Central sleep apnea: implications for congestive heart failure

Congestive heart failure (HF), an exceedingly common and costly disease, is frequently seen in association with central sleep apnea (CSA), which often manifests as a periodic breathing rhythm referred to as Cheyne-Stokes respiration. CSA has historically been considered to be a marker of heart disease, since improvement in cardiac status is often associated with the attenuation of CSA. However, this mirroring of HF and CSA may suggest bidirectional importance to their relationship. In fact, observational data suggest that CSA, associated with repetitive oxyhemoglobin desaturations and surges in sympathetic neural activity, may be of pathophysiologic significance in HF outcomes. In light of the disappointing results from the first large trial assessing therapy with continuous positive airway pressure in patients with CSA and HF, further large-scale interventional trials will be needed to assess the role, if any, of CSA treatment on the outcomes of patients with HF. This review will discuss epidemiologic, pathophysiologic, diagnostic, and therapeutic considerations of CSA in the setting of HF.     

Obstructive sleep apnea in a laryngectomy patient: “External obstructive sleep apnea”

Obstructive sleep apnea was diagnosed in a man after a total laryngectomy. Excessive daytime sleepiness led to a diagnostic investigation. He had occlusion of the tracheal stoma while asleep by his chin and neck structures. This “external” obstructive sleep apnea caused repetitive desaturations and arousals typical of sleep apnea. Therapeutic measures to keep the chin off the stoma were successful in preventing the apneas with complete symptom relief. This is the first case of obstructive sleep apnea syndrome occurring from an obstruction external to the airway.     

Evidence for liver injury in the setting of obstructive sleep apnea

Introduction. Obstructive sleep apnea (OSA) and non-alcoholic fatty liver disease (NAFLD) are both strongly associated with obesity. Whether OSA is an independent risk factor for liver injury is uncertain.Objective. To assess the hypothesis that OSA is associated with liver injury independent of obesity.Materials and methods. We reviewed the histories of 73 consecutive patients referred to a hospital-based sleep lab because of suspected OSA. OSA was determined to be present if the apnea-hypopnea index was > 10. Obesity was defined as a BMI ≥ 30 kg/m². Patients were included for analysis if they had aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels obtained within 60 days of sleep study. Patients with evidence of viral hepatitis, autoimmune-, metabolic-or established alcoholic-liver disease were excluded. Patients who reported alcohol intake equivalent to a dose ≥ 20 g/day were also excluded. 53 of 73 patients met study criteria. Patients were subdivided for analysis into groups meeting or not meeting OSA and obesity criteria, and having or not having elevated aminotransferase levels.Results. 35/53 patients (66%) had OSA. 31/53 (58%) patients were obese. 15 (28%) and 12 (23%) patients had elevated AST and ALT, respectively. Mean age, gender distribution, mean BMI and percentage with either diabetes or hyperlipi-demia were not significantly different in those with or without OSA. Elevated ALT was found in 11/35 (31%) patients with OSA, compared to 1/18 patients without OSA (p = 0.041). Frequency of elevated AST [obese 11/31 (35%); non-obese 4/22 (18%)] or ALT [obese 10/31 (32%); non-obese 2/22 (9%)] was not significantly different in the obese and non-obese cohorts.Conclusions. OSA may be a risk factor for liver injury independent of obesity. The prevalence and nature of liver disease in the setting of OSA should be determined with larger, prospective studies. The impact of OSA treatment, if any, on liver injury should be similarly evaluated.     

Excessive daytime sleepiness in obstructive sleep apnea: implications for driving licenses

Sleep and Breathing - Excessive daytime sleepiness (EDS) while driving is a major international public health issue resulting in a more than doubled risk of motor vehicle accidents (MVAs)....     

Obesity-related cardiovascular disease: implications of obstructive sleep apnea

Obesity and obstructive sleep apnea (OSA) often coexist. OSA has been linked to cardiovascular disease. Thus, OSA may contribute to the cardiovascular consequences of obesity. In this review, we explore clinical and pathophysiological interactions between obesity, cardiovascular disease and OSA. We discuss the mechanisms whereby OSA may contribute to hypertension, atherosclerosis, insulin resistance and atrial fibrillation associated with obesity, and emphasize the potential implications for understanding why only a subgroup of obese patients develop cardiovascular disease. Identification of the OSA-dependent and OSA-independent pathways in the cardiovascular pathophysiology of obesity may hold clinical and therapeutic promise.     

Pediatric sleep apnea: implications of the epidemic of childhood overweight

Over the last 30 years, the prevalence of overweight across all pediatric age groups and ethnicities has increased substantially, with the current prevalence of overweight among adolescents estimated to be approximately 30%. Current evidence suggests that overweight is modestly associated with obstructive sleep apnea syndrome (OSAS) among young children, but strongly associated with OSAS in older children and adolescents. The rising incidence of pediatric overweight likely will impact the prevalence, presentation, and treatment of childhood OSAS. The subgroup of children who may be especially susceptible include ethnic minorities and those from households with caregivers from low socioeconomic groups. OSAS, by exposing children to recurrent intermittent hypoxemia or oxidative stress, may amplify the adverse effects of adiposity on systemic inflammation and metabolic perturbations associated with vascular disease and diabetes. When these conditions manifest early in life, they have the potential to alter physiology at critical developmental stages, or, if persistent, provide cumulative exposures that may powerfully alter long-term health profiles. An increased prevalence of overweight also may impact the response to adenotonsillectomy as a primary treatment for childhood OSAS. The high and anticipated increased prevalence of pediatric OSAS mandates assessment of optimal approaches for preventing and treating both OSAS and overweight across the pediatric age range. In this Pulmonary Perspective, the interrelationships between pediatric OSAS and overweight are reviewed, and the implications of the overweight epidemic on childhood OSAS are discussed.     

