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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

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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.

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Obstructive sleep apnea (OSA) is associated with increased cardiovascular risk, mediated through pathophysiological mechanisms that include intermittent hypoxia, excessive sympathetic nervous activation and exaggerated swings in negative intrathoracic pressure (2, 3). While it has previously been established from randomized controlled trials (RCT) that treatment of OSA with continuous positive airway pressure (CPAP) reduces blood pressure, with the most marked effects seen in drug-resistant hypertension (4), data to support a role for CPAP therapy to reduce cardiovascular mortality comes largely from observational studies (5, 6). To address this, McEvoy et al. conducted a multicentre, randomized, parallel-group trial to evaluate the efficacy of CPAP in reducing cardiovascular mortality in patients with moderate-to-severe OSA (oxygen desaturation index ≥ 12) and a history of coronary artery disease or cerebrovascular disease , who were mildlyor non-sleepy (Epworth Sleepiness Scale less or equal to 15) (1). Patients were excluded if they had severe hypoxia (oxygen saturation <80%) or if they had a Cheyne-Stokes respiration pattern. The primary endpoint included a composite of death from cardiovascular causes, myocardial infarction, stroke or hospitalization for unstable angina, heart failure or transient ischemic attack. 2687 subjects were randomized to either "usual care" (n=1341) or "usual care" plus CPAP (n=1346). After a mean follow up of 3.7 years, there was no significant difference in the occurrence of the primary endpoint between the groups (hazard ratio (HR) with CPAP added, 1.10; 95% confidence interval (CI) 0.91 to 1.32; p = 0.34). Mean duration of adherence to CPAP therapy was 3.3 hours per night. A one-to-one propensity score analysis performed to compare 561 adherent patients (CPAP used for more than 4h/night) and 561 patients in the usual care group, showed no significant difference in the primary endpoint (HR 0.80; 95% CI : 0.60-1.07; p = 0.13), but a lower risk of cerebrovascular events among the CPAP group (HR 0.52; 95% CI : 0.30-0.90; p = 0.02). The results of this relatively large RCT are clearly an important addition to the current knowledge base and certainly, on the basis of this one study, CPAP cannot be recommended as a therapy in moderate to severe OSA patients with established cardiovascular disease if the sole purpose is to reduce cardiovascular complications. This trial affirms the results of other studies in highlighting the uncertain efficacy of CPAP therapy in the reduction of cardiovascular risk in non-symptomatic OSA patients over the short to medium term, and also highlights the challenge of CPAP adherence (7, 8). However, it is important that these results are not extrapolated to those OSA patients who do have excessive daytime sleepiness or significant hypoxia given these patients were excluded from the study. (AU)

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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.

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