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Original Research |

Effects of Dynamic Bilevel Positive Airway Pressure Support on Central Sleep Apnea in Men With Heart Failure* FREE TO VIEW

Michael Arzt, MD; Roland Wensel, MD, PhD; Sylvia Montalvan, MD; Thomas Schichtl, MD; Stephan Schroll, MD; Stephan Budweiser, MD; Friedrich C. Blumberg, MD; Günther A. J. Riegger, MD; Michael Pfeifer, MD
Author and Funding Information

*From the Department of Internal Medicine II, Divisions of Pneumology and Cardiology (Drs. Arzt, Wensel, Schroll, and Riegger), University of Regensburg, Regensburg; the Center for Pneumology (Drs. Schichtl, Montalvan, Budweiser, and Pfeifer), Donaustauf Hospital, Donaustauf; and Prosper Hospital (Dr. Blumberg), Recklinghausen, Germany.

Correspondence to: Michael Arzt, MD, Department of Internal Medicine II, Pneumology, University of Regensburg, Franz-Josef-Strauβ-Allee 11, 93042 Regensburg, Germany; e-mail: michael.arzt@klinik.uni-regensburg.de


Chest. 2008;134(1):61-66. doi:10.1378/chest.07-1620
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Published online

Background: Treatment with continuous positive airway pressure (CPAP) improves cardiac function in chronic heart failure (CHF) patients with central sleep apnea (CSA)-Cheyne-Stokes respiration (CSR) by stabilizing ventilation, but frequently central apneas and hypopneas persist. Our objective was to test the hypothesis that flow-targeted dynamic bilevel positive airway pressure (BPAP) support (BiPAP autoSV; Respironics; Murrysville, PA) effectively suppresses CSR-CSA in CHF patients.

Methods: We studied 14 CHF patients with CSR-CSA (and residual CSA on positive airway pressure therapy) during 3 consecutive nights: (1) diagnostic polysomnography, (2) CPAP (n = 10) or BPAP (n = 4) titration, and (3) dynamic flow-targeted dynamic BPAP support with an expiratory positive airway pressure (EPAP) set to suppress obstructive respiratory events, and an inspiratory positive airway pressure (IPAP) dynamically ranging between 0 and 15 cm H2O above the EPAP.

Results: CPAP or BPAP significantly reduced the apnea-hypopnea index (AHI) [mean ± SD, 46 ± 4 events/h to 22 ± 4 events/h; p = 0.001] compared to the first night without treatment. Flow-targeted dynamic BPAP support (mean EPAP, 6.5 ± 1.7 cm H2O; maximal IPAP, 21.9 ± 2.1 cm H2O) further reduced the AHI to 4 ± 1/h of sleep compared to the untreated (p < 0.001) and CPAP or BPAP night (p = 0.002). After the first night of flow-targeted dynamic BPAP support, patients rated on an analog scale (range, 0 to 10) the treatment as comfortable (6.9 ± 0.6), and the sleep quality as improved compared to previous nights (7.4 ± 0.6).

Conclusion: Flow-targeted dynamic BPAP support effectively suppresses CSR-CSA in patients with CHF and is well tolerated.

Figures in this Article

Cheyne-Stokes respiration (CSR)-central sleep apnea (CSA) is a common breathing disorder in 25 to 40% of patients with chronic heart failure (CHF).13 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.37 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.8Ultimately, the presence of CSR-CSA and its adverse effects confer an increased risk of mortality in CHF patients independent of underlying cardiac function.911

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.1214 In the largest trial14of 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. However, a stratified analysis15 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.

As a large proportion of CPAP-treated CHF patients with CSR-CSA have residual apneas and hypopneas,14 and suppression of CSR-CSA appears to be a possible mechanism by which positive airway pressure support can improve cardiovascular outcome in CHF patients,10,1213,1516 conventional CPAP may not be the optimal therapeutic approach in these patients. Therefore, devices that suppress CSR-CSA more effectively are needed.

