Depression and comorbid obstructive sleep apnea: Association between positive airway pressure adherence, occurrence of self-harm events, healthcare resource utilization, and costs.

OBJECTIVE: Previous studies have shown that treatment of obstructive sleep apnea (OSA) with positive airway pressure (PAP) therapy in patients with depression may improve depression symptoms and response to antidepressant therapy. We investigated the association between PAP therapy adherence, self-harm events, healthcare resource utilization (HCRU), and costs over 2 years in a national sample of patients with pre-existing depression and newly diagnosed comorbid OSA. METHODS: Administrative claims data were linked to objective PAP therapy usage. Inverse probability treatment weighting was used to compare outcomes over 2 years across PAP adherence levels. The predicted numbers of emergency room (ER) visits and hospitalizations by adherence level were assessed using risk-adjusted generalized linear models. RESULTS: 37,459 patients were included. Relative to non-adherent patients, consistently adherent patients had fewer self-harm events (0.04 vs 0.05, p < 0.001) after 1 year, and significantly (all p < 0.001) fewer ER visits (0.66 vs 0.86) and all-cause hospitalizations (0.13 vs 0.17), and lower total ($11,847 vs $11,955), inpatient hospitalization ($1634 vs $2274), and ER visit ($760 vs $1006) costs per patient in the second year of PAP therapy. Consistently adherent patients showed lower risk for hospitalizations and ER visits. LIMITATIONS: Using observational claims data, we were unable to assess clinical characteristics including sleep, sleepiness, and daytime symptoms, or important social determinants of health. We were limited in assessing care received outside of the included health plans. CONCLUSION: Consistent adherence to PAP therapy over 2 years was associated with improved HCRU outcomes for patients with pre-existing depression newly diagnosed with comorbid OSA.

Critical Issues in Dental and Medical Management of Obstructive Sleep Apnea.

This critical review focuses on obstructive sleep apnea (OSA) and its management from a dental medicine perspective. OSA is characterized by ≥10-s cessation of breathing (apnea) or reduction in airflow (hypopnea) ≥5 times per hour with a drop in oxygen and/or rise in carbon dioxide. It can be associated with sleepiness and fatigue, impaired mood and cognition, cardiometabolic complications, and risk for transportation and work accidents. Although sleep apnea is diagnosed by a sleep physician, its management is interdisciplinary. The dentist's role includes 1) screening patients for OSA risk factors (e.g., retrognathia, high arched palate, enlarged tonsils or tongue, enlarged tori, high Mallampati score, poor sleep, supine sleep position, obesity, hypertension, morning headache or orofacial pain, bruxism); 2) referring to an appropriate health professional as indicated; and 3) providing oral appliance therapy followed by regular dental and sleep medical follow-up. In addition to the device features and provider expertise, anatomic, behavioral, demographic, and neurophysiologic characteristics can influence oral appliance effectiveness in managing OSA. Therefore, OSA treatment should be tailored to each patient individually. This review highlights some of the putative action mechanisms related to oral appliance effectiveness and proposes future research directions.

The use of bronchodilators in people with recently acquired tetraplegia: a randomised cross-over trial.

STUDY DESIGN: A within-participant, double-blind, cross-over, randomised control trial. OBJECTIVES: To determine the short-term effects of bronchodilator therapy on respiratory function in people with recently acquired motor complete tetraplegia. SETTING: Hospital, Australia. METHODS: A total of 12 people with recently acquired tetraplegia were randomised to receive either a one-off dose of a bronchodilator followed by an equivalent dose of a placebo propellant between 1 day and 1 week later or visa versa. The three outcomes were forced expiratory volume in 1 s (FEV1), peak expiratory flow rate (PEF) and forced vital capacity (FVC). These were measured while supine by a blinded assessor 10 and 30 min after treatment. Data were analysed on 11 participants and reported as percentage of predicted. RESULTS: The FEV1, FVC and PEF mean between-group differences (95% confidence interval) at 10 min post treatment were 7.3% (2.7-11.9%; P=0.003), 5.5% (1.6-9.4%; P=0.008) and 20.1% (1.1-40.4%; P=0.039). Similar effects were observed at 30 min for FVC and FEV1 but not for PEF. CONCLUSION: Bronchodilator therapy has a beneficial effect on FEV1, FVC and PEF in participants with recently acquired tetraplegia.

