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Published ahead of print on November 3, 2003, doi:10.1164/rccm.200306-752OC
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American Journal of Respiratory and Critical Care Medicine Vol 169. pp. 361-366, (2004)
© 2004 American Thoracic Society

Controlled Trial of Continuous Positive Airway Pressure in Obstructive Sleep Apnea and Heart Failure

Darren R. Mansfield, N. Claire Gollogly, David M. Kaye, Meroula Richardson, Peter Bergin and Matthew T. Naughton

Departments of Respiratory Medicine and Cardiology, Alfred Hospital, Monash University; and Baker Heart Research Institute, Melbourne, Australia

Correspondence and requests for reprints should be addressed to Matthew T. Naughton, M.D., Department of Respiratory Medicine, Alfred Hospital, Commercial Road, Melbourne, Victoria 3181, Australia. E-mail: m.naughton{at}alfred.org.au


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Obstructive sleep apnea (OSA) is highly prevalent among patients with congestive heart failure (CHF) and may contribute to progression of cardiac dysfunction via hypoxia, elevated sympathetic nervous system activity, and systemic hypertension. Our aim was to assess the long-term effect of OSA treatment with nocturnal continuous positive airway pressure (CPAP) on systolic heart function, sympathetic activity, blood pressure, and quality of life in patients with CHF. Fifty-five patients with CHF and OSA were randomized to 3 months of CPAP or control groups. End points were changes in left ventricular ejection fraction, overnight urinary norepinephrine excretion, blood pressure, and quality of life. Nineteen patients in the CPAP group and 21 control subjects completed the study. Compared with the control group, CPAP treatment was associated with significant improvements in left ventricular ejection fraction ({Delta} 1.5 ± 1.4% vs. 5.0 ± 1.0%, respectively, p = 0.04), reductions in overnight urinary norepinephrine excretion ({Delta} 1.6 ± 3.7 vs. -9.9 ± 3.6 nmol/mmol creatinine, p = 0.036), and improvements in quality of life. There were no significant changes in systemic blood pressure. In conclusion, treatment of OSA among patients with CHF leads to improvement in cardiac function, sympathetic activity, and quality of life.

Key Words: congestive heart failure • obstructive sleep apnea • continuous positive airway pressure

Congestive heart failure (CHF) remains common in western communities and contributes significantly to the burden of morbidity and mortality (1). Cross-sectional results from the large Sleep Heart Health Study have shown a significant association between obstructive sleep apnea (OSA) and CHF (2). Moreover, the prevalence of OSA in a population with CHF has been shown to be as high as 40% (3–5). Factors associated with OSA, including systemic hypertension and obesity (2), are also associated with the development of CHF (6, 7)

Emerging data suggest that OSA may not only be associated with but may also contribute to the progression of CHF through several mechanisms. Large epidemiologic (8), animal (9) and human intervention studies (10) indicate that OSA contributes to the development of systemic hypertension, a precursor of CHF. Recurrent hypoxemia, hypercapnia (11), and baroreflex inhibition resulting from repetitive surges in nocturnal blood pressure (12) may contribute to elevated sympathetic nerve activity, which is known to be cardiotoxic in CHF (13). Hypoxemia may also independently lead to oxidative vascular wall injury (14, 15).

Although there is an increasing understanding of the physiologic consequences of OSA, until recently little was known of the clinical response to OSA treatment in patients with CHF. Small case series and uncontrolled trials suggest treatment of OSA with continuous positive airway pressure (CPAP) in patients with idiopathic cardiomyopathy led to significant improvements in heart function (16–18). Moreover, dogs exposed to simulated OSA develop left ventricular dysfunction (19). A recently published randomized controlled trial by Kaneko and coworkers demonstrated a significant improvement in cardiac function associated with a fall in systemic blood pressure with 1 month CPAP in patients with idiopathic and ischemic cardiomyopathy (20). There are several mechanisms by which this improvement may have occurred. In human intervention studies, the application of CPAP has been shown to reduce left ventricular transmural pressure gradient (21) and cardiac sympathetic tone (22) in patients with CHF and reduce systemic blood pressure (10) in patients with OSA.

The aim of this study was to measure the medium-term effect of treating OSA with CPAP on left ventricular systolic function, sympathetic nerve activity, and systemic blood pressure as well as functional outcomes including quality of life and exercise performance. Some of the results of this study were reported in the form of an abstract (23).