One such approach is flow-targeted dynamic bilevel positive airway pressure (BPAP) support (BiPAP autoSV; Respironics; Murrysville, PA), which has been developed to normalize breathing in patients with both obstructive sleep apnea and CSR-CSA. The flow-targeted dynamic BPAP device provides a minimum expiratory positive airway pressure (EPAP) to maintain upper-airway patency and eliminate obstructive apneas and hypopneas. In addition, the device modulates inspiratory positive airway pressure (IPAP) in order to maintain a target inspiratory airflow and eliminate central apneas and hypopneas. In this first clinical evaluation of flow-targeted dynamic BPAP, our objective was to test the hypothesis that it effectively suppresses CSR-CSA in CHF patients in whom CSR-CSA persisted using conventional CPAP or BPAP therapy.

Patients

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 radionuclidventriculography; (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 trial17 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.

Baseline Assessment

Demographic information, anthropometric measurements, and status of CHF including objective evidence of systolic left ventricular dysfunction and status of sleep-disordered breathing (without positive pressure support) were assessed in all 14 eligible patients. During the first night of polysomnography, body position, eye and leg movements, cardiotachography, nasobuccal airflow (pressure cannula), thoracoabdominal movements (Inductotrace; Ambulatory Monitoring; Ardsley, NY), and pulse oximetry were recorded (Alice 3.5; Respironics). Bedtime and awakening time were at the discretion of each subject. Sleep studies were scored by an experienced clinician who was blinded to the applied treatment modality, using standard criteria.18 Apneas were defined as absence of tidal volume for ≥ 10 s (measured reduction of airflow to < 10% peak “nominal” airflow). Hypopneas were defined as a ≥ 50% reduction in air flow from baseline for ≥ 10 s or with a discernable reduction in airflow associated with a 4% oxygen desaturation or an arousal. Apneas and hypopneas were classified obstructive if out-of-phase thoracoabdominal motion or airflow limitation was present. The AHI was defined as the mean number of apneas and hypopneas per hour of sleep, and the oxygen desaturation index was defined as the number of oxygen desaturations ≥ 4%/h of sleep.

Principles of Operation of Flow-Targeted Dynamic BPAP

Flow-targeted dynamic BPAP provides positive airway pressure support to sustain upper-airway patency. The EPAP is manually set to eliminate obstructive apnea/hypopnea during sleep, which can be determined during conventional in-laboratory polysomnography in CPAP mode. In this clinical evaluation, the minimal IPAP is manually set at the determined EPAP level (minimal IPAP = EPAP). In addition, the flow-targeted dynamic BPAP device modulates the IPAP above the EPAP as required to maintain a target peak inspiratory airflow: when the device detects normal breathing, flow-targeted dynamic BPAP operates like conventional CPAP by providing the minimal IPAP (= EPAP); when the patient does not maintain the target peak inspiratory airflow, the device increases the IPAP above the EPAP up to a maximum IPAP, which can be set by the user (15 cm H2O above EPAP in this clinical evaluation). The device also provides an automatic back-up rate should sustained apnea be detected. In order to avoid hyperventilating the patient and to promote spontaneous breathing, the target inspiratory flow is set to below the mean inspiratory flow during spontaneous breathing by the patient, and the timing of the back-up rate begins with time delay and is set to a slower rate than the average respiratory rate of the patient.

Protocol and Intervention

After one diagnostic polysomnography, flow-targeted dynamic BPAP was initiated during 2 consecutive nights with full polysomnography. Patients were blinded to the applied treatment modality: during the first night, positive pressure support was titrated using the flow-targeted dynamic BPAP device in CPAP (n = 10) or BPAP (n = 4) mode (depending of the treatment of sleep-disordered breathing the patients received before entry into the study) in order to achieve maximal suppression of apneas and hypopneas. Titration was started at 5.4 ± 1.9 cm H2O CPAP/EPAP pressure, which was increased in increments of 1 to 2.5 cm H2O until obstructive apneas and hypopneas were optimally treated. Patients spent 81 ± 14% of the time receiving optimal positive airway pressure settings. During the second consecutive night, flow-targeted dynamic BPAP was initiated; EPAP was set to the optimal CPAP/EPAP levels determined during the second (previous) night. IPAP dynamically ranged from 0 to 15 cm H2O above EPAP. CPAP/BPAP and flow-targeted dynamic BPAP were applied in a fixed order rather than a randomized order because the optimal EPAP had to be determined by retitration of CPAP or BPAP using a standardized protocol to evaluate the optimal settings for CPAP, BPAP, and flow-targeted dynamic BPAP treatment. The morning following initiation of flow-targeted dynamic BPAP, subjects completed a visual analog scale of perceived treatment comfort and sleep quality. The analog scale included two items: (1) how would you describe the comfort of the therapy you received through the night? Values ranged from 0 (treatment was very uncomfortable) to 10 (treatment was very comfortable); and (2) how would you describe the quality of the rest you had last night? Values ranged from 0 (this was the worst night of sleep I have had in quite some time) and 10 (this was the best night of sleep I have had in quite some time).