Continuous positive airway pressure requirements in patients with tetraplegia and obstructive sleep apnoea.

STUDY DESIGN: Clinic-based retrospective case-control study. OBJECTIVES: To compare continuous positive airway pressure (CPAP) requirements between patients with tetraplegia and able-bodied patients with obstructive sleep apnoea (OSA). SETTING: Melbourne, Australia. METHODS: Diagnostic and CPAP titration polysomnograms of 219 able-bodied, and 25 patients with tetraplegia and OSA were compared for apnoea hypopnoea index (AHI) and CPAP levels required to effectively treat OSA. Demographics and body mass index (BMI) were obtained for each patient. ASIA score and injury date were obtained for patients with tetraplegia. RESULTS: There was no significant difference in AHI (P=0.102) between the two groups; however, able-bodied patients were significantly older (P=0.003), required significantly higher levels of CPAP to control their OSA (P<0.001) and had higher BMIs (P=0.009) than patients with tetraplegia. In the tetraplegia group, there was no significant correlation between AHI and effective CPAP (r=0.022, P=0.92) or between AHI and BMI (r=-0.196, P=0.35). There was a significant correlation between effective CPAP and BMI (r=0.411, P=0.041). Among able-bodied patients, over two-thirds (68.8%) required 10-16 cm H(2)0 to control their OSA and nearly one-third required over 16 cm H(2)0. In contrast, over two-thirds (68.8%) in the tetraplegia group required less than 10 cm H(2)0 of CPAP to control their OSA. CONCLUSION: This retrospective study suggests that OSA patients with tetraplegia require significantly less CPAP to treat their OSA at any given AHI than those who are able-bodied. This suggests that additional unknown factors may contribute to the high prevalence of OSA in tetraplegia.

Nasopharyngoscopic evaluation of oral appliance therapy for obstructive sleep apnoea.

This study aimed to explore the effect of mandibular advancement splints (MAS) on upper airway anatomy during wakefulness in obstructive sleep apnoea (OSA). Patients commencing treatment for OSA with MAS were recruited. Response to treatment was defined by a >or=50% reduction in the apnoea/hypopnoea index. Nasopharyngoscopy was performed in the supine position. Nasopharyngoscopy was performed in 18 responders and 17 nonresponders. Mandibular advancement caused an increase in the calibre of the velopharynx (mean+/- sem +40+/-10%), with relatively minor changes occurring in the oropharynx and hypopharynx. An increase in cross-sectional area of the velopharynx with mandibular advancement occurred to a greater extent in responders than nonresponders (+56+/-16% versus +22+/-13%; p<0.05). Upper airway collapse during the Müller manoeuvre, relative to the baseline cross-sectional area, was greater in nonresponders than responders in the velopharynx (-94+/-4% versus -69+/-9%; p<0.01) and oropharynx (-37+/-6% versus -16+/-3%; p<0.01). When the Müller manoeuvre was performed with mandibular advancement, airway collapse was greater in nonresponders than responders in the velopharynx (-80+/-11% versus +9+/-37%; p<0.001), oropharynx (-36+/-6% versus -20+/-5%; p<0.05) and hypopharynx (-64+/-6% versus -42+/-6%; p<0.05). These results indicate that velopharyngeal calibre is modified by MAS treatment and this may be useful for predicting treatment response.

Obstructive sleep apnoea--an update.

Obstructive sleep apnoea (OSA) is a common disorder characterized by the repetitive complete or partial collapse of the upper airway during sleep. It results in intermittent hypoxaemia and hypercapnia, cortical arousals and surges of sympathetic activity. The occurrence of OSA has also been linked to serious long-term adverse health consequences; such as hypertension, metabolic dysfunction, cardiovascular disease, neurocognitive deficits and motor vehicle accidents. There have been several advances in the field of particular clinical importance: (i) the development of portable monitoring as part of a simplified clinical algorithm for the diagnosis of OSA in selected patients; (ii) growing awareness of the cardio-metabolic health consequences of OSA and (iii) emerging evidence to support a range of non-continuous positive airway pressure (CPAP) treatment modalities, such as oral appliances.

Obstructive sleep apnea and hypertension: epidemiology, mechanisms and treatment effects.

