Obesity and obstructive sleep apnea: Or is it OSA and obesity?

Obstructive sleep apnea (OSA) consists of repetitive choking spells due to sleep-induced reduction of upper airway muscle tone. Millions of adults and children live unaware of this condition, which can have a profound affect on their health and quality of life. Obesity, gender, genetic, and hormonal factors mediate risk for OSA and interact in a multifaceted manner in the pathogenesis of this disease. Obesity is the most established and primary risk factor given that body mass index, visceral fat, and neck circumference are major predictors in the clinical expression of OSA. Many studies have shown weight loss or gain significantly impacts OSA severity. More recently, accumulating evidence indicates OSA promotes weight gain, obesity, and type II diabetes in a variety of ways, such that obesity and OSA form multiple interleaved vicious cycles. Thus, creative strategies to increase physical activity, improve diet, and otherwise facilitate weight management become particularly vital given the epidemics of obesity and OSA in the United States. In this regard, the American College of Sports Medicine recently launched the "Exercise is Medicine" (initiative exerciseismedicine.org). In the future, medications may emerge to treat obesity, OSA, and their sequelae with minimal side effects. However, there are effective ways to approach these problems now without waiting for "the magic pill".     

Is treatment of obstructive sleep apnea syndrome with auto-CPAP useful?

Automatic CPAP therapy has been developed to constantly adapt the positive pressure level to the required needs. The automatic devices have been used in two different ways, one being to determine the pressure level to be prescribed at home for fixed CPAP therapy, and the other one to replace fixed CPAP as an home treatment. This last application should alleviate the need for a titration study. The benefits reported up to now in the literature vary from one machine to another, but usually these machine are effective in abolishing obstructive breathing disturbances and the consecutive sleep fragmentation. The mean positive pressure level applied during automatic CPAP treatment is usually less than the effective pressure level measured during a conventional titration sleep study. Some results suggest that automatic CPAP therapy may improve compliance to CPAP therapy. There is a need to better define if automatic CPAP therapy may benefit to specific groups of sleep apnea patients.     

Complex sleep apnea syndrome: is it a unique clinical syndrome?

STUDY OBJECTIVES: Some patients with apparent obstructive sleep apnea hypopnea syndrome (OSAHS) have elimination of obstructive events but emergence of problematic central apneas or Cheyne-Stokes breathing pattern. Patients with this sleep-disordered breathing problem, which for the sake of study we call the "complex sleep apnea syndrome," are not well characterized. We sought to determine the prevalence of complex sleep apnea syndrome and hypothesized that the clinical characteristics of patients with complex sleep apnea syndrome would more nearly resemble those of patients with central sleep apnea syndrome (CSA) than with those of patients with OSAHS. DESIGN: Retrospective review SETTING: Sleep disorders center. PATIENTS OR PARTICIPANTS: Two hundred twenty-three adults consecutively referred over 1 month plus 20 consecutive patients diagnosed with CSA. INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: Prevalence of complex sleep apnea syndrome, OSAHS, and CSA in the 1-month sample was 15%, 84%, and 0.4%, respectively. Patients with complex sleep apnea syndrome differed in gender from patients with OSAHS (81% vs 60% men, p < .05) but were otherwise similar in sleep and cardiovascular history. Patients with complex sleep apnea syndrome had fewer maintenance-insomnia complaints (32% vs 79%; p < .05) than patients with CSA but were otherwise not significantly different clinically. Diagnostic apnea-hypopnea index for patients with complex sleep apnea syndrome, OSAHS, and CSA was 32.3 +/- 26.8, 20.6 +/- 23.7, and 38.3 +/- 36.2, respectively (p = .005). Continuous positive airway pressure suppressed obstructive breathing, but residual apnea-hypopnea index, mostly from central apneas, remained high in patients with complex sleep apnea syndrome and CSA (21.7 +/- 18.6 in complex sleep apnea syndrome, 32.9 +/- 30.8 in CSA vs 2.14 +/- 3.14 in OSAHS; p < .001). CONCLUSIONS: Patients with complex sleep apnea syndrome are mostly similar to those with OSAHS until one applies continuous positive airway pressure. They are left with very disrupted breathing and sleep on continuous positive airway pressure. Clinical risk factors don't predict the emergence of complex sleep apnea syndrome, and best treatment is not known.     