Statistical Analysis

All data were analyzed using statistical software (SPSS, version 11.0; SPSS; Chicago, IL). Data are shown as mean ± SD. To assess differences in the number of respiratory events, oxygen saturation and polysomnographic measures of sleep quality between the sleep study at baseline, the CPAP/BPAP titration night, and the treatment night with flow-targeted dynamic BPAP, a repeated-measures analysis of variance with post hoc contrasts by t tests was used. A two-sided p value < 0.05 was considered to indicate statistical significance.

Patient Characteristics

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
Applied Pressures

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 flow-targeted 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.

Breathing During Sleep

Both therapies, CPAP/BPAP and flow-targeted dynamic BPAP, improved CSR-CSA compared to the untreated night as indicated by a significant fall in AHI, apnea index, central apnea index, and oxygen desaturation index as well as a significant increase in mean nocturnal oxygen saturation (Table 2). The reduction of AHI by CPAP (n = 10) and BPAP (n = 4) compared to the diagnostic polysomnography was similar (53 ± 18% vs 52 ± 55%, p = 0.723). Flow-targeted dynamic BPAP reduced AHI, apnea index, central apnea index, and oxygen desaturation index significantly more than CPAP/BPAP therapy. Minimal oxygen saturation was also significantly higher with flow-targeted dynamic BPAP than with CPAP/BPAP. In contrast to CPAP/BPAP, flow- targeted dynamic BPAP further reduced the initial AHI (range, 23 to 72/h of sleep) to below the threshold of 15 apneas and hypopneas per hour of sleep (which defined the presence of CSR-CSA in this clinical evaluation) in all individuals (Fig 1 ). In addition, the suppression of residual AHI by flow-targeted dynamic BPAP compared to the CPAP (n = 10) or BPAP (n = 4) night was similar (85 ± 11% vs 84 ± 6%, p = 0.751).

Sleep Quality and Treatment Comfort

With both CPAP/BPAP and flow-targeted dynamic BPAP therapies, reductions in CSR-CSA were accompanied by trends (not statistically significant) toward improvement in objective measures of sleep quality and quantity (Table 2). With CPAP/BPAP and flow-targeted dynamic BPAP, the arousal index was reduced by 17% and 40%, respectively; patients slept 40 min longer and had 8% and 18% higher sleep efficiency. Again, none of these changes reached statistical significance. As depicted in Figure 2 , CHF patients perceived the first night of nocturnal treatment with flow-targeted dynamic BPAP as comfortable and rated the quality of sleep as better than average. Only one patient, who completed the study but did not tolerate wearing a face mask, rated below average in both analog scales.

In the first clinical evaluation of the flow-targeted dynamic BPAP device, patients with CHF and moderate-to-severe CSR-CSA were evaluated. The major findings are that CPAP/BPAP and flow-targeted dynamic BPAP reduced the frequency of apneas and hypopneas during sleep. While the CHF patients had substantial residual CSR-CSA with CPAP/BPAP therapy, flow-targeted dynamic BPAP effectively eliminated apneas and hypopneas during sleep on the first night of treatment. These effects were accompanied by a trend toward improved sleep continuity and sleep architecture. Treatment with flow-targeted dynamic BPAP was perceived as comfortable, and sleep quality during the first night of device use was subjectively improved compared to recent nights.