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Eligible patients aged between 18 and 80 years, under the care of a cardiologist, had a diagnosis of symptomatic, stable, and optimally treated CHF. CHF eligibility criteria included New York Heart Association Class II or greater and objective evidence of systolic dysfunction (left ventricular ejection fraction [LVEF] < 55%). Patients were questioned for symptoms of snoring and one or more of excessive daytime sleepiness, witnessed apneas, or nocturnal choking. Suitable patients were invited to undergo screening overnight polysomnography, and those with an apnea/hypopnea index (AHI) of more than 5 obstructive events per hour were eligible to participate and be randomized. Exclusion criteria included significant central sleep apnea (> 20% events central in type), clinical evidence of neurologic disease, renal disease with serum creatinine higher than 150 mmol/L, or spirometric confirmation of pulmonary disease with forced expiratory ratio of less than 70%. Patients with valvular heart disease were excluded.

Protocol
Consenting eligible patients were randomized to either 3 months of overnight nasal CPAP or to an untreated control group. All patients received lifestyle advice from the Australian National Heart Foundation guidelines (24) on diet, alcohol consumption, and on exercise for patients with CHF. The protocol was approved by the Alfred Hospital Ethics Committee (4/99), and all patients provided written consent.

Fixed-level CPAP was titrated manually during overnight polysomnography and continued at the optimally determined fixed pressure for 3 months (Autoset-T; ResMed, Sydney, Australia). All patients received one home visit and were contacted every second week by telephone. At 3 months, patients underwent repeat measurements at the same time of day. All patients underwent repeat overnight polysomnography: the treatment group on nasal CPAP.

Measurements at Baseline and 3 Months
At baseline and 3 months, patients underwent (1) right and left ventricular nuclear gated scans (Starcam 400AC; GE Medical Systems, Madison, WI), (2) symptom-limited incremental cycle ergometry (Sensormedics 2900; Sensormedics Corp., Anaheim, CA), and (3) overnight collection of urinary norepinephrine (UNE) and arterial blood gas sampling (Model 865; Ciba Corning, Medfield, MA) at the time of in-laboratory polysomnography (Somnostar; Sensormedics Corp.). Detailed methods for nuclear gated scanning, UNE determination, and polysomnography have been published elsewhere (25, 26). Quality of life was also assessed at baseline and 3 months using general (SF-36) and disease-specific questionnaires (Chronic Heart Failure questionnaire [27], New York Heart Association, Epworth Sleepiness Scale [28]). After a period of supine rest for 15 minutes, blood pressure was measured in a seated position using the average of three readings from a mercury sphygmomanometer.

Statistical Analysis
Statistical analyses were performed on the software package SPSS version 10 (SPAA Inc, Chicago, IL). All data were normally distributed and are expressed as arithmetic mean ± SE. The level of significance was accepted when the p value was less than 0.05. Outcomes were defined as the between-groups difference from baseline measurements and those recorded at 3 months. Two-way analyses of variance were completed for each of the independent variables. Post hoc analysis of covariants was performed for primary endpoints against AHI to measure effect of OSA severity on outcomes. Effect size was calculated from the difference in group changes divided by the pooled SDs of the groups at baseline.


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
One hundred fifty-six patients with a clinical diagnosis of CHF and a clinical suspicion of OSA underwent overnight polysomnography screening (Figure 1) . Of the 156 patients, 35 did not have systolic heart failure with LVEF more than or equal to 55% and 43 failed to meet OSA criteria. Nine patients subsequently became unstable before randomization, and 14 declined participation. Fifty-five patients enrolled and were randomized (28 to CPAP and 27 to the control group (Table 1 and Table E1 in the online supplement).



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  		Figure 1. Fate of participating patients. Bold boxes represent the patients who completed the study.

