Treating Central Sleep Apnea in Heart Failure

recent enhanced appreciation of sleep-cardiovascu- lar interactions, particularly in patients with conges- tive heart failure (CHF), has prompted careful con- sideration of the relevance of sleep-disordered breathing to CHF pathophysiology, progression, and treatment.1 Sleep- disordered 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 chemosen- sitivity may play a role in the genesis of the periodic breathing that characterizes this disorder.1,2 Article p 3173 Of 5 million North Americans with CHF, an estimated 50% may have coexistent sleep apnea. Although the preva- lence 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 2:1 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,5-7 in- creased neurohormonal activation,1 increased ventricular ar- rhythmia,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 acti- vation10 independently promote disease progression and ad- verse outcomes remains unknown. Because OSA and CSA have different primary causes, optimal therapy may differ for these 2 distinct disorders. However, for patients with CHF, a paucity of data exists from prospective, randomized, controlled trials addressing the potential benefits of treatment for either OSA or CSA. Such studies have generally been limited to evaluation of the short-term effects of continuous positive airway pressure (CPAP) on left ventricular ejection fraction in patients with OSA.11,12 An exception is the Canadian Continuous Positive Airway Pressure for Patients With Central Sleep Apnea and Heart Failure (CANPAP), described later.13