Does sleep deprivation worsen mild obstructive sleep apnea?

STUDY OBJECTIVES: Sleep deprivation is believed to worsen obstructive sleep apnea (OSA). We assessed the effect of acute sleep deprivation on polysomnography in a cohort of subjects with mild OSA and a cohort of subjects without OSA. DESIGN: Crossover study in which subjects initially had polysomnography after a normal night's sleep or after 36 hours of sleep deprivation, followed by a 2- to 4-week interval, after which subjects were restudied under the alternate testing condition. SETTING AND PARTICIPANTS: 13 subjects with mild OSA and 16 subjects without OSA were studied in a university teaching hospital sleep laboratory. INTERVENTIONS: 36 hours of supervised sleep deprivation. MEASUREMENTS: Subjects' age, body mass index, neck circumference and Epworth Sleepiness Scale scores were measured; actigraphy and sleep diaries were used to estimate prior sleep debt before each sleep study. RESULTS: Sleep deprivation was found to significantly increase total sleep time, sleep efficiency, and rapid eye movement and slow-wave sleep time. Subjects with OSA showed a lower minimum oxygen saturation after sleep deprivation. However, subjects did not show a significantly different respiratory disturbance index, arousal index, or length of the longest apnea after sleep deprivation. CONCLUSIONS: Acute sleep deprivation did not worsen most OSA parameters as measured by polysomnography. A lower minimum oxygen saturation in mild OSA subjects after sleep deprivation may be important in patients with significant cardiorespiratory disease. More research is needed to assess whether daytime performance and function (eg, driving, sleepiness) is more greatly impaired in OSA subjects who are sleep deprived, compared to normal subjects who are sleep deprived.     

Does nasal decongestion improve obstructive sleep apnea?

Whether nasal congestion promotes obstructive sleep apnea is controversial. Therefore, we performed a randomized placebo-controlled cross-over trial on the effects of topical nasal decongestion in patients with obstructive sleep apnea syndrome (OSA) and nasal congestion. Twelve OSA patients with chronic nasal congestion (mean +/- SD age 49.1 +/- 11.1 years, apnea/hypopnea index 32.6 +/- 24.5/h) were treated with nasal xylometazoline or placebo for 1 week each. At the end of treatment periods, polysomnography including monitoring of nasal conductance by an unobtrusive technique, vigilance by the OSLER test, and symptom scores were assessed. Data from xylometazoline and placebo treatments were compared. Mean nocturnal nasal conductance on xylometazoline was significantly higher than on placebo (8.6 +/- 5.3 versus 6.3 +/- 5.8 mL s(-1)Pa(-1), P < 0.05) but the apnea/hypopnea index was similar (29.3 +/- 32.5/h versus 33.2 +/- 32.8/h, P = NS). However, 30-210 min after application of xylometazoline, at the time of the maximal pharmacologic effect, the apnea/hypopnea index was slightly reduced (27.3 +/- 30.5/h versus 33.2 +/- 33.9/h, P < 0.05). Xylometazoline did not alter sleep quality, sleep resistance time (33.6 +/- 8.8 versus 33.4 +/- 10.1 min, P = NS) and subjective sleepiness (Epworth score 10.5 +/- 3.8 versus 11.8 +/- 4.4, P = NS). The reduced apnea/hypopnea index during maximal nasal decongestion by xylometazoline suggests a pathophysiologic link but the efficacy of nasal decongestion was not sufficient to provide a clinically substantial improvement of OSA.     

Can snoring induce or worsen obstructive sleep apnea?