For this study, we selected CHF patients who had residual CSR-CSA (AHI ≥ 10/h) during a previous sleep study with conventional CPAP or BPAP. Compared to the first night without treatment, we found a significant reduction of AHI and central apnea index of 52% and 53%, respectively, during the night with CPAP or BPAP. These findings are similar to those reported from the CANPAP trial14 involving 258 heart failure patients with CSR-CSA (AHI > 15/h of sleep). The CANPAP investigators14 found that CPAP reduced the AHI from 40 to 19/h of sleep, indicating that a large proportion of patients still had substantial CSR-CSA (AHI > 15/h of sleep) when receiving CPAP. In the only trial that compared the CPAP and BPAP (without back-up rate) treatment after > 1 night, Köhnlein et al17 found that BPAP and CPAP led to similar improvements in CSR-CSA in 16 CHF patients.

In our clinical evaluation of flow-targeted dynamic BPAP in CHF patients with CSR-CSA, we observed a near elimination of CSR-CSA (AHI from 46 to 4/h of sleep) during the first night of treatment. The comparison of the approximately 90% AHI reduction with flow-targeted dynamic BPAP to the approximately 50% AHI reduction with CPAP or BPAP in our clinical evaluation as well as in the CANPAP trial14 strongly suggests that flow-targeted dynamic BPAP is more effective than CPAP in normalizing nocturnal breathing in CHF patients with CSR-CSA.

Our observed results with flow-targeted dynamic BPAP on CSR-CSA were similar to those trials evaluating a device with volume-targeted adaptive servoventilation. Teschler and colleagues19studied 14 CHF patients with similar CSR-CSA severity and observed an 86% reduction in AHI, with a residual AHI of 6/h of sleep. In another study, Morgenthaler and collegues20 observed a near elimination of respiratory events (AHI of 1/h of sleep) in 21 patients with predominantly normal cardiac function and CSR-CSA, mixed sleep apnea, or complex sleep apnea, who had a residual AHI of 34/h of sleep with conventional CPAP (not part of the trial).

Suppression of CSR-CSA and normalization of nocturnal oxygenation by flow-targeted dynamic BPAP were accompanied by trends toward improved objective measures of sleep continuity and quality. However, none of these effects reached statistical significance, which may be a result of a lack of study power rather than a lack of effect. The magnitude of effects of flow-targeted dynamic BPAP on sleep efficiency and slow-wave sleep compare to those of Teschler and colleagues19 with volume-triggered adaptive servoventilation.

This first clinical evaluation of flow-targeted dynamic BPAP has to be interpreted considering the following limitations: it is possible that a full night of fixed optimal CPAP or BPAP would have suppressed CSR-CSA more effectively as our CPAP/BPAP night that included titration. However, we do not believe that this influenced our results significantly because only patients with a residual AHI ≥ 10/h during a previous sleep study with conventional CPAP or BPAP therapy (not part of this trial) were included, and patients spent > 80% receiving optimal CPAP/BPAP settings during the titration night in our trial. Moreover, the observed 52% reduction of CSR-CSA events by CPAP/BPAP conforms with the CPAP effects on CSR-CSA demonstrated in the CANPAP trial14 after long-term treatment, indicating that full suppression of CSR-CSA by CPAP is not possible in all patients.

BPAP with a timed back-up rate may have suppressed CSA more effectively than conventional CPAP19 or BPAP without a back-up rate. However, this treatment modality has not been tested for > 1 night of treatment in patients with CHF and CSA,19 and hence its effect on cardiovascular outcomes and clinical significance in such patients is unknown. Therefore, we tested the effects of flow-targeted dynamic BPAP on CSA in CHF patients with residual CSA on conventional treatment modalities such as CPAP or BPAP without a back-up rate who were studied over longer periods of time.14,17 Our clinical evaluation assessed the effects on CSR-CSA only during the first night of flow-targeted dynamic BPAP. Although it has been demonstrated in the CANPAP trial14 that the alleviation of CSR-CSA by positive airway pressure support are sustained over 2 years, it has to be confirmed in longer-term trials whether the elimination of CSR-CSA by flow-targeted dynamic BPAP is sustained over such time periods.