Obstructive sleep apnea (OSA) is a highly prevalent disorder of breathing during sleep. A growing body of evidence suggests that OSA is independently associated with an increased risk of cardiovascular disease, although the extent of this risk and underlying mechanisms remain to be elucidated. However, there is clearer evidence from epidemiological and pathophysiological research of a causal link between OSA and hypertension. The acute hemodynamic and autonomic perturbations that accompany obstructive apneas during sleep, with associated repeated arousals and intermittent hypoxemia, appear to result in sustained hypertension. In addition to the metabolic and humoral effects from obesity, OSA appears to predispose individuals to autonomic imbalance characterized by sympathetic overactivity and altered baroreflex mechanisms as well as alterations to vascular function. Treatment of OSA restores normal sleep architecture and generally mitigates the acute hemodynamic effects of OSA. Treatment of symptomatic OSA, particular at the severe end of the spectrum, appears to be associated with improvements in blood pressure, both during sleep and wakefulness, and there may also be additional gains in subjects who are hypertensive and/or resistant to antihypertensive medications. The severe group appears to be particularly at risk for developing fatal and non-fatal cardiovascular events and treatment with continuous positive airway pressure appears to markedly reduce that risk. Future treatment studies will need to be extended for greater than the current average of 1-2 months in order to more fully evaluate any time dependent improvements in blood pressure, and consequent cardiovascular risk.

Relationship between craniofacial abnormalities and sleep-disordered breathing in Marfan's syndrome.

OBJECTIVES: To examine the prevalence and nature of craniofacial abnormalities in patients with Marfan's syndrome and to investigate the relationship between craniofacial abnormalities and obstructive sleep apnea (OSA) severity in these patients. DESIGN: Cross-sectional. SETTING: Marfan's syndrome clinic in a tertiary teaching hospital. PATIENTS: Fifteen consecutive adult patients (7 men and 8 women; mean [+/- SD] age, 34.8 +/- 13.2 years) who had Marfan's syndrome. MEASUREMENTS AND RESULTS: Apneic status was determined from standard overnight polysomnography testing. Measurements from standardized lateral cephalometric radiographs were compared to normative data. Thirteen patients had OSA, which was defined as an apnea/hypopnea index (AHI) of > 5 episodes per hour (mean AHI, 22 +/- 15 episodes per hour). A high prevalence of craniofacial abnormalities was found with significant gender differences for some of the variables. Significant abnormalities for the entire group were bimaxillary retrusion, a reduced maxillary length, an increased total anterior face height, a long lower anterior face height, an obtuse gonial angle, a steep mandibular plane, a reduced posterior nasal airway height, a reduced posterior airway space, and an increased distance from the mandibular plane to the hyoid bone. Univariate analysis revealed significant correlations among the total anterior face height, the upper anterior and posterior face heights, the mandibular length, and AHI. There was a significant correlation between the rank of the number of cephalometric abnormalities per patient and AHI in those patients with OSA. CONCLUSIONS: Craniofacial abnormalities are common in patients with Marfan's syndrome. The relationship between some cephalometric parameters and apnea severity suggests a potential role of craniofacial structure in the pathogenesis of OSA in these patients.

A randomized, controlled study of a mandibular advancement splint for obstructive sleep apnea.

Although there is increasing interest in the use of oral appliances to treat obstructive sleep apnea (OSA), the evidence base for this is weak. Furthermore, the precise mechanisms of action are uncertain. We aimed to systematically investigate the efficacy of a novel mandibular advancement splint (MAS) in patients with OSA. The sample consisted of 28 patients with proven OSA. A randomized, controlled three-period (ABB/BAA) crossover study design was used. After an acclimatization period, patients underwent three polysomnographs with either a control oral plate, which did not advance the mandible (A), or MAS (B), 1 wk apart, in either the ABB or BAA sequence. Complete response (CR) was defined as a resolution of symptoms and a reduction in Apnea/Hypopnea Index (AHI) to < 5/h, and partial response (PR) as a > or = 50% reduction in AHI, but remaining > or = 5/h. Twenty-four patients (19 men, 5 women) completed the protocol. Subjective improvements with the MAS were reported by the majority of patients (96%). There were significant improvements in AHI (30 +/- 2/h versus 14 +/- 2/h, p < 0.0001), MinSa(O(2)) (87 +/- 1% versus 91 +/- 1%, p < 0.0001), and arousal index (41 +/- 2/h versus 27 +/- 2/h, p < 0.0001) with MAS, compared with the control. The control plate had no significant effect on AHI and MinSa(O(2)). CR (n = 9) or PR (n = 6) was achieved in 62.5% of patients. The MAS is an effective treatment in some patients with OSA, including those patients with moderate or severe OSA.

