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Introduction Obstructive sleep apnea (OSA) is a heterogeneous disease dependent on many factors including the sleep stage and the body position. OSA is often more severe during the rapid eye movement (REM) sleep stage, a phenomenon known as REM predominance. Prior studies suggested associations of higher REM predominance of OSA with younger age, higher obesity, and lower adherence to continuous positive airway pressure (CPAP) therapy, but these studies had small cohort sizes. Here we leverage home-based sleep tests (HST) that estimate REM sleep and measure body position to study REM predominance in a larger cohort of OSA patients. Methods We retrospectively reviewed patients who took HST at our clinic using devices based on peripheral arterial tonometry (WatchPAT, Itamar Medical). The HST results included estimated REM sleep periods and measured body positions. Auto-titrating CPAP therapy was prescribed for the majority of OSA patients diagnosed by the HST. Our inclusion criteria were: apnea-hypopnea index (AHI) above 5 /hour, estimated REM sleep time above 30 minutes, oxygen saturation below 90% (T90) for less than 10 minutes, and successful retrieval of CPAP usage data. CPAP adherence was defined as the percentage of nights with CPAP usage above four hours, and REM predominance as the ratio between REM AHI and non-REM AHI. Additionally, the percentage of estimated sleep time in supine position was calculated. Results Among 292 consecutive patients whose HST were reviewed, 113 patients met the inclusion criteria. The 25th-75th percentile ranges of age, body mass index (BMI), AHI, REM predominance, CPAP adherence and supine sleep percentage were 36–56 years, 28.1–38.4 kg/m2, 8.9–25.9 /hour, 1.27–2.89, 40%-97% and 28%-72%, respectively. REM predominance was not associated with CPAP adherence (P > 0.05), but was significantly associated with lower age, higher BMI, and higher supine sleep percentage (all P < 0.01). Conclusion We found that REM-predominant OSA is relatively more prevalent not only in young and obese patients, but in patients who sleep relatively more in the supine position. This association of REM predominance with body position is a novel finding to our knowledge. Contrary to prior studies, we did not find association of REM predominance with adherence to CPAP therapy. Support (if any):

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INTRODUCTION: Polysomnography (PSG) is usually conducted on patients who are not acutely ill, in order to assess the baseline status of sleep-disordered breathing, including obstructive (OSA) and central sleep apnea (CSA). Here we present a unique case of PSG that was unknowingly performed on a patient suffering from acute submassive pulmonary embolism (PE). CASE PRESENTATION:In 2018, a 53-year-old male with no presented to our clinic for snoring and witnessed apneas. We conducted a PSG that showed mild OSA, with an apnea-hypopnea index (AHI) of 6.4 and an oxygen saturation (SaO2) nadir of 90%. All scored events in this PSG were obstructive hypopneas. He did not tolerate the therapy and was lost to follow-up. In 2021, he returned with persistent symptoms. We ordered a repeat PSG to reassess the severity of OSA. An Echocardiogram done 11 days prior was entirely normal. In the week prior to the PSG, the patient developed chest pain but did not seek medical care. Despite a weight loss of 11 kg, his second PSG showed an overall AHI of 39.2 per hour, and a SaO2 nadir of 81%. The majority of respiratory events in this PSG were central in nature (26 per hour) and displayed a crescendo-decrescendo pattern. The cycle length was shorter than 40 seconds. After completing this PSG, the patient went to the emergency room for chest pain. His vitals were within normal ranges. However, the D-Dimer level was elevated to 8.6 mg/L. CT angiogram showed a saddle pulmonary embolus. Troponin-T was 59 ng/L, and NT-proBNP was 3990 pg/mL. Echocardiogram two days later showed normal left ventricular function, but the right ventricle was enlarged, and the pulmonary artery systolic pressure was estimated at 57 mmHg.DISCUSSION: This case offers a rare opportunity to showcase the effect of acute submassive PE on sleep-disordered breathing. We had expected the second PSG to show mild OSA similar to the first PSG, but instead, it showed severe central sleep apnea (CSA). In this patient, the most likely culprit for CSA is the acute submassive PE with right ventricular strain, based on the normal echocardiogram shortly before the PE occurred. CSA is commonly associated with left ventricular heart failure through several well-elucidated mechanisms (1), but its association with right ventricular heart failure is much less known. Because acute submassive PE primarily causes dysfunction of the right ventricle, our case sheds new light on the role of the right ventricle in the pathophysiology of cardiogenic CSA. As the cycle length of CSA is relatively short in our case, despite a crescendo-decrescendo pattern, our case may be similar in physiology to the CSA associated with heart failure with preserved ejection fraction.CONCLUSIONS: To our knowledge, this is the first reported case of CSA that is primarily associated with acute submassive PE. Our case illustrates that acute right-sided heart failure (cor pulmonale) can cause CSA.