The reader is referred to a recent comprehensive review by Eckert et al6of the various forms and manifestations of CSA, as well as the physiologic underpinnings related to the ventilatory control system. We will refer to components of that system that may relate more intimately, either directly or indirectly, to HF. The form of CSA most commonly observed in the setting of HF is Cheyne-Stokes respiration, which was first recognized 2 centuries ago.7–8 (For the purpose of this review, the term CSA will be inclusive of the Cheyne-Stokes respiratory pattern.) Cheyne-Stokes respiration, also referred to by some as periodic breathing, is characterized by oscillatory ventilation, with periods of central apneas or hypopneas alternating with intervals of hyperpnea. As in patients with OSA, disordered breathing events result in polysomnographic evidence of CNS arousals and sleep disruption. In patients with CSA, arousals are more likely to occur at the height of hyperpnea and may contribute to complaints of paroxysmal nocturnal dyspnea in patients with HF. Based on a 1999 consensus statement,9 the severity of CSA, like OSA, has been quantified by the hourly frequency of disordered breathing events (known as the apnea-hypopnea index [AHI]). While an obstructive AHI of at least five events per hour has traditionally been considered the minimum for the development of daytime symptoms that may respond to treatment, evidence to support any equivalent threshold for the treatment of CSA is absent.9In fact, in a recently published revision of the sleep scoring manual,10 an American Academy of Sleep Medicine task force found insufficient evidence linking the extent of Cheyne-Stokes breathing with morbidity and mortality to provide a recommendation on the severity rating.