Maxillary morphology in obstructive sleep apnoea syndrome.

The aim of this case-control study was to test the hypothesis that maxillary morphology differs between obstructive sleep apnoea (OSA) patients and non-snoring, non-apnoeic subjects. Forty randomly selected patients [36 M, 4 F; mean age 49 +/- 2 (SEM) years] with varying degrees of OSA (mean Apnoea/Hypopnoea Index 32 +/- 4/hour) were compared with 21 non-snoring, non-apnoeic control subjects (18 M, 3 F; mean age 40 +/- 2 years). An intra-oral assessment of the occlusion was carried out, particularly for the presence or absence of posterior transverse discrepancies. Maxillary dental arch width was assessed by standardized lateral inter-tooth measurements (inter-canine, inter-premolar, and inter-molar) from dental models. Palatal height and maxillary depth were also measured. The maxillary dental arch was described by a 4th order polynomial equation. The ratios of maxillary to mandibular width (max/mand) and maxillary to facial width (max/facial) were determined from standardized postero-anterior cephalometric radiographs in a subgroup of patients (n = 29) and all controls. Twenty patients (50 per cent) had evidence of posterior transverse discrepancies compared with one control subject (5 per cent; P < 0.01). All patients had significantly reduced inter-canine, inter-premolar, and inter-molar distances (P < 0.05). The maxillary depth was also shorter (P < 0.05), but palatal height was not different. The quadratic coefficient of the polynomial equation was greater in the patients than in the controls (P < 0.05), indicative of greater arch tapering. Patients had smaller maxillary to mandibular and maxillary to facial width ratios (P < 0.01). These results suggest that OSA patients have narrower, more tapered, and shorter maxillary arches than non-snoring, non-apnoeic controls. Further work is required to determine the relevance of these findings in the pathophysiology of OSA.

Influence of maxillary morphology on nasal airway resistance in Marfan's syndrome.

High nasal airway resistance (NAR) has been reported in Marfan's syndrome, and this appears to contribute to the development of obstructive sleep apnoea in these patients. The cause of high NAR in Marfan's syndrome is unknown, but these patients characteristically have a narrow maxilla, which could have an influence on nasal dimensions. The aim of this study was to define the mechanism(s) mediating high NAR in Marfan's syndrome. Five patients with Marfan's syndrome (mean age 29+/-4 (SEM) years) were compared with an equivalent number of normal control subjects (31+/-1 years). NAR was measured by posterior rhinomanometry, before and after topical decongestant, nasal stenting, or both. Dental impressions were taken to evaluate maxillary arch morphology, allowing measurement of the following lateral distances: inter-canine (ICD), inter-premolar (IPD), and inter-molar (IMD). NAR (at a flow of 500 ccm/s) was considerably higher in patients compared with controls at baseline (0.93+/-0.08 vs 0.35+/-0.08 Pa/ccm/s, p < 0.001), and following decongestant and/or stenting. The maxillary arch was considerably narrower in patients. There were strong inverse correlations between the lateral maxillary dimensions and NAR after nasal decongestant, with or without stenting. These results indicate a strong association between maxillary width and NAR, and suggest that maxillary constriction is the dominant mechanism for the high NAR in Marfan's syndrome. The therapeutic implications of this finding warrant further investigation.

Treatment of obstructive sleep apnea syndrome by rapid maxillary expansion.

The precise role of maxillary constriction in the pathophysiology of obstructive sleep apnea (OSA) is unclear. However, it is known that subjects with maxillary constriction have increased nasal resistance and resultant mouth-breathing, features typically seen in OSA patients. Maxillary constriction is also associated with alterations in tongue posture which could result in retroglossal airway narrowing, another feature of OSA. Rapid maxillary expansion (RME) is an orthodontic treatment for maxillary constriction which increases the width of the maxilla and reduces nasal resistance. The aim of this pilot study was to investigate the effect of rapid maxillary expansion in OSA. We studied 10 young adults (8 male, 2 female, mean age 27 +/- 2 [sem] years) with mild to moderate OSA (apnea/hypopnea index-AHI 19 +/- 4 and minimum SaO2 89 +/- 1%), and evidence of maxillary constriction on orthodontic evaluation. All patients underwent treatment with RME, six cases requiring elective surgical assistance. Polysomnography was repeated at the completion of treatment. Nine of the 10 patients reported improvements in snoring and hypersomnolence. There was a significant reduction in AHI (19 +/- 4 vs 7 +/- 4, p < 0.05) in the entire group. In seven patients, the AHI returned to normal (i.e., = < 5); only one patient showed no improvement. These preliminary data suggest that RME may be a useful treatment alternative for selected patients with OSA.

