Rationale for Treating Central Sleep Apnea in Pa- Tients with Heart Failure

T are 2 possible rationales for treating Cheyne-Stokes respiration or central sleep apnea (CSA) in patients with congestive heart failure (CHF). First, alleviation of CSA might alleviate symptoms directly related to CSA, such as sleep disruption and excessive daytime sleepiness. Second, treating CSA might improve cardiovascular outcomes, such as cardiovascular function, as well as morbidity and mortality due to CHF. Regarding the first rationale, there is little evidence that CSA itself gives rise to symptoms of a sleep apnea syndrome. For example, most CHF patients with CSA do not snore and do not complain of excessive daytime sleepiness.1,2 Thus, relief of symptoms of CSA is not a strong rationale to treat CSA in patients with CHF. Regarding the second rationale, this is largely based on observations from some,3,4 but not all, reports5,6 that, in patients with CHF, CSA increases the risk of death and cardiac transplantation independently of known risk factors. This observation suggests the possibility that, in patients with CHF, treating and alleviating coexisting CSA might reduce some of the excess morbidity and mortality attributable to this condition. Closely linked to this notion is evidence that CSA arises secondary to CHF itself and is, to some extent, a sign of the severity of CHF. For example, although cardiac output does not appear to differ between CHF patients with and without CSA, patients with CSA have higher left ventricular (LV) filling pressures, LV end-diastolic volumes, and sympathetic nervous system activity, as compared with CHF patients without CSA.7,8 These are signs of worse cardiovascular function in patients with CSA that should have adverse prognostic implications. In CHF, CSA is associated with chronic hypocapnia.9 This is related to elevated LV filling pressures and end-diastolic volumes, and pulmonary congestion that may provoke hyperventilation through stimulation of pulmonary vagal irritant receptors, and to increases in central and peripheral chemosensitivity.7,8,10 Hence, treating CSA might improve cardiovascular outcomes either by alleviating CSA per se or by alleviating underlying cardiovascular dysfunction that is associated with CSA. The prevalence of CSA in patients with stable CHF is approximately 25% to 40%,1,6,11 compared with less than 1% in the general population.12 This high prevalence in the setting of CHF is probably attributable to derangements in cardiovascular physiology that influence the respiratory system, as described above. Accordingly, because CSA is largely a consequence of CHF, one could anticipate that treatments for CHF that relieved pulmonary edema and/or lowered LV filling pressures might also relieve CSA. Case series suggest that intensification of pharmacologic therapy for CHF can attenuate CSA.13,14 Similarly, in nonrandomized trials, cardiac resynchronization pacemaker therapy was accompanied by alleviation of CSA in association with an improvement of cardiac function.15,16 Heart transplantation can also alleviate CSA in patients with CHF.17 Thus, optimizing CHF therapy can stabilize ventilatory control and attenuate CSA in some patients. These observations suggest that, in addition to optimal contemporary CHF therapy, specific interventions for CSA in patients with CHF would be most effective if the therapy also had direct beneficial effects on cardiovascular function.