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OBJECTIVE Despite evidence of a relationship among obstructive sleep apnea (OSA), metabolic dysregulation, and diabetes, it is uncertain whether OSA treatment can improve metabolic parameters. We sought to determine effects of long-term continuous positive airway pressure (CPAP) treatment on glycemic control and diabetes risk in patients with cardiovascular disease (CVD) and OSA. RESEARCH DESIGN AND METHODS Blood, medical history, and personal data were collected in a substudy of 888 participants in the Sleep Apnea cardioVascular Endpoints (SAVE) trial in which patients with OSA and stable CVD were randomized to receive CPAP plus usual care, or usual care alone. Serum glucose and glycated hemoglobin A1c (HbA1c) were measured at baseline, 6 months, and 2 and 4 years and incident diabetes diagnoses recorded. RESULTS Median follow-up was 4.3 years. In those with preexisting diabetes (n = 274), there was no significant difference between the CPAP and usual care groups in serum glucose, HbA1c, or antidiabetic medications during follow-up. There were also no significant between-group differences in participants with prediabetes (n = 452) or new diagnoses of diabetes. Interaction testing suggested that women with diabetes did poorly in the usual care group, while their counterparts on CPAP therapy remained stable. CONCLUSIONS Among patients with established CVD and OSA, we found no evidence that CPAP therapy over several years affects glycemic control in those with diabetes or prediabetes or diabetes risk over standard-of-care treatment. The potential differential effect according to sex deserves further investigation.

Overnight extracellular rostral fluid shifts have been shown to be of importance in patients with fluid-retaining states and are associated with a higher prevalence of sleep apnea. Pulmonary hypertension is frequently associated with right ventricular dysfunction and progressive right ventricular failure, and an increased prevalence of sleep apnea has been described. In light of the importance of fluid shifts in the pathophysiology of sleep apnea, we aimed to explore temporal fluid shifts in patients with pulmonary hypertension with and without sleep apnea. Patients with pulmonary hypertension (WHO Group 1 or 4) had overnight extracellular rostral fluid shift assessment before and a minimum of 3 months after initiation of pulmonary hypertension-specific therapy. Fluid shift measurements of extracellular leg, abdominal, thoracic and neck fluid volumes were performed simultaneously. Twenty-nine patients with pulmonary hypertension (age 55 ± 16 years, 69% female) participated. Sleep apnea was diagnosed in 15 subjects (apnea-hypopnea index 14 [8-27] per hr). There were no significant differences in baseline or overnight leg extracellular rostral fluid, abdominal extracellular rostral fluid, thoracic extracellular rostral fluid or neck extracellular rostral fluid between those with and without sleep apnea. There was a significant inverse correlation between the sleep apnea severity and the overnight change in leg extracellular rostral fluid (r = -0.375, p = 0.049). There were no significant differences detected in overnight extracellular rostral fluid shifts from baseline to follow-up. Treatment-naïve patients with pulmonary hypertension both with and without sleep apnea demonstrate overnight extracellular rostral fluid shifts from the legs into the thorax and neck. Pulmonary hypertension-specific treatment, while significantly improving cardiac haemodynamics, had little impact on nocturnal extracellular rostral fluid shifts or the presence of sleep apnea.

Objectives To evaluate if treatment with continuous positive airway pressure (CPAP) compared to usual care in stroke patients with obstructive sleep apnea (OSA) over one month reduces delta and alpha oscillations on quantitative electroencephalography (EEG) in association with improvements in cognitive or functional outcomes. Methods Spectral EEG analysis was performed in patients with subacute stroke and OSA randomized to usual care or CPAP treatment from a previous study. Results A total of 23 subjects were included. Compared to CPAP (n = 14), those in the control (n = 9) group demonstrated a significant increase in alpha power (p = 0.042). There was no between group differences for delta, theta or beta power. No significant correlation was demonstrated between the change in alpha power and indices of OSA severity or sleepiness. The increase in alpha power did not correlate with improvements in outcomes. Conclusion Contrary to expectations CPAP treatment of OSA did not significantly decrease alpha and delta oscillations in stroke subjects.

Objectives Our aims were to evaluate HRV in pulmonary hypertension (WHO Group 1 and 4) compared to control subjects, and to assess whether the presence of sleep apnea in those with pulmonary hypertension would be deleterious and cause greater impairment in HRV. Methods This retrospective case-control study analyzed electrocardiogram segments obtained from diagnostic polysomnography. Results Forty-one pulmonary hypertension patients were compared to 41 age, sex and apnea-hypopnea index matched healthy controls. The pulmonary hypertension group had decreased high frequency, very low frequency, low frequency, and percentage of normal R-R intervals that differ by > 50 ms compared to control subjects. Moderate to severe right ventricle dysfunction on echocardiography was a predictor of lower high frequency in pulmonary hypertension patients. Conclusions There were no differences in any HRV measures in pulmonary hypertension patients with or without sleep apnea. Impaired HRV was demonstrated in pulmonary hypertension patients however, the presence of sleep apnea did not appear to further reduce vagal modulation.