There was a possible order effect in our study because the CPAP/BPAP study always preceded the flow-targeted dynamic BPAP evaluation. However, because subjects were exposed to the nightly use of a positive airway pressure device already for 27 weeks before this clinical evaluation, an order effect is unlikely to influence sleep quality and apnea/hypopnea frequency. Thus, we do not believe this influenced our results. Finally, our results cannot be extrapolated to women because we studied only men.

In summary, flow-targeted dynamic BPAP effectively suppresses apneas and hypopneas in CHF patients with residual CSR-CSA receiving conventional CPAP/BPAP therapy. Flow-targeted dynamic BPAP was perceived as a comfortable treatment and subjectively improved sleep quality. In view of the current literature10,1213,1516 that suggests that suppression of CSR-CSA is a possible mechanism through which forms of positive airway pressure exert beneficial cardiovascular effects in patients with CHF and CSR-CSA, the longer-term effects on hemodynamics, cardiac function, and survival of dynamic BPAP support in patients with CHF merit further investigation.

Abbreviations: AHI = apnea-hypopnea index; BPAP = bilevel positive airway pressure; CANPAP = Canadian Trial of Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure; CHF = chronic heart failure; CPAP = continuous positive airway pressure; CSA = central sleep apnea; CSR = Cheyne-Stokes respiration; EPAP = expiratory positive airway pressure; IPAP = inspiratory positive airway pressure

Dr. Arzt received lecture fees from Respironics ($1,500 in 2007). The other authors have no actual and potential conflicts of interest to disclose.

Table Graphic Jump Location
Table 1. Baseline Characteristics of Heart Failure Patients*
* 

Data are presented as mean ± SE or No. (%) unless otherwise indicated. NYHA = New York Heart Association.

Table Graphic Jump Location
Table 2. Short-term Effects of CPAP/BPAP and Flow-Targeted Dynamic BPAP in Patients With CHF and CSR-CSA*
* 

Data are presented as mean ± SD.

Figure Jump LinkFigure 1. Individual data of 14 patients with CHF and moderate-to-severe CSR-CSA (mean AHI, 46 ± 4/h of sleep) are displayed. With CPAP or BPAP therapy, significant CSR-CSA persists in 50% of CHF patients (mean AHI, 22 ± 4/h of sleep). Flow-targeted dynamic BPAP (BiPAP autoSV; Respironics) effectively suppresses AHI (mean AHI, 4 ± 1/h of sleep) in all individuals below the threshold of 15 apneas and hypopneas per hour of sleep (dashed line), which defined the presence of CSR-CSA in this clinical evaluation. Patients who were treated with CPAP before the trial and during the second night of the trial are depicted as Δ. Patients who were treated with BPAP before the trial and during the second night of the trial are depicted as ▴.Grahic Jump Location
Figure Jump LinkFigure 2. The morning following 1 night of treatment with flow-targeted dynamic BPAP, the subjects completed a visual analog scale. The analog scale included two items: (1) top, A: how would you describe the comfort of the therapy you received through the night? and (2) bottom, B: how would you describe the quality of the rest you had last night? Possible values ranged from 0 to 10. The mean rating ± SE after the first night with flow-targeted dynamic BPAP for item 1 was 6.9 ± 0.6 and for item 2 was 7.4 ± 0.6.Grahic Jump Location
Javaheri, S, Parker, TJ, Liming, JD, et al (1998) Sleep apnea in 81 ambulatory male patients with stable heart failure: types and their prevalences, consequences, and presentations.Circulation97,2154-2159
 
Sin, DD, Fitzgerald, F, Parker, JD, et al Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure.Am J Respir Crit Care Med1999;160,1101-1106
 
Solin, P, Bergin, P, Richardson, M, et al Influence of pulmonary capillary wedge pressure on central apnea in heart failure.Circulation1999;99,1574-1579
 
Javaheri, S A mechanism of central sleep apnea in patients with heart failure.N Engl J Med1999;341,949-954
 