Aortic root dilatation in Marfan's syndrome: a contribution from obstructive sleep apnea?

We report two cases of Marfan's syndrome with coexistent obstructive sleep apnea (OSA) in which treatment with nasal continuous positive airway pressure was associated with attenuation of aortic root dilatation, a serious complication of the syndrome. We speculate that coexistent OSA promotes progressive aortic dilatation in some patients with Marfan's syndrome.

Influence of maxillary constriction on nasal resistance and sleep apnea severity in patients with Marfan's syndrome.

BACKGROUND: Marfan's syndrome is associated with a high prevalence of obstructive sleep apnea (OSA). As this syndrome is associated with a characteristic constricted maxilla and high-arched palate, we reasoned that nasal airway constriction and resultant high nasal airway resistance (NAR) may contribute to the development of OSA. Therefore, the aim of this study was to measure NAR in patients with Marfan's syndrome. In addition, we aimed to examine the influence of maxillary morphology on both NAR and the severity of OSA. METHOD: We measured NAR in 13 consecutive patients with Marfan's syndrome and 13 control subjects. NAR was measured by posterior rhinomanometry, and expressed as the inspiratory resistance at a flow of 0.5 L/s. Dental impressions were taken to evaluate maxillary arch morphology, allowing measurement of the following distances: intercuspid (ICD), interpremolar (IPD), intermolar (IMD), and maximum hard palate height (MPH). Ten of the patients and four of the control subjects had previously undergone nocturnal polysomnography. RESULTS: Mean NAR for the Marfan group was more than twice that in the control group (7.7 +/- 1.2 vs 2.9 +/- 0.4 cm H2O/L/s; p < 0.005). The patients also had marked constriction of the maxillary arch compared with control subjects. Two of the lateral maxillary measurements were significantly inversely correlated with NAR. There were significant correlations between various maxillary arch measurements (MPH/ICD, MPH/IPD, MPH/IMD) and the apnea/hypopnea index. CONCLUSION: These data suggest that high NAR is a common feature of Marfan's syndrome. Maxillary constriction with a relatively high hard palate appears to be a major reason for the high NAR. The significant correlations between indexes of maxillary constriction and sleep apnea severity suggest that maxillary morphology may play an important role in the pathophysiology of OSA in Marfan's syndrome.

Craniofacial abnormalities in obstructive sleep apnoea: implications for treatment.

Obstructive sleep apnoea (OSA) is a common disorder, and is characterized by repetitive closure of the upper airway during sleep. Upper airway narrowing and sleep-induced loss of muscle tone are important factors in the development of OSA. Over the last decade there has been a growing recognition that craniofacial abnormalities occur commonly in OSA patients. The more commonly identified abnormalities include mandibular deficiency, an inferiorly placed hyoid bone relative to the mandibular plane, a narrowed posterior air space, a greater flexion of the cranial base, and elongation of the soft palate. It is thought that these abnormalities result in upper airway narrowing, thereby predisposing to OSA. When the well established role of obesity in the development of OSA is taken into account, a model of OSA emerges in which the degree of craniofacial abnormalities determines the extent of obesity required to produce OSA in a given individual. The recognition of the role of craniofacial abnormalities in the development of OSA has led to a number of treatment strategies aimed at correcting or improving craniofacial structure, thereby preventing upper airway collapse during sleep. These treatments include dental appliances, and various maxillofacial surgical procedures. An improved understanding of the evolution of OSA from childhood to adulthood, in relation to facial development, may lead to a preventative strategy for this disorder.

Mouth leak with nasal continuous positive airway pressure increases nasal airway resistance.