 

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  		TABLE 1. Baseline characteristics

 
Fifteen patients failed to complete the trial (9 from the CPAP and 6 from the control group), leaving 40 patients for complete analysis. Seven patients withdrew from the study. In the CPAP group, two patients were intolerant of CPAP and withdrew, and two patients withdrew for personal reasons. In the control group, three patients withdrew for personal reasons. Three patients in each group became unstable and required a new class of therapy. In the CPAP group, one patient received cardiac transplant and 2 patients received introduction of a new drug class likely to impact significantly on LVEF. In the control group, one patient received insertion of a biventricular pacemaker and two patients received introduction of a new drug class likely to impact significantly on LVEF. Two patients with ischemic cardiomyopathy in the CPAP group died. One patient suffered sudden death immediately after a game of tennis, likely due to an arrhythmia. The second patient developed pacemaker lead failure from a previously inserted biventricular pacemaker and died of cardiac tamponade after reinsertion of a pacemaker lead. Both patients had been compliant with CPAP and had symptomatically improved. Thus, baseline versus follow-up data were available on 40 subjects who completed the study (Table 2 and Tables E2 and E3 in the online supplement). The severity of CHF and OSA were similar between the patients who completed the study and those who dropped out (Table 2 and Table E2 in the online supplement). Two patients (one in each group) in sinus rhythm at entry into the study were found to be in atrial fibrillation at the end of the study. They had not altered the drug class and were included in the final analysis.


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  		TABLE 2. Endpoint outcome measures

 
The two groups were similar at baseline including age, sex, body mass index, LVEF, and AHI for both the patients who had enrolled in the study and for those who had completed the study (Table 1 and Tables E1 and E2 in the online supplement). Compared with the control group that completed the study, the CPAP group had a slightly greater O2 peak at baseline (Table 2). The mean CPAP pressure was 8.8 ± 1.4 mm Hg, and the average nightly usage was 5.6 ± 0.4 hours. CPAP therapy was effective in the treatment of OSA as demonstrated by a fall in AHI and rise in minimum oxygen saturation (pulse oximetry) (Table 2 and Table E4 in the online supplement). There was an associated 42% reduction in UNE, and the Epworth Sleepiness Scale score improved by 27%. There was a small reduction in AHI in the control group over the 3 months (p = 0.02), which was not explained by changes in body weight, sleep quality, or positioning. This did not translate into changes in UNE or the Epworth Sleepiness Scale score (Table 2).

Figure 2 and Table 2 show a significant improvement in the LVEF in the CPAP group compared with the control group ({Delta}5.0 ± 1.0% vs. 1.5 ± 1.4% respectively, p = 0.04). There was however greater fluctuation in {Delta}LVEF in the control group resulting from one patient with idiopathic cardiomyopathy showing a spontaneous improvement of {Delta}LVEF of +14% and another (who developed atrial fibrillation) with {Delta}LVEF of -14% (Figure 2). In contrast, the LVEF of a CPAP-treated patient, who also developed atrial fibrillation during the study, fell by 2%. Otherwise, the CPAP group demonstrated a significant unidirectional shift to improvement (within-group comparison, p < 0.001). The analysis of covariants was unable to show that AHI severity impacted on {Delta}LVEF (R2 = 0.1, p = 0.3).



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  		Figure 2. Display of left ventricular ejection fraction (LVEF baseline) and follow-up in control and continuous positive airway pressure (CPAP)–treated groups. Open circles represent idiopathic and closed circles the ischemic cardiomyopathies. There was significant improvement in LVEF in the CPAP group compared with the control group. Patients marked with an asterisk were in sinus rhythm at study commencement and found to be in atrial fibrillation at the end of the study.

 
The CPAP group demonstrated improvement in quality of life as measured by both SF-36 and the Chronic Heart Failure questionnaire (Figure 3) , whereas the control group remained unchanged. Neither was there any change in patients' exercise performance determined by the cycle ergometry O2 peak in either group nor was there any significant change in the New York Heart Association class of either group (Table 2 and Table E3 in the online supplement).



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  		Figure 3. The SF-36 quality of life questionnaire. (A) Note improvements in the eight domains of the SF-36 questionnaire with significant improvements in the domains of physical role (*p = 0.03), vitality ({dagger}p = 0.02), social functioning (*p = 0.03), and mental health ({ddagger}p = 0.01). Note also the calculated treatment effect size of 0.31 for physical function, 0.62 for physical role, 0.37 for bodily pain, 0.38 for general health, 0.77 for vitality, 0.53 for social function, 0.36 for emotional well being, and 0.61 for mental health. (B) The Chronic Heart Failure questionnaire. Mastery scale 4–28, dyspnea scale 5–35, fatigue scale 4–28, and emotional function scale 7–49. Note significant improvements in three of four domains (fatigue, {dagger}p = 0.01; emotional well being, *p = 0.02; and disease mastery, *p = 0.02), with corresponding treatment effect sizes of 0.71, 0.46, and 0.47, respectively. The dyspnea domain did not significantly change, and the effect size was only modest (0.27).

