RT Book, Section A1 Javaheri, Shahrokh A1 Pevernagie, Dirk A1 Javaheri, Ali A2 Fuster, Valentin A2 Narula, Jagat A2 Vaishnava, Prashant A2 Leon, Martin B. A2 Callans, David J. A2 Rumsfeld, John S. A2 Poppas, Athena SR Print(0) ID 1202456660 T1 Sleep-Disordered Breathing T2 Fuster and Hurst's The Heart, 15e YR 2022 FD 2022 PB McGraw-Hill Education PP New York, NY SN 9781264257560 LK accesscardiology.mhmedical.com/content.aspx?aid=1202456660 RD 2024/11/14 AB Chapter SummaryThis chapter explores the pathophysiology of obstructive and central sleep apnea, as well as the purported causal relationship between these and hypertension, atherosclerosis, cardiac rhythm disorders, and cardiac failure. Obstructive sleep apnea (OSA)—involving cyclic asphyxia, microarousals from sleep, and negative swings in intrathoracic pressure—induces adverse systemic effects that disrupt normal cardiovascular physiology and function (see Fuster and Hurst’s Central Illustration). Notably, however, central sleep apnea of the Hunter-Cheyne-Stokes type is a consequence of cardiac failure rather than a cause. Treatment of sleep-disordered breathing with positive airway pressure devices and other therapeutic regimens has been shown to improve cardiovascular outcomes in patients with OSA. Randomized controlled trials have failed to show any mortality benefit, but this is likely related to methodological issues with the trials. Treatment of central sleep apnea remains difficult. Two randomized, controlled trials are ongoing: one with low-flow nocturnal oxygen and another with improved adaptive servo-ventilation. Phrenic nerve stimulation has shown benefits in a randomized, controlled trial. Finally, cardiac transplant recipients have been of particular interest because it was anticipated that preexisting central sleep apnea might be cured; however, OSA is prevalent in this patient population due to weight gain, potentially contributing to hypertension, poor quality of life, and even cardiac rejection.