Snoring and sleep apneas are breathing disorders intimately associated during sleep. Most snorers are ‘simple’ or ‘nonapneic’, as the prevalence of snoring is much higher than that of sleep apneas. The vibrations transmitted to the pharyngeal structures by snoring span a large range of frequencies, while the energy transmitted may reach high values. A deleterious effect of these vibrations can therefore be considered.In 1983 a group of investigators from Bologna described five cases of heavy snorers of increasing severity, suggesting that they correspond to the natural history of ‘heavy snorers’ disease'. The present article reviews the data published since 1983 in favor of this hypothesis: anatomic lesions of the upper airway mucosa, pharyngeal muscles and nerves, and clinical observations in snorers. The conclusion stresses the absence of ultimate proof in favor of this attractive hypothesis: we lack the demonstration of a significant increase of the incidence of sleep apnea in a group of nonapneic snorers in a longitudinal follow-up study.     

Does cognitive dysfunction conform to a distinctive pattern in obstructive sleep apnea syndrome?

Obstructive sleep apnea (OSA) is a recognized cause of cognitive dysfunction. By using a cross-sectional comparative study, we aimed to verify whether neuropsychological performance of untreated OSA patients conforms to a distinctive pattern. Forty-nine newly diagnosed, untreated OSA patients, 27 with multi-infarctual dementia (MID), 31 with mild to moderate dementia of Alzheimer type (DAT) and 63 with severe chronic obstructive pulmonary disease (COPD), all free from major comorbid dementing conditions were chosen for the study. The groups were matched for age and education. We found a bimodal distribution of cognitive performance in OSA group, which was therefore divided into two clusters having better (OSAb, n = 35) and worse (OSAw, n = 14) performance on a battery of 10 cognitive indexes. Cognitive performances of OSAb, OSAw, MID, DAT and COPD were compared by discriminant analysis. OSAb performed better than OSAw in all but one test. Deductive thinking and verbal attainment were more severely impaired in OSAw than in COPD patients. Constructive ability, deductive thinking and both verbal attainment and immediate memory were comparably impaired in OSAw and DAT. The mean neuropsychological scores of OSAw and MID were comparable, but 71% of OSAw patients had a distinctive cognitive profile, i.e. a group specific pattern of cognitive dysfunction, according to discriminant analysis. One of four newly diagnosed OSA patients had a severe and distinctive neuropsychological dysfunction mainly involving inductive and deductive thinking, and constructive ability. Some analogy with cognitive pattern of MID suggests that a mainly subcortical damage underlies this dysfunction.     

Sleepiness in obstructive sleep apnea: a harbinger of impaired cardiac function?

STUDY OBJECTIVES: Daytime sleepiness is a common clinical presentation in both obstructive sleep apnea (OSA) and cardiovascular diseases. The purpose of this study was to assess the relationship between degree of subjective daytime sleepiness and cardiac performance in patients with obstructive sleep apnea. DESIGN: Observational study. SETTING: General Clinical Research Center. PATIENTS: The study sample was comprised of 86 patients (68 men and 18 women) with an average age of 47 years. All were suspected of having obstructive sleep apnea and underwent confirmatory diagnostic polysomnography (respiratory disturbance index > or = 15). MEASUREMENTS AND RESULTS: Stroke volume and cardiac output were measured using impedance cardiography and corrected for body surface area to yield stroke index and cardiac index. Daytime sleepiness was quantified using the Epworth Sleepiness Scale. A higher Epworth Sleepiness Scale score, suggesting more daytime sleepiness, was significantly related to lower stroke index and cardiac index. In multiple regression analyses, the relationships of Epworth Sleepiness Scale score with both stroke index and cardiac index were significant (p < .05), even after controlling for age, sex, ethnicity, respiratory disturbance index, and mean sleep oxygen saturation. CONCLUSIONS: These results suggest that daytime sleepiness is independently associated with decreases in cardiac function as assessed by impedance cardiography in patients with obstructive sleep apnea.     

Is there a vicious cycle between obstructive sleep apnea and laryngopharyngeal reflux disease?

Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder which is mainly characterized by the repetitive episodes of obstructive apneas and/or hypopneas. It is associated with daytime sleepiness, decrements in quality of life, cardiovascular and cerebrovascular diseases and endocrine disturbances. In addition, there is a high prevalence of gastric reflux (including both gastroesophageal reflux and laryngopharyngeal reflux diseases) in patients with OSA. However, the mechanism underlying this association has not been completely established. Herein, we hypothesize that there is a vicious cycle between OSA and laryngopharyngeal reflux disease. Increased respiratory efforts in OSA generate more-negative intrathoracic pressure, contributing to reflux of gastric contents, which in turn creates inflammation and sensory deficits in the laryngeal and pharyngeal tissues that contributes to progression of OSA through both inflammatory and neuromuscular pathways.     

Clinical value of polymesam recording in diagnosis of obstructive sleep apnea. Can we replace polysomnography with polymesam?

Polymesam (PM) recordings was performed in 320 patients admitted to Sleep Laboratory with suspicion of OSA. OSA was diagnosed in 179 of them (55.9%), group (PM-Ch). These patients were obese (BMI--34.3 +/- 6.7 kg/m2) and had moderately-severe OSA (RDI--41.5 +/- 19.9 and ODI--43.7 +/- 21.5). They suffered from excessive daytime sleepiness (ESS = 12.2 +/- 5.5). PM was negative in 141 person (44.1%), (PM-Z). Subjects PM-Z had significantly lower BMI and rarely suffered from excessive daytime sleepiness. In 38 subjects PM-Z a full PSG was performed. In 12 PSG confirmed OSA (AHI--31.6 +/- 19.9). Both studies (PM and PSG) were negative in 26 subjects. In 10 obese subjects PM-Ch full PSG confirmed diagnosis. CONCLUSIONS: PM recording can replace full PSG in majority of patients suspected of OSA. Patients with typical symptoms of OSA and negative PM require PSG.     

Ischemic vascular disease and solid cancers: opposing ends of the angiogenic spectrum?

Angiogenesis is a key pathway crucial to the patho-physiology of both vascular disease and solid cancer. In physiological conditions, a fine balance of pro- and anti-angiogenic factors is maintained as part of normal homeostatic mechanisms. It is widely accepted that excess angiogenesis influences the development or progression of tumours whilst insufficient angiogenesis may predispose to ischemic vascular disease. Although there are some factors, which predispose to both cancers and vascular disease, we believe there is a reasonable body of literature that suggests an inverse association between the two. We hypothesise that pro-angiogenic and anti-angiogenic phenotypes exist in the population. This may be due to a combination of underlying genetic variations and/or environmental factors. Pro-angiogenic phenotypes would have increased susceptibility to solid cancers and decreased predisposition to cardiovascular diseases and vice versa with the anti-angiogenic phenotypes. We propose that genetic and environmental factors causing a shift in the balance of angiogenesis will predispose individuals towards one group of pathologies while protecting them from another. Evaluation of this hypothesis will in the first instance involve carefully designed large population based observational studies to determine if an inverse relationship exists between the predisposition to ischemic vascular disease and the predisposition to solid cancer. Further detailed study of the pathways and underlying mechanisms of angiogenesis especially in disease states would facilitate better understanding of its regulation. Evaluation and validation of molecular markers that affect the 'angiogenesis pathway' may be helpful in determining the angiogenic potential of individual subjects. Determining where individuals lie along this spectrum may have a potential role in the prediction and stratification of risk of cancer and vascular disease. Modifying risk for patients at high risk of disease at the two opposing ends of the spectrum may then be possible by either lifestyle or dietary alterations or drugs targeting the angiogenic pathway.     

Obstructive sleep apnea syndrome: who should be treated?

Most, if not all patients referred for assessment require some form of therapeutic intervention. In particular, general lifestyle advice, sleep hygiene, and weight reduction in overweight patients should always be promoted, even where additional specific therapy such as NCPAP is also being considered. Treatment decisions are relatively easy at the extremes of the clinical spectrum, but there is an increasing choice of therapeutic options available for those patients in the mid-range of severity. Criteria based on AHI levels are inappropriate to dictate treatment choice, particularly NCPAP.