Implantable pacing devices and sleep apnea: implications for diagnosis and therapy

Sleep apnea has been increasingly recognized for its prevalence and its impact on cardiovascular health. The disorder has considerable impact on cardiovascular disease states, particularly congestive heart failure. Implantable cardiac pacing devices may have a role in both the diagnosis and therapy of sleep apnea, which may be of particular importance given the seemingly wide coprevalence of cardiac disorders and sleep apnea.     

Effects of surgical weight loss for treating obstructive sleep apnea

Purpose

Weight loss has been reported to reduce the severity of obstructive sleep apnea (OSA), particularly in the obese population. However, prospective studies with polysomnography (PSG) for the precise evaluation of OSA are lacking especially in Asian countries. We evaluated the effects of surgical weight loss for treating OSA using PSG data obtained before and after surgery.

Methods

We performed a prospective study analyzing the clinical and PSG data obtained from our cohort of bariatric surgical candidates with moderate to severe OSA, as confirmed by preoperative PSG. The patients underwent follow-up PSG at least 12 months after bariatric surgery (laparoscopic Roux-en-Y gastric bypass).

Results

Of the 47 patients (70.1 %) with moderate to severe OSA among 67 patients who underwent preoperative PSG, 10 patients underwent postoperative PSG. The mean apnea-hypopnea index (AHI) of these 10 patients significantly reduced from 51.0?±?34.2 to 9.3?±?12.9 events/h, while their mean body mass index (BMI) loss was from 39.9?±?8.3 to 26.9?±?4.4 kg/m². Although the severity of OSA improved considerably, OSA resolution was achieved in only five patients (50 %). When compared to the patients who achieved OSA resolution, the patients with residual OSA showed a tendency to have lower minimum arterial oxygen saturation (SaO₂) levels and higher supine AHI values in preoperative PSG.

Conclusions

Surgical weight loss resulted in the significant improvement of OSA associated with obesity. However, OSA remained in a considerable proportion of patients even after substantial weight loss. We recommend that postoperative PSG be considered for the evaluation of residual OSA, especially in patients with low minimum SaO₂ levels and high supine AHI in preoperative PSG.     

Obstructive sleep apnea and heart failure: pathophysiologic and therapeutic implications

Obstructive sleep apnea (OSA) exposes the cardiovascular system to intermittent hypoxia, oxidative stress, systemic inflammation, exaggerated negative intrathoracic pressure, sympathetic overactivation, and elevated blood pressure (BP). These can impair myocardial contractility and cause development and progression of heart failure (HF). Epidemiological studies have shown significant independent associations between OSA and HF. On the other hand, recent prospective observational studies reported a significant association between the presence of moderate to severe OSA and increased risk of mortality in patients with HF. In randomized trials, treating OSA with continuous positive airway pressure suppressed sympathetic activity, lowered BP, and improved myocardial systolic function in patients with HF. These data suggest the potential for treatment of OSA to improve clinical outcomes for patients with HF. However, large-scale randomized trials with sufficient statistical power will be needed to ascertain whether treatment of OSA will prevent development of, or reduce morbidity and mortality from HF.     

Hemostatic implications of endothelial cell apoptosis in obstructive sleep apnea

Patients with obstructive sleep apnea (OSA) are at increased risk of atherothrombosis independent of the Framingham risk factors. Studies on hemostasis factors in OSA are scarce and inconsistent. We sought to understand the variation in atherothrombotic propensity as a function of apoptotic circulating endothelial cells (CECs) in OSA by investigating the relationship between CEC apoptosis and plasma levels of hemostatic factors tissue factor (TF) and von Willebrand Factor (vWF) in apneic subjects. Apoptotic CECs were detected by flow cytometry in 35 male subjects free of cardiovascular diseases (AHI range 8–43) and 12 healthy male controls (AHI range 2–5) before and after 8 weeks of nasal continuous positive airway pressure (nCPAP). Quantitative determination of TF and vWF was performed using an enzyme-linked immunosorbent assay (ELISA) kit. The mean levels of TF (66.78 ± 41.59 pg/ml) and vWF (189.70 ± 69.24 IU/dl) were significantly higher in OSA patients compared with those in healthy subjects (42.83 ± 14.18 pg/ml; and 124.48 ± 31.43 IU/dl). Apoptotic CECs were elevated in patients with OSA and correlated strongly with TF and vWF levels (p = 0.02 and p < 0.001; respectively). There were no correlations between TF, vWF and apnea hypopnea index, or arousal index. Only the percentage of time spent <90% oxygen saturation was inversely associated with TF (r = 0.38; p = 0.02). Following nCPAP therapy, there was significant decrease in TF levels that correlated with decrease in apoptotic CECs. In patients with OSA, increased prothrombotic factors are strongly determined by apoptotic CECs. Treatment with nCPAP may alleviate the coagulation propensity.