality. CPAP is considered the treatment of choice for OSA syndrome, but poor patient acceptance and compliance remain problematic. Surgical procedures have been developed to alter the offending anatomic abnormalities responsible for OSA. Identification of the offending anatomic site with application of the most appropriate surgical procedure is essential for effective surgical treatment of OSA. When the region of the retropalate is correctly identified as the site of obstruction, UPPP can effectively treat OSA in a majority of patients. Surgical correction of nasal obstruction is advocated in conjunction with sleep apnea surgery when nasal obstruction exists. In OSA patients with retrolingual airway obstruction, a number of surgical procedures have been performed, with or without UPPP, with some improvement over UPPP alone. MMO has been effective in the treatment of OSA in patients with significant retrolingual airway obstruction with contributing skeletal abnormalities and in patients who have failed multiple other surgical procedures. MMO, however, is a procedure of considerable magnitude, requiring extensive oromaxillofacial surgical expertise. MMO is likely appropriate only in a limited number of patients. Tracheostomy is completely effective in the treatment of OSA syndrome but is undesirable to patients and is associated with significant physical and emotional morbidity. Nonetheless, tracheostomy can be lifesaving and remains an option for patients with severe OSA with serious associated cardiovascular complications, who cannot tolerate CPAP, and for whom other interventions are ineffective or unacceptable. Effective surgical treatment of snoring has been accomplished with UPPP and LAUP. LAUP is less invasive, less morbid, more cost-effective, and better tolerated and is likely the most appropriate procedure for debilitating symptomatic snoring. Currently, LAUP is not recommended for the treatment of OSA, despite some efficacy in patients with mild OSA. Exclusion of OSA in patients undergoing LAUP for snoring is important.

Airway Obstruction↗

PubMed2000

Obstructive sleep apnoea: multiple comparisons of cephalometric variables of obese and non-obese patients.

BACKGROUND: Pathogenesis of obstructive sleep apnoea (OSA) is complex and not yet fully understood. Several factors contribute to OSA severity. Obesity is believed to play an important role. Nevertheless, not all OSA patients are obese. Therefore, the different features that cause nocturnal upper airway obstruction in obese and non-obese OSA patients could be expected. PURPOSE: To investigate the different components of cervico-craniofacial skeletal and upper airway soft tissue morphology among obese OSA, non-obese OSA patients and the controls. PATIENTS: One hundred male OSA patients were classified into two groups on the basis of body mass index (BMI) as obese (BMI > or = 30 kg/m2) and non-obese (BMI < 30 kg/m2). Consequently, 57 obese and 43 non-obese OSA patients were examined and compared with a control group of 36 healthy males. STUDY DESIGN: A comprehensive cephalometric analysis of cervico-craniofacial skeletal and upper airway soft tissue morphology was performed. Sixty-eight cephalometric variables were compared among the three groups by one way analysis of variance with Bonferroni's test. RESULTS: Both OSA groups had aberrations of cervico-craniofacial skeletal as well as upper airway soft tissue morphology when compared with the controls. These anatomic deviations were confined to cervico-craniofacial skeletal structures in the non-obese OSA patients, whereas the obese OSA patients had more abnormalities in the upper airway soft tissue morphology, head posture and position of the hyoid bone. CONCLUSION: The findings imply that there should be different treatment regimens for the two subgroups of OSA patients. Cephalometric analysis together with various considerations of BMI is highly recommended as one of the most important tools in diagnosis and treatment planning for OSA patients.

Adult↗

PubMed2000

Obstructive sleep apnea in infants: relation to family history of sudden infant death syndrome, apparent life-threatening events, and obstructive sleep apnea.

OBJECTIVES: Familial aggregation of obstructive sleep apnea (OSA) has been shown to be associated with sudden infant death syndrome (SIDS) and apparent life-threatening events (ALTE) in infants. We wanted to determine the incidence of OSA in infants with siblings with ALTE and SIDS referred to our sleep clinic and to ascertain whether OSA was more common in infants who have family histories of SIDS, ALTE, and OSA. STUDY DESIGN: We studied 125 infants (mean age, 11.5 +/- 0.6 weeks) who were separated into 2 groups on the basis of their family history; polysomnographic studies were performed on each infant. RESULTS: Twenty infants had a multiple family history of SIDS, ALTE, or OSA (group 1), whereas the other 105 infants (group 2) had only one case of SIDS or ALTE within the family and no known history of OSA. We found that 19 of 20 infants in group 1 had OSA, whereas only 31 of 105 infants in group 2 had OSA (chi-squared analysis, P <.05). The OSA recorded was more frequent in infants of group 1 than in those of group 2. Follow-up studies in some infants with OSA demonstrated a progressive decrease in OSA, which resolved between 6 and 12 months of age. CONCLUSION: We conclude that infants of families with multiple histories of SIDS, ALTE, and OSA are more likely to have OSA than infants of families with only one case of SIDS or ALTE.

Age Factors↗

PubMed2006

Obstructive sleep apnoea syndrome, plasma adiponectin levels, and insulin resistance.