Lorenzi-Filho, G, Azevedo, ER, Parker, JD, et al Relationship of carbon dioxide tension in arterial blood to pulmonary wedge pressure in heart failure.Eur Respir J2002;19,37-40
 
Lorenzi-Filho, G, Rankin, F, Bies, I, et al Effects of inhaled carbon dioxide and oxygen on Cheyne-Stokes respiration in patients with heart failure.Am J Respir Crit Care Med1999;159,1490-1498
 
Wilcox, I, Grunstein, RR, Collins, FL, et al The role of central chemosensitivity in central apnea of heart failure.Sleep1993;16,S37-S38
 
Leung, RS, Floras, JS, Lorenzi-Filho, G, et al Influence of Cheyne-Stokes respiration on cardiovascular oscillations in heart failure.Am J Respir Crit Care Med2003;167,1534-1539
 
Lanfranchi, PA, Braghiroli, A, Bosimini, E, et al Prognostic value of nocturnal Cheyne-Stokes respiration in chronic heart failure.Circulation1999;99,1435-1440
 
Sin, DD, Logan, AG, Fitzgerald, FS, et al Effects of continuous positive airway pressure on cardiovascular outcomes in heart failure patients with and without Cheyne-Stokes respiration.Circulation2000;102,61-66
 
Javaheri, S, Shukla, R, Zeigler, H, et al Central sleep apnea, right ventricular dysfunction, and low diastolic blood pressure are predictors of mortality in systolic heart failure.J Am Coll Cardiol2007;49,2028-2034
 
Naughton, MT, Benard, DC, Liu, PP, et al Effects of nasal CPAP on sympathetic activity in patients with heart failure and central sleep apnea.Am J Respir Crit Care Med1995;152,473-479
 
Naughton, MT, Liu, PP, Bernard, DC, et al Treatment of congestive heart failure and Cheyne-Stokes respiration during sleep by continuous positive airway pressure.Am J Respir Crit Care Med1995;151,92-97
 
Bradley, TD, Logan, AG, Kimoff, RJ, et al Continuous positive airway pressure for central sleep apnea and heart failure.N Engl J Med2005;353,2025-2033
 
Arzt, M, Floras, JS, Logan, AG, et al Suppression of central sleep apnea by continuous positive airway pressure and transplant-free survival in heart failure: a post hoc analysis of the Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure Trial (CANPAP).Circulation2007;115,3173-3180
 
Davies, RJ, Harrington, KJ, Ormerod, OJ, et al Nasal continuous positive airway pressure in chronic heart failure with sleep-disordered breathing.Am Rev Respir Dis1993;147,630-634
 
Kohnlein, T, Welte, T, Tan, LB, et al Assisted ventilation for heart failure patients with Cheyne-Stokes respiration.Eur Respir J2002;20,934-941
 
Rechtschaffen, A, Kales, A. A manual of standardized terminology, techniques and scoring systems for sleep stages of human subjects. 1968; UCLA Brain Information Service/Brain Research Institute. Los Angeles, CA:.
 
Teschler, H, Dohring, J, Wang, YM, et al Adaptive pressure support servo-ventilation: a novel treatment for Cheyne-Stokes respiration in heart failure.Am J Respir Crit Care Med2001;164,614-619
 
Morgenthaler, TI, Gay, PC, Gordon, N, et al Adaptive servoventilation versus noninvasive positive pressure ventilation for central, mixed, and complex sleep apnea syndromes.Sleep2007;30,468-475
 

