CPAP is the standard treatment for OSA even in patients with CHF. As in patients without CHF, CPAP splints the pharynx and maintains its patency, thereby preventing apnea and hypopnea. In addition, independent from treating OSA, CPAP may have beneficial positive airway pressure effects on CHF, such as cardiac unloading. For instance, CPAP reduces LV transmural pressure and afterload in patients with CHF by increasing intrathoracic pressure. It also reduces LV preload and consequently LV end-diastolic volume and pressure. The acute response of cardiac output to CPAP therapy in awake patients with CHF is dependent on cardiac preload [8]. In patients with CHF and high LV filling pressure (i.e., ≥12 mmHg), CPAP of 5–10 cm H₂O generally augments cardiac output, but in patients with CHF and low LV filling pressure (i.e., <12 mmHg), it generally reduces cardiac output [8].

As an OSA treatment, in addition to the alleviation of OSA, one-night application of CPAP caused abolition of negative intrathoracic pressure swings and reductions in nocturnal BP that caused a dramatic reduction in LV afterload that was accompanied by a decrease in HR. [9] A recent study extended these findings by demonstrating that treatment of OSA by CPAP reversed overnight decreases in stroke volume and cardiac output and increases in peripheral resistance [7].

Other studies have shown that treatment of OSA by CPAP in CHF patients for 3–9 weeks improved the cardiac work metabolic index, indicating the energy-sparing effect of CPAP [10]. In a study in which subjects were randomized to receive either 6–8 weeks of CPAP therapy or not, cardiac positron emission tomography-derived indices of oxidative metabolism and cardiac sympathetic nerve presynaptic function were assessed in patients with CHF and OSA [11]. Although significant improvement in cardiac sympathetic nerve presynaptic function was observed in patients randomized to CPAP, oxidative metabolism was not improved with CPAP, probably due to the short time periods of CPAP treatment. However, it should be noted that improvement in oxidative metabolism with CPAP was observed in a subset of patients with more severe OSA.

In a 1-month randomized trial involving HF patients with severe OSA, fixed-pressure CPAP increased the LV ejection fraction (LVEF) by 9 % in association with reduced systolic BP and HR [12]. Considering that CPAP reduced sympathetic vasoconstrictor activity [13], it was suggested that this was a mechanism by which BP was lowered. Egea et al. [14] also reported that in 50 patients with CHF, fixed-pressure CPAP improved the LVEF after 3 months. In a 3-month randomized trial involving 40 patients with less severe CHF and OSA, Mansfield et al. [15] reported that fixed-pressure CPAP reduced urinary norepinephrine concentration and improved the LVEF and quality of life, but not BP. In another randomized trial, Smith et al. [16] found no improvement in the LVEF in CHF patients with OSA while on CPAP. In contrast to the previously mentioned trials, they used auto-titrating CPAP, and they did not confirm that it eliminated OSA in a sleep study at the end of the trial. Furthermore, short-term CPAP treatment increased high-frequency heart rate variability and baroreflex sensitivity, indicating an increase in parasympathetic modulation of the heart rate [17, 18].

These observations, along with the short-term beneficial effects on the LVEF and autonomic nervous system, suggest that CPAP may have beneficial effects on long-term clinical outcomes. In terms of long-term clinical outcomes, although there are no randomized, controlled trials, two observational studies exist. In a study involving 218 patients with CHF, of whom 51 had OSA and an apnea-hypopnea index (AHI) ≥15, there was a trend toward lower mortality in the 14 who accepted CPAP therapy than in the 37 who did not (p = 0.07) over mean and maximum follow-up periods of 2.9 and 7.3 years, respectively [2]. In another study of 88 CHF patients with moderate to severe OSA, 65 CPAP-treated patients had significantly greater hospitalization-free survival than 23 untreated patients over mean and maximum follow-up periods of 2.1 and 4.8 years, respectively [19]. In the latter study, among the 65 CPAP-treated patients, the hospitalization-free survival rate was significantly higher in the more compliant group (N = 32), whose average nightly usage was more than the median level (4.9 h), than in the less compliant group (N = 33), whose average nightly usage was 4.9 h or less [19].