OBJECTIVE: To investigate whether sleep-disordered breathing and/or plasma adiponectin levels are associated with insulin resistance independent of obesity or fat distribution in obstructive sleep apnoea syndrome (OSAS). DESIGN: Cross-sectional clinical study. PATIENTS: Two-hundred and thirteen Japanese patients with OSAS aged 27-80 years were divided into three groups: 30 with mild OSAS [apnoea-hypopnoea index (AHI) = 10.3 +/- 0.9 episodes/h, minimum oxygen saturation (min SpO2) = 87.3 +/- 0.9%], 98 with moderate OSAS (AHI = 28.9 +/- 0.6 episodes/h, min SpO2 = 82.1 +/- 0.7%), and 85 with severe OSAS (AHI = 68.1 +/- 2.8 episodes/h, min SpO2 = 72.3 +/- 1.6%). Twenty-one patients undergoing diabetic treatments (two mild, nine moderate and 10 severe) were excluded from the assessment of insulin resistance and plasma adiponectin measurements. MEASUREMENTS: Fat distribution [evaluated according to visceral (V) and subcutaneous (S) fat areas using computed tomography scanning at the umbilical level], blood pressure, metabolic parameters and hormones including insulin and adiponectin were measured. After full polysomnography, venous blood was collected between 0600 and 0700 h. RESULTS: Severe OSAS patients were more hypertensive than mild and moderate OSAS. Fasting plasma glucose (FPG) and fasting plasma insulin and homeostasis model assessment of insulin resistance (HOMA-IR) levels were all higher in severe OSAS than mild and moderate OSAS patients. HOMA-IR was correlated not only with obesity [body mass index (BMI), V and S areas] but also with apnoea (AHI, min SpO2 and desaturation time). Additionally, HOMA-IR was correlated positively with haemoglobin (Hb)A1c, systolic (SBP) and diastolic blood pressure (DBP), triglycerides and free fatty acids (FFA), and negatively with high density lipoprotein (HDL)-cholesterol, suggesting that insulin resistance is a key component of the metabolic syndrome in OSAS. Plasma adiponectin levels were not different between mild, moderate and severe OSAS groups. Plasma adiponectin levels were correlated with HOMA-IR and V area, but not AHI or min SpO2. Stepwise multiple regression analysis, however, revealed that BMI, AHI and plasma adiponectin were independently associated with HOMA-IR. CONCLUSION: Sleep-disordered breathing was associated with insulin resistance independent of obesity. Although plasma adiponectin was also an independent determinant of HOMA-IR in OSAS patients, plasma adiponectin was more closely related to obesity than to sleep apnoea. Although treatment of sleep-disordered breathing with nasal continuous positive airway pressure reportedly improves insulin sensitivity, our findings suggest that treatment of obesity is also essential in ameliorating insulin resistance at least through increased plasma adiponectin levels in OSAS.

Adiponectin↗

PubMed1999

pSa causes oncogenic suppression of Agrobacterium by inhibiting VirE2 protein export.

When coresident with the Ti (tumor-inducing) plasmid, the 21-kDa product of the osa gene of the plasmid pSa can suppress crown gall tumorigenesis incited by Agrobacterium tumefaciens. Neither T-DNA processing nor vir (virulence) gene induction is affected by the presence of osa in the bacterium. We used Arabidopsis thaliana root segments and tobacco leaf discs to demonstrate that Osa inhibits A. tumefaciens from transforming these plants to the stable phenotypes of tumorigenesis, kanamycin resistance, and stable beta-glucuronidase (GUS) expression. When A. tumefaciens contained osa, the lack of expression of transient GUS activity in infected plant tissues, as well as the lack of systemic viral symptoms following agroinfection of Nicotiana benthamiana by tomato mottle virus, suggested that oncogenic suppression by Osa occurs before T-DNA enters the plant nucleus. The extracellular complementation of an A. tumefaciens virE2 mutant (the T-DNA donor strain) by an A. tumefaciens strain lacking T-DNA but containing a wild-type virE2 gene (the VirE2 donor strain) was blocked when osa was present in the VirE2 donor strain, but not when osa was present in the T-DNA donor strain. These data indicate that osa inhibits VirE2 protein, but not T-DNA export from A. tumefaciens. These data further suggest that VirE2 protein and T-DNA are separately exported from the bacterium. The successful infection of Datura stramonium plants and leaf discs of transgenic tobacco plants expressing VirE2 protein by an A. tumefaciens virE2 mutant carrying osa confirmed that oncogenic suppression by osa does not occur by blocking T-DNA transfer. Overexpression of virB9, virB10, and virB11 in A. tumefaciens did not overcome oncogenic suppression by osa. The finding that the expression of the osa gene by itself, rather than the formation of a conjugal intermediate with pSa, blocks transformation suggests that the mechanism of oncogenic suppression by osa may differ from that of the IncQ plasmid RSF1010.

Agrobacterium tumefaciens↗