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Circulation. 2007;115:3173-3180
Published online before print June 11, 2007, doi: 10.1161/CIRCULATIONAHA.106.683482
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(Circulation. 2007;115:3173-3180.)
© 2007 American Heart Association, Inc.


Heart Failure

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)

Michael Arzt, MD; John S. Floras, MD, DPhil; Alexander G. Logan, MD; R. John Kimoff, MD; Frederic Series, MD; Debra Morrison, MD; Kathleen Ferguson, MD; Israel Belenkie, MD; Michael Pfeifer, MD; John Fleetham, MD; Patrick Hanly, MD; Mark Smilovitch, MD; Clodagh Ryan, MD; George Tomlinson, PhD; T. Douglas Bradley, MD, for the CANPAP Investigators

From the University of Toronto (M.A., J.S.F., A.G.L., P.H., C.R., G.T., T.D.B.), Toronto, Ontario, Canada; University of British Columbia (J.F.), Vancouver, British Columbia, Canada; University of Calgary (I.B., P.H.), Calgary, Alberta, Canada; University of Western Ontario (K.F.), London, Ontario, Canada; McGill University (R.J.K., M.S.), Montreal, Quebec, Canada; Laval University (F.S.), Quebec City, Quebec, Canada; Dalhousie University (D.M.), Halifax, Nova Scotia, Canada; and the University of Regensburg (M.P.), Regensburg, Germany.

Correspondence to T. Douglas Bradley, MD, Toronto General Hospital/University Health Network, 9N-943, 200 Elizabeth St, Toronto, Ontario, M5G 2C4, Canada. E-mail douglas.bradley{at}utoronto.ca

Received December 11, 2006; accepted April 9, 2007.

Background— In the main analysis of the Canadian Continuous Positive Airway Pressure (CPAP) for Patients with Central Sleep Apnea (CSA) and Heart Failure Trial (CANPAP), CPAP had no effect on heart transplant–free survival; however, CPAP only reduced the mean apnea-hypopnea index to 19 events per hour of sleep, which remained above the trial inclusion threshold of 15. This stratified analysis of CANPAP tested the hypothesis that suppression of CSA below this threshold by CPAP would improve left ventricular ejection fraction and heart transplant–free survival.

Methods and Results— Of the 258 heart failure patients with CSA in CANPAP, 110 of the 130 randomized to the control group and 100 of the 128 randomized to CPAP had sleep studies 3 months later. CPAP patients were divided post hoc into those whose apnea-hypopnea index was or was not reduced below 15 at this time (CPAP-CSA suppressed, n=57, and CPAP-CSA unsuppressed, n=43, respectively). Their changes in left ventricular ejection fraction and heart transplant–free survival were compared with those in the control group. Despite similar CPAP pressure and hours of use in the 2 groups, CPAP-CSA–suppressed subjects experienced a greater increase in left ventricular ejection fraction at 3 months (P=0.001) and significantly better transplant-free survival (hazard ratio [95% confidence interval] 0.371 [0.142 to 0.967], P=0.043) than control subjects, whereas the CPAP-CSA–unsuppressed group did not (for left ventricular ejection fraction, P=0.984, and for transplant-free survival, hazard ratio 1.463 [95% confidence interval 0.751 to 2.850], P=0.260).

Conclusions— These results suggest that in heart failure patients, CPAP might improve both left ventricular ejection fraction and heart transplant–free survival if CSA is suppressed soon after its initiation.


 

CLINICAL PERSPECTIVE


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