 

   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
We have demonstrated significant 3-month improvements in cardiac function and attenuation of sympathetic nerve activity associated with reduced hypoxemia with nasal CPAP treatment of OSA in patients with CHF, using a randomized controlled trial design. These physiologic improvements were associated with significant improvements in general and disease-specific symptoms of the quality of life.

The magnitude of the change in LVEF in the current study is similar to (29, 30) or greater than (30, 31) other large CHF pharmacologic intervention trials that have shown important mortality improvements. Given that the patients in the current trial were already on optimal medical treatment under the guidance of a cardiologist, our findings indicate an advance in the treatment of patients with CHF.

Our results confirm the recently published results by Kaneko and coworkers in which LVEF improved by 9% with CPAP in a 1-month controlled trial involving 24 patients with OSA and CHF (20). Our study included a larger sample size and was conducted on patients for a 3-month period. We explored mechanisms by which cardiac function may improve by measuring surrogate measures of sympathetic nerve activity and assessed functional outcomes in terms of quality of life and exercise performance.

The improvement in LVEF in the current study (+5%) was not as great as that in the study of Kaneko and coworkers (+9%). This could be explained by our group having less severe OSA (AHI, 26 vs. 42/hour) and higher baseline LVEF (35 vs. 28%). The mechanisms underlying the improvement in LVEF include the significant fall noted in sympathetic nerve activity, reflected by the 42% decrease in overnight UNE, in the CPAP group. Overnight UNE has been shown to correlate with plasma norepinephrine, mean sleep heart rate, hypoxemia, and sleep fragmentation (32). Sympathoexcitation is believed to have detrimental consequences on the failing heart (13). OSA contributes to sympathoexcitation through ventilatory inhibition (33), hypoxemia, and hypercapnia (11). Furthermore, effective treatment of OSA has been shown to attenuate sympathetic nerve activity in previous studies of patients without CHF (33), whereas the current study is the first to show a fall in UNE in the setting of CHF and OSA with CPAP. Given the abolition of hypoxemia and the nonsignificant change in arousals, it is likely that the fall in UNE is related to abolition of hypoxemia rather than alterations in arousal frequency.

An alternative mechanism through which OSA treatment with CPAP may improve LVEF is by inducing a fall in blood pressure. OSA has been causally linked to hypertension (10, 34). The current study, however, did not demonstrate a fall in awake blood pressure with CPAP treatment, suggesting that this mechanism may be less important in improving LVEF over the time frame measured. We also surmise that the changes to LVEF are likely to reflect improvements in systolic function per se rather than a potential effect of reduced afterload and more favorable hemodynamics secondary to lowered blood pressure. Our blood pressure findings contrast with those reported in OSA with the study of Kaneko and coworkers (20) and studies of patients without CHF (10, 34). In these three studies, blood pressure was measured over varying time frames from 15 minutes (20) to 24 hours (10, 34) with photoplethysmography (10, 20) or automated sphygmomanometry (34). In addition, all patients in the current study were on vasodilators, which may have blunted any additional effect of CPAP on blood pressure.

We were unable to demonstrate a significant improvement in maximal exercise capacity with CPAP. This may be explained by the high baseline O2 peak, which would have limited the magnitude of any further improvement. Our group mean baseline O2 peak of approximately 17.5 ml/minute/kg was similar to that reported in patient survivors with CHF (16.4 ml/minute/kg) and was significantly greater than that of nonsurvivors (13.2 ml/minute/kg) in a large prospective 3-year study (35). Alternatively, the lack of change in O2 peak may simply have reflected the inflexibility of O2 to change with therapies, as illustrated by recent large ß-blocker studies in which several markers of exercise capacity did not change with ß-blockers despite improvements in LVEF and survival (29, 36).

The responses to both quality of life questionnaires, the SF-36 and Chronic Heart Failure questionnaire, revealed significant improvements across most domains in the CPAP group. The effect size of CPAP on quality of life observed in the current study, approximately 0.3 to 0.8 indicates a clinically important treatment effect (37). This represents a substantial improvement in symptomatology, given that our patient sample was recruited proactively through heart failure clinics rather than patients presenting of their own volition volunteering symptoms.

