Central sleep apnea: implications for congestive heart failure

Abstract

Congestive heart failure (HF), an exceedingly common and costly disease, is frequently seen in association with central sleep apnea (CSA), which often manifests as a periodic breathing rhythm referred to as Cheyne-Stokes respiration. CSA has historically been considered to be a marker of heart disease, since improvement in cardiac status is often associated with the attenuation of CSA. However, this mirroring of HF and CSA may suggest bidirectional importance to their relationship. In fact, observational data suggest that CSA, associated with repetitive oxyhemoglobin desaturations and surges in sympathetic neural activity, may be of pathophysiologic significance in HF outcomes. In light of the disappointing results from the first large trial assessing therapy with continuous positive airway pressure in patients with CSA and HF, further large-scale interventional trials will be needed to assess the role, if any, of CSA treatment on the outcomes of patients with HF. This review will discuss epidemiologic, pathophysiologic, diagnostic, and therapeutic considerations of CSA in the setting of HF.

Figure 1

Prognostic value of CSA in patients with HF. The risk of cardiac death (vertical axis) progressively increases with an increase in the AHI and in left atrial (LA) dimensions; patients who are at very high risk for fatal outcome can be identified by an AHI of > 30 events per hour and LA enlargement of > 25 cm². Reprinted from the study by Lanfranchi et al with permission.

Figure 2

Influence of pulmonary capillary wedge pressure (PCWP) on central apnea in patients with HF. PCWP is elevated in HF patients with CSA compared with those with OSA or without apnea. Left, A: in patients with CSA, PCWP correlated with the frequency and severity of CSA. Right, B: in patients with CSA and high PCWP, intensive medical therapy for 1 to 6 months reduced both mean (± SD) PCWP (from 29 ± 3 mm Hg [range, 20 to 38 mm Hg] to 22 ± 2 mm Hg [range, 17 to 27 mm Hg]; p < 0.001) and mean AHI (from 39 ± 8 events per hour [range, 7 to 62 events per hour] to 19 ± 5 events per hour [range, 1 to 31 events per hour]; p = 0.005). Arrows indicate the direction of change with time and therapy. Reprinted from the study by Solin et al with permission.

Figure 3

Long-term effects of CPAP therapy in HF patients. Sin et al reported a significant reduction of the combined mortality-cardiac transplantation rate (and therefore improved transplant-free survival time) in HF patients who were randomized to receive treatment with CPAP who complied with therapy compared to control subjects (relative risk reduction, 60%; 95% confidence interval, 2 to 84%; p = 0.047). From Sin et al with permission. These findings are not supported by those of the larger CANPAP study.

Figure 4

Effects of CRT on AHI in patients with and without CSA. Area under the dotted line = normal AHI (less than five events per hour); square = mean ± SD of all patients; triangle = mean ± SD of patients with CSA; octagon = mean ± SD of patients without CSA; star = p < 0.005 vs baseline. Reprinted from the study by Sinha et al with permission.