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J Am Coll Cardiol, 2005; 45:2008-2011, doi:10.1016/j.jacc.2004.12.080
© 2005 by the American College of Cardiology Foundation
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CLINICAL RESEARCH: HEART FAILURE

Inhibition of Awake Sympathetic Nerve Activity of Heart Failure Patients With Obstructive Sleep Apnea by Nocturnal Continuous Positive Airway Pressure

Kengo Usui, MD, PhD, T. Douglas Bradley, MD, FRCPC, Jonas Spaak, MD, PhD, Clodagh M. Ryan, MB, BCh, Toshihiko Kubo, MD, PhD, Yasuyuki Kaneko, MD and John S. Floras, MD, DPhil, FRCPC, FACC*

University Health Network and Mount Sinai Hospital Department of Medicine and Sleep Research Laboratories of the Toronto Rehabilitation Institute, University of Toronto, Toronto, Canada.

Manuscript received July 15, 2004; revised manuscript received November 29, 2004, accepted December 6, 2004.

* Reprint requests and correspondence: Dr. John S. Floras, Suite 1614, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada. (Email: john.floras{at}utoronto.ca).

OBJECTIVES: This study was designed to determine whether reductions in morning systolic blood pressure (BP) elicited by treatment of moderate to severe obstructive sleep apnea (OSA) in heart failure (HF) patients are associated with a reduction in sympathetic vasoconstrictor tone.

BACKGROUND: Daytime muscle sympathetic nerve activity (MSNA) is elevated in HF patients with coexisting OSA. In our recent randomized trial in HF, abolition of OSA by continuous positive airway pressure (CPAP) increased left ventricular ejection fraction (LVEF) and lowered morning systolic BP.

METHODS: Muscle sympathetic nerve activity, BP, and heart rate (HR) of medically treated HF patients (EF <45%) and OSA (apnea-hypopnea index ≥20/h of sleep) were recorded on the morning after overnight polysomnography, and again one month after patients were randomly allocated nocturnal CPAP treatment or no CPAP (control).

RESULTS: In nine control patients, there were no significant changes in the severity of OSA, MSNA, systolic BP, or HR. In contrast, in the 8 CPAP-treated patients, OSA was attenuated, and there were significant reductions in daytime MSNA (from 58 ± 4 bursts/min to 48 ± 5 bursts/min; 84 ± 4 bursts/100 heart beats to 72 ± 5 bursts/100 heart beats; p < 0.001 and p = 0.003, respectively), systolic BP (from 135 ± 5 mm Hg to 120 ± 6 mm Hg, p = 0.03), and HR (from 69 ± 2 min–1 to 66 ± 2 min–1; p = 0.013).

CONCLUSIONS: Treatment of coexisting OSA by CPAP in HF patients lowers daytime MSNA, systolic BP, and HR. Inhibition of increased central sympathetic vasoconstrictor outflow is one mechanism by which nocturnal CPAP reduces awake BP in HF patients with moderate to severe OSA.

Abbreviations and Acronyms
  AHI = apnea-hypopnea index
  BP = blood pressure
  CPAP = continuous positive airway pressure
  HF = heart failure
  HR = heart rate
  LV = left ventricular
  LVEF = left ventricular ejection fraction
  MSNA = muscle sympathetic nerve activity
  OSA = obstructive sleep apnea
  SaO2 = oxyhemoglobin saturation


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