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Using the Mueller maneuver (MM) to simulate obstructive sleep apnea (OSA), we sought to investigate the acute changes in left sided heart morphology and function that develop with apneas occurring during sleep. Strong evidence supports a relationship between OSA and both atrial fibrillation (AF) and heart failure (HF). However, the acute effects of airway obstruction on cardiac structure and function have not been well defined. In addition, it is unclear how OSA might contribute to the development of AF and HF. We utilized echocardiography in healthy young adults to measure various parameters of cardiac structure and function. Subjects were studied at baseline, during and immediately after performance of the MM, and after a 10 minute recovery. Continuous heart rate, blood pressure and pulse oximetry measurements were made. During the MM, left atrial (LA) volume index markedly decreased. Left ventricular (LV) end systolic dimension increased in association with a decrement in LV ejection fraction. On release of the maneuver, there was a compensatory increase in blood flow to the left side of the heart with stroke volume, ejection fraction and cardiac output exceeding baseline. After 10 minutes of recovery all parameters had returned to baseline. In conclusion, sudden imposition of severe negative intrathoracic pressure leads to an abrupt decrease in LA volume and a decrease in LV systolic performance. These changes reflect an increase in LV afterload. Repeated swings in afterload burden and chamber volumes may have implications for future development of AF and HF.

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Despite a high prevalence of SDB in this population with AF, most patients do not report EDS. Furthermore, EDS does not appear to correlate with severity of SDB or to accurately predict the presence of SDB. Further research is needed to determine whether EDS affects the natural history of AF or modifies the response to SDB treatment.

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Abnormal nocturnal oximetry is common in patients with HCM, suggesting that OSA is prevalent. OSA may impact hemodynamics and symptoms in HCM. Further studies are needed to determine the long-term benefit of OSA treatment on hemodynamics and disease progression in HCM.

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