Nasal congestion, dry nose and throat, and sore throat affect approximately 40% of patients using nasal continuous positive airway pressure (CPAP). The mechanisms causing nasal symptoms are unclear, but mouth leaks causing high unidirectional nasal airflow may be important. We conducted a study to investigate the effects of mouth leak and the influence of humidification on nasal resistance in normal subjects. Nasal resistance was measured with posterior rhinomanometry in six normal subjects who deliberately produced a mouth leak for 10 min while using nasal CPAP. Nasal resistance was measured regularly for 20 min after the challenge. A series of tests were performed using air at differing temperatures and humidities. There was no change in nasal resistance when subjects breathed through their noses while on CPAP, but a mouth leak caused a large increase in resistance (at a flow of 0.5 L/s) from a baseline mean of 2.21 cm H2O/L/s to a maximum mean of 7.52 cm H2O/L/s at 1 min after the challenge. Use of a cold passover humidifier caused little change in the response (maximum mean: 8.27 cm H2O/L/s), but a hot water bath humidifier greatly attenuated the magnitude (maximum mean: 4.02 cm H2O/L/s) and duration of the response. Mouth leak with nasal CPAP leads to high unidirectional nasal airflow, which causes a large increase in nasal resistance. This response can be largely prevented by fully humidifying the inspired air.

Sleep apnea in Marfan's syndrome. Increased upper airway collapsibility during sleep.

Marfan's syndrome is a hereditary disorder characterized by a defect in connective tissue, resulting in tissue laxity. It is associated with a high prevalence of obstructive sleep apnea (OSA). The aim of this study was to determine whether excessive upper airway collapsibility during sleep is an important pathophysiologic factor predisposing these individuals to OSA. We measured upper airway closing pressures (UACP) during sleep in 12 patients with Marfan's syndrome and 6 age-, and height-, and weight-matched control subjects. Ten of the patients had OSA, defined as an apnea/hypopnea index > 5. All patients with Marfan's syndrome, including the two patients without OSA, demonstrated increased upper airway collapsibility during sleep, with a mean UACP of -2.5 +/- 0.5 cm H2O during slow-wave sleep (SWS). In contrast, only two control subjects demonstrated upper airway closure. However, this was at significantly higher suction pressures, with a mean UACP of -5.6 +/- 0.4 cm H2O during SWS (p < 0.005). These data suggest that patients with Marfan's syndrome have abnormally increased upper airway collapsibility during sleep. It is possible that this is related to the characteristic connective tissue defect of this disorder.

Obstructive sleep apnea in obese noninsulin-dependent diabetic patients: effect of continuous positive airway pressure treatment on insulin responsiveness.

Patients with noninsulin-dependent diabetes mellitus (NIDDM) are often obese and frequently complain of tiredness. These features are also characteristically seen in patients with obstructive sleep apnea (OSA). Therefore, it was the aim of this study to assess the prevalence of OSA among a group of obese NIDDM patients who have some clinical features of OSA. The effect of reversal of OSA by nasal continuous positive airway pressure (CPAP) treatment on insulin responsiveness was also investigated. From a population of 179 NIDDM patients with a body mass index (BMI) greater than 35 kg/m2, we performed ambulatory sleep monitoring on 31 (15 males and 16 females) who admitted to either heavy snoring or excessive sleepiness. Results were reviewed by a sleep physician blinded to the clinical status of the patients, and 22 (70%) were found to have moderate or severe OSA, with mean oxygen desaturation indexes of 10.3 +/- 5.3 and 30.7 +/- 13.2 episodes/h, respectively. A subgroup of 10 patients (seven males and three females) with a mean BMI of 42.7 +/- 4.3 kg/m2 was treated with nightly CPAP for 4 months. These subjects all had significant OSA, with frequent obstructive apneas (mean, 47 +/- 31.6 episodes/h) and oxygen desaturation (mean minimum O2 saturation, 74 +/- 9.5%), as determined by polysomnography. One patient was excluded from analysis because of infrequent use of CPAP. Insulin responsiveness in terms of glucose disposal measured by hyperinsulinemic euglycemic clamps improved from 11.4 +/- 6.2 to 15.1 +/- 4.6 mumol/kg.min (P < 0.05) during CPAP treatment. These results indicate that OSA occurs commonly in obese NIDDM patients with excessive sleepiness or heavy snoring. Treatment of their OSA may improve insulin responsiveness.