Table 1 displays the baseline characteristics of the 14 male patients. They were mildly overweight and had moderate-to-severe CHF due to ischemic, idiopathic, and hypertensive cardiomyopathy. All patients were receiving stable and optimal cardiac medication for at least 4 weeks before entry into the trial (Table 1). During the diagnostic polysomnography, untreated patients had moderate-to-severe CSR-CSA with 94% central apneas and frequent mild oxygen desaturations (Table 2). Patients slept for only 5.5 h, and sleep efficiency (total sleep time/time in bed) was reduced (73 + 3%).
Effects of CPAP/BPAP and Flow-Targeted Dynamic BPAP
During the CPAP/BPAP titration night, CPAP was increased up to a mean maximum of 8.3 ± 0.9 cm H2O (n = 10) and a mean maximum IPAP/EPAP of 13.5 ± 3.0 cm H2O/7.6 ± 1.7 cm H2O (n = 4), and patients spent at least 80% (81 ± 14%) of the time receiving pressure settings optimally suppressing apneas and hypopneas. During the first night of flowtargeted dynamic BPAP, maximum IPAP and mean EPAP were set at 21.8 ± 2.1 cm H2O and 6.5 ± 1.7 cm H2O, respectively. The mean IPAP that was actually applied by the flow-targeted dynamic BPAP device was 8.0 ± 2.4 cm H2O, significantly below the maximum IPAP. No adverse clinical event occurred.
Inclusion criteria were as follows: (1) age between 18 and 80 years; (2) CHF due to ischemic, hypertensive, or idiopathic dilated cardiomyopathy with a left ventricular ejection fraction < 45% as determined by resting echocardiography or by radio-nuclidventnculography; (3) CSR-CSA (AHI > 15/h, > 80% central apneas and hypopneas); and (4) a residual AHI > 10/h during a previous sleep study (not part of this trial) on conventional CPAP or BPAP (without back-up rate) therapy. Patients who had a residual AHI > 10/h after 27 ± 11 weeks of CPAP or BPAP therapy were pooled in one group because the only mid-term (cross-over) randomized trial comparing the effects of BPAP and CPAP on CSA in CHF patients demonstrated that the pretreatment AHI of 26.7 ± 10.7/h was similar significantly reduced by CPAP and BPAP to 7.7 ± 5.6/h and 6.5 ± 6.6/h, respectively.
Exclusion criteria were as follows: (1) a history of unstable angina, cardiac surgery, or documented myocardial infarction within 3 months of entry into the study; (2) CHF due to valvular heart disease; (3) daytime hypercapnia or the need for mechanical ventilatory assistance for comorbid conditions; (4) important COPD (FEV1 < 70% of predicted value or FEV1/FVC < 60%); (5) pregnancy; and (6) a history of pneumothorax and/or pneumomediastinum. We studied 14 consecutive sleep clinic patients with CHF who met the inclusion and exclusion criteria above. The investigation conforms with the principles outlined in the Declaration of Helsinki. The patients gave written informed consent to participate in this prospective study, which had been approved by the Ethics of Human Research Committee of the University of Regensburg.
Cheyne-Stokes respiration (CSR)-central sleep apnea (CSA) is a common breathing disorder in 25 to 40% of patients with chronic heart failure (CHF). In such patients, ventilation is destabilized by a combination of high controller gain (increased carbon dioxide responsiveness), hypocapnia resulting from lung edema (high filling pressures), and a long circulation time. CSR-CSA may contribute to disease progression by exposing the failing ventricle to intermittent hypoxia, arousals from sleep, and surges in sympathetic nervous system activity and BP. Ultimately, the presence of CSR-CSA and its adverse effects confer an increased risk of mortality in CHF patients independent of underlying cardiac function.
Treatment of CSR-CSA with continuous positive airway pressure (CPAP) has been demonstrated to stabilize ventilation, attenuate sympathetic activation, and improve left ventricular function in patients with CHF and CSR-CSA. In the largest trial of CPAP in CHF patients with CSR-CSA (Canadian Trial of Continuous Positive Airway Pressure for Patients With Central Sleep Apnea and Heart Failure [CANPAP]), the investigators found only a 50% reduction in the apnea-hypopnea index (AHI) [apneas and hypopneas per hour of sleep] and no beneficial effects on prognosis offered by My Canadian Pharmacy www.my-medstore-canada.net. However, a stratified analysis of the CANPAP trial demonstrated that increases in left ventricular ejection fraction and transplant-free survival were greater in those CHF patients in whom CPAP suppressed CSR-CSA than in the control group. These data suggest that a reduction in AHI in response to CPAP is a predictor of improved cardiovascular outcome in CHF patients with CSR-CSA.