Study Limitations
First, although this was a randomized controlled trial, it lacked a placebo. Although placebo pills (37) and subtherapeutic or sham CPAP (38) have been administered in OSA trials other studies have used untreated control subjects (39), indicating a lack of consensus amongst clinicians conducting nasal CPAP trials. Given these difficulties and the fact that a recent metaanalysis suggested that placebo therapy has little benefit over untreated control groups (40), the control group in the current study was not offered placebo. As a result, the participants could not be blinded to treatment; however, the objective measurements (LVEF, UNE) were analyzed by scientists blinded to the patients' treatment status.

Our study included only three females. Although there is a consistent finding among prevalence trials of OSA in CHF (3–5) of a very high male predominance (~ 90%), caution should be taken when generalizing these results to all patients.

We included a higher LVEF cutoff than other heart failure trials. The objective of this trial was to measure effects of alleviating OSA on systolic dysfunction. Unlike CHF trials including mortality or hospitalization rates, in which low LVEF cutoffs were required to attain sufficient endpoints, our objectives could be satisfied at higher LVEF ranges. We acknowledge that left ventricular diastolic dysfunction may have coexisted with systolic dysfunction and possibly contributed to our patients' symptomatology, but it was not assessed.

We included patients with mild OSA (AHI, 5–15 events per hour) on the basis of the results of the Sleep Heart Health study (2), demonstrating a relationship between CHF, other cardiovascular diseases, and AHI more than five events per hour. Thus, our results not only confirm the findings of the Kaneko study but also demonstrate generalizability to a more mild and clinically prevalent population.

The study incurred a dropout rate of 27%. The reasons for dropouts are outlined in RESULTS. This dropout rate is similar to that experienced in other clinical trials of CPAP of 19 (34) to 47% (10). The study was limited by a higher than expected death rate and rate of other interventions initiated during the trial period that would have significantly impacted study endpoints. The latter outcome is explained by the vast array of therapeutic options available to clinicians for the management of CHF. In addition, clinical decision making was performed by cardiologists who were, in the main, not study investigators and were instructed in the study protocol that necessary additional interventions could not to be withheld for trial purposes.

In summary we have demonstrated that CPAP therapy for moderately severe OSA in patients with CHF augments systolic heart function, restores normoxia during sleep, reduces sympathetic nerve activity, and improves the quality of life. Further studies are required to assess the mortality benefits of this therapy.


   Acknowledgments
 
The authors thank Dr. Peter Little, Baker Heart Research Institute, who performed the urinary norepinephrine analysis; Drs. Michael Kelly and Victor Kalff, Department of Nuclear Medicine, Alfred Hospital; Di Holst, R.N., Coordinator Heart Failure Program; Dr. Michael Bailey, Statistician, Monash University; Ms. Teanau Roebuck, Senior Medical Scientist; and the Departments of Respiratory Medicine and Cardiology, Alfred Hospital.


   FOOTNOTES
 
Supported by the Australian National Health and Medical Research Council (NH&MRC) and by an unconditional grant from ResMed. D.R.M. was a recipient of an NH&MRC scholarship.

This article has an online supplement, which in accessible from this issue's table of contents online at www.atsjournals.org

Conflict of Interest Statement: D.R.M. has no declared conflict of interest; N.C.G. has no declared conflict of interest; D.M.K. has no declared conflict of interest; M.R. has no declared conflict of interest; P.B. has no declared conflict of interest; M.T.N. is a member of an Australian Medical Advisory Board for a device company that makes CPAP machines and as a result is paid a small stipend <$3,000 Australian to attend board meetings and has also been a recipient of an unconditional research grant of $50,000 Australian for two years to conduct this clinician initiated research project.