Figures

Figure Jump LinkFigure 1. Individual data of 14 patients with CHF and moderate-to-severe CSR-CSA (mean AHI, 46 ± 4/h of sleep) are displayed. With CPAP or BPAP therapy, significant CSR-CSA persists in 50% of CHF patients (mean AHI, 22 ± 4/h of sleep). Flow-targeted dynamic BPAP (BiPAP autoSV; Respironics) effectively suppresses AHI (mean AHI, 4 ± 1/h of sleep) in all individuals below the threshold of 15 apneas and hypopneas per hour of sleep (dashed line), which defined the presence of CSR-CSA in this clinical evaluation. Patients who were treated with CPAP before the trial and during the second night of the trial are depicted as Δ. Patients who were treated with BPAP before the trial and during the second night of the trial are depicted as ▴.Grahic Jump Location
Figure Jump LinkFigure 2. The morning following 1 night of treatment with flow-targeted dynamic BPAP, the subjects completed a visual analog scale. The analog scale included two items: (1) top, A: how would you describe the comfort of the therapy you received through the night? and (2) bottom, B: how would you describe the quality of the rest you had last night? Possible values ranged from 0 to 10. The mean rating ± SE after the first night with flow-targeted dynamic BPAP for item 1 was 6.9 ± 0.6 and for item 2 was 7.4 ± 0.6.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. Baseline Characteristics of Heart Failure Patients*
* 

Data are presented as mean ± SE or No. (%) unless otherwise indicated. NYHA = New York Heart Association.

Table Graphic Jump Location
Table 2. Short-term Effects of CPAP/BPAP and Flow-Targeted Dynamic BPAP in Patients With CHF and CSR-CSA*
* 

Data are presented as mean ± SD.

References

Javaheri, S, Parker, TJ, Liming, JD, et al (1998) Sleep apnea in 81 ambulatory male patients with stable heart failure: types and their prevalences, consequences, and presentations.Circulation97,2154-2159
 
Sin, DD, Fitzgerald, F, Parker, JD, et al Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure.Am J Respir Crit Care Med1999;160,1101-1106
 
Solin, P, Bergin, P, Richardson, M, et al Influence of pulmonary capillary wedge pressure on central apnea in heart failure.Circulation1999;99,1574-1579
 
Javaheri, S A mechanism of central sleep apnea in patients with heart failure.N Engl J Med1999;341,949-954
 
Lorenzi-Filho, G, Azevedo, ER, Parker, JD, et al Relationship of carbon dioxide tension in arterial blood to pulmonary wedge pressure in heart failure.Eur Respir J2002;19,37-40
 
Lorenzi-Filho, G, Rankin, F, Bies, I, et al Effects of inhaled carbon dioxide and oxygen on Cheyne-Stokes respiration in patients with heart failure.Am J Respir Crit Care Med1999;159,1490-1498
 
Wilcox, I, Grunstein, RR, Collins, FL, et al The role of central chemosensitivity in central apnea of heart failure.Sleep1993;16,S37-S38
 
Leung, RS, Floras, JS, Lorenzi-Filho, G, et al Influence of Cheyne-Stokes respiration on cardiovascular oscillations in heart failure.Am J Respir Crit Care Med2003;167,1534-1539
 
Lanfranchi, PA, Braghiroli, A, Bosimini, E, et al Prognostic value of nocturnal Cheyne-Stokes respiration in chronic heart failure.Circulation1999;99,1435-1440
 
Sin, DD, Logan, AG, Fitzgerald, FS, et al Effects of continuous positive airway pressure on cardiovascular outcomes in heart failure patients with and without Cheyne-Stokes respiration.Circulation2000;102,61-66
 
Javaheri, S, Shukla, R, Zeigler, H, et al Central sleep apnea, right ventricular dysfunction, and low diastolic blood pressure are predictors of mortality in systolic heart failure.J Am Coll Cardiol2007;49,2028-2034
 
Naughton, MT, Benard, DC, Liu, PP, et al Effects of nasal CPAP on sympathetic activity in patients with heart failure and central sleep apnea.Am J Respir Crit Care Med1995;152,473-479
 
Naughton, MT, Liu, PP, Bernard, DC, et al Treatment of congestive heart failure and Cheyne-Stokes respiration during sleep by continuous positive airway pressure.Am J Respir Crit Care Med1995;151,92-97
 
Bradley, TD, Logan, AG, Kimoff, RJ, et al Continuous positive airway pressure for central sleep apnea and heart failure.N Engl J Med2005;353,2025-2033
 
Arzt, M, Floras, JS, Logan, AG, et al Suppression of central sleep apnea by continuous positive airway pressure and transplant-free survival in heart failure: a post hoc analysis of the Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure Trial (CANPAP).Circulation2007;115,3173-3180
 
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