Treating Central Sleep Apnea in Heart Failure

A recent enhanced appreciation of sleep-cardiovascular interactions, particularly in patients with congestive heart failure (CHF), has prompted careful consideration of the relevance of sleep-disordered breathing to CHF pathophysiology, progression, and treatment.1 Sleepdisordered breathing may be broadly classified as either obstructive sleep apnea (OSA) or central sleep apnea (CSA). 1 The former is characterized by repetitive collapse of the upper airway, whereas in patients with CHF, the latter is most often due to periodic alternation of diminished ventilatory drive and compensatory hyperventilation typical of Cheyne-Stokes respiration (Figure 1).CSA is likely a consequence rather than a cause of CHF.Although the mechanisms that underlie CSA/Cheyne-Stokes respiration in patients with CHF are not well understood, pulmonary congestion with increased lung J-receptor stimulation and greater chemosensitivity may play a role in the genesis of the periodic breathing that characterizes this disorder.1,2 Article p 3173Of 5 million North Americans with CHF, an estimated 50% may have coexistent sleep apnea.Although the prevalence of OSA is much higher than CSA in the general population, 3 it appears that this relationship may be reversed among patients with systolic heart failure.Case series have reported frequencies of CSA exceeding 40% for stable, ambulatory patients with CHF in a ratio Ͼ2:1 relative to the frequency of OSA.Indeed, the frequency of OSA in these same series was similar to that observed in the general population, whereas the frequency of CSA was strikingly higher.4,5 Furthermore, in patients with CHF, CSA has been associated with increased morbidity and mortality, [5][6][7] increased neurohormonal activation, 1 increased ventricular arrhythmia, 8 decreased exercise capacity, 5,9 and more advanced New York Heart Association class.5 However, whether these associations merely reflect more advanced CHF or whether repetitive apneas with hypoxia and sympathetic neural activation 10 independently promote disease progression and adverse outcomes remains unknown.