Received in original form June 6, 2003; accepted in final form October 24, 2003


   REFERENCES
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Levy D, Kenchaiah S, Larson MG, Benjamin EJ, Kupka MJ, Ho KK, Murabito JM, Vasan RS. Long-term trends in the incidence of and survival with heart failure. N Engl J Med 2002;347:1397–1402.[Abstract/Free Full Text]
  2. Shahar E, Whitney CW, Redline S, Lee ET, Newman AB, Javier Nieto F, O'Connor GT, Boland LL, Schwartz JE, Samet JM. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med 2001;163:19–25.[Abstract/Free Full Text]
  3. Javaheri S, Parker TJ, Liming JD, Corbett WS, Nishiyama H, Wexler L, Roselle GA. Sleep apnea in 81 ambulatory male patients with stable heart failure: types and their prevalences, consequences, and presentations. Circulation 1998;97:2154–2159.[Abstract/Free Full Text]
  4. Sin DD, Fitzgerald F, Parker JD, Newton G, Floras JS, Bradley TD. Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure. Am J Respir Crit Care Med 1999;160:1101–1106.[Abstract/Free Full Text]
  5. Solin P, Bergin P, Richardson M, Kaye DM, Walters EH, Naughton MT. Influence of pulmonary capillary wedge pressure on central apnea in heart failure. Circulation 1999;99:1574–1579.[Abstract/Free Full Text]
  6. Dahlof B, Lindholm LH, Hansson L, Schersten B, Ekbom T, Wester PO. Morbidity and mortality in the Swedish Trial in Old Patients with Hypertension (STOP-Hypertension). Lancet 1991;338:1281–1285.[CrossRef][Medline]
  7. Kenchaiah S, Evans JC, Levy D, Wilson PW, Benjamin EJ, Larson MG, Kannel WB, Vasan RS. Obesity and the risk of heart failure. N Engl J Med 2002;347:305–313.[Abstract/Free Full Text]
  8. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000;342:1378–1384.[Abstract/Free Full Text]
  9. Brooks D, Horner RL, Kozar LF, Render-Teixeira CL, Phillipson EA. Obstructive sleep apnea as a cause of systemic hypertension: evidence from a canine model. J Clin Invest 1997;99:106–109.[Medline]
  10. Becker HF, Jerrentrup A, Ploch T, Grote L, Penzel T, Sullivan CE, Peter JH. Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation 2003;107:68–73.[Abstract/Free Full Text]
  11. Morgan BJ, Crabtree DC, Palta M, Skatrud JB. Combined hypoxia and hypercapnia evokes long-lasting sympathetic activation in humans. J Appl Physiol 1995;79:205–213.[Abstract/Free Full Text]
  12. Carlson JT, Hedner JA, Sellgren J, Elam M, Wallin BG. Depressed baroreflex sensitivity in patients with obstructive sleep apnea. Am J Respir Crit Care Med 1996;154:1490–1496.[Abstract]
  13. Mann DL, Kent RL, Parsons B, Cooper G IV. Adrenergic effects on the biology of the adult mammalian cardiocyte. Circulation 1992;85:790–804.[Abstract/Free Full Text]
  14. Prabhakar NR. Sleep apneas: an oxidative stress? Am J Respir Crit Care Med 2002;165:859–860.[Free Full Text]
  15. Ip MSM, Lam B, Chan L-Y, Zheng L, Tsang KWT, Fung PCW, Lam W-K. Circulating nitric oxide is suppressed in obstructive sleep apnea and is reversed by nasal continuous positive airway pressure. Am J Respir Crit Care Med 2000;162:2166–2171.[Abstract/Free Full Text]
  16. Malone S, Liu PP, Holloway R, Rutherford R, Xie A, Bradley TD. Obstructive sleep apnoea in patients with dilated cardiomyopathy: effects of continuous positive airway pressure. Lancet 1991;338:1480–1484.[CrossRef][Medline]
  17. Alchanatis M, Tourkohoriti G, Kosmas EN, Panoutsopoulos G, Kakouros S, Papadima K, Gaga M, Jordanoglou JB. Evidence for left ventricular dysfunction in patients with obstructive sleep apnoea syndrome. Eur Respir J 2002;20:1239–1245.[Abstract/Free Full Text]
  18. Laaban JP, Pascal-Sebaoun S, Bloch E, Orvoen-Frija E, Oppert JM, Huchon G. Left ventricular systolic dysfunction in patients with obstructive sleep apnea syndrome. Chest 2002;122:1133–1138.[Abstract/Free Full Text]
  19. Parker JD, Brooks D, Kozar LF, Render-Teixeira CL, Horner RL, Douglas Bradley T, Phillipson EA. Acute and chronic effects of airway obstruction on canine left ventricular performance. Am J Respir Crit Care Med 1999;160:1888–1896.[Abstract/Free Full Text]
  20. Kaneko Y, Floras JS, Usui K, Plante J, Tkacova R, Kubo T, Ando S, Bradley TD. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med 2003;348:1233–1241.[Abstract/Free Full Text]
  21. Naughton MT, Rahman MA, Hara K, Floras JS, Bradley TD. Effect of continuous positive airway pressure on intrathoracic and left ventricular transmural pressures in patients with congestive heart failure. Circulation 1995;91:1725–1731.[Abstract/Free Full Text]
  22. Kaye DM, Mansfield D, Aggarwal A, Naughton MT, Esler MD. Acute effects of continuous positive airway pressure on cardiac sympathetic tone in congestive heart failure. Circulation 2001;103:2336–2338.[Abstract/Free Full Text]
  23. Mansfield D, Gollogly NC, Bergin P, Kaye DM, Naughton MT. Cardiomyopathy, (obstructive) apnea and trial of nasal positive airway pressure (CATNAP) [abstract]. Am J Respir Crit Care Med 2003;167:A835.
  24. National Heart Foundation of Australia. Accessible online at www.heartfoundation.com.au (accessed December 2003).
  25. Pitt A, Kalff V, Kelly M, Lim YL, Anderson ST, Harper RW. Isotope angiocardiography of the left ventricle. Med J Aust 1980;1:573–580.[Medline]
  26. Solin P, Kaye DM, Little PJ, Bergin P, Richardson M, Naughton MT. Impact of sleep apnea on sympathetic nervous system activity in heart failure. Chest 2003;123:1119–1126.[Abstract/Free Full Text]
  27. Guyatt GH, Nogradi S, Halcrow S, Singer J, Sullivan MJ, Fallen EL. Development and testing of a new measure of health status for clinical trials in heart failure. J Gen Intern Med 1989;4:101–107.[Medline]
  28. Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep 1991;14:540–545.[Medline]
  29. Packer M, Colucci WS, Sackner-Bernstein JD, Liang C-S, Goldscher DA, Freeman I, Kukin ML, Kinhal V, Udelson JE, Klapholz M, et al. Double-blind, placebo-controlled study of the effects of carvedilol in patients with moderate to severe heart failure: The PRECISE Trial: prospective randomized evaluation of carvedilol on symptoms and exercise. Circulation 1996;94:2793–2799.[Abstract/Free Full Text]
  30. Cohn JN. Effect of vasodilator therapy on mortality in chronic congestive heart failure. Eur Heart J 1988;9:171–173.
  31. Cohn JN, Johnson G, Ziesche S, Cobb F, Francis G, Tristani F, Smith R, Dunkman WB, Loeb H, Wong M, et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med 1991;325:303–310.[Abstract]
  32. Naughton MT, Benard DC, Liu PP, Rutherford R, Rankin F, Bradley TD. Effects of nasal CPAP on sympathetic activity in patients with heart failure and central sleep apnea. Am J Respir Crit Care Med 1995;152:473–479.[Abstract]
  33. Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest 1995;96:1897–1904.
  34. Pepperell JC, Ramdassingh-Dow S, Crosthwaite N, Mullins R, Jenkinson C, Stradling JR, Davies RJ. Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised parallel trial. Lancet 2002;359:204–210.[CrossRef][Medline]
  35. Gitt AK, Wasserman K, Kilkowski C, Kleemann T, Kilkowski A, Bangert M, Schneider S, Schwarz A, Senges J. Exercise anaerobic threshold and ventilatory efficiency identify heart failure patients for high risk of early death. Circulation 2002;106:3079–3084.[Abstract/Free Full Text]
  36. Australia/New Zealand heart failure research collaborative group. Randomised, placebo-controlled trial of carvedilol in patients with congestive heart failure due to ischaemic heart disease. Lancet 1997;349:375–380.[CrossRef][Medline]
  37. Engleman HM, Kingshott RN, Wraith PK, Mackay TW, Deary IJ, Douglas NJ. Randomized placebo-controlled crossover trial of continuous positive airway pressure for mild sleep apnea/hypopnea syndrome. Am J Respir Crit Care Med 1999;159:461–467.[Abstract/Free Full Text]
  38. Jenkinson C, Davies RJ, Mullins R, Stradling JR. Comparison of therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised prospective parallel trial. Lancet 1999;353:2100–2105.[CrossRef][Medline]
  39. Naughton MT, Liu PP, Bernard DC, Goldstein RS, Bradley TD. Treatment of congestive heart failure and Cheyne-Stokes respiration during sleep by continuous positive airway pressure. Am J Respir Crit Care Med 1995;151:92–97.[Abstract]
  40. Beldoch, M. Is the placebo powerless? N Engl J Med 2001;345:1278–1279.



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[Full Text] [PDF]

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[Full Text] [PDF]

Home page
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[Abstract] [Full Text] [PDF]

Home page
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