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Occult Sleep-Disordered Breathing in Stable Congestive Heart Failure

Shahrokh Javaheri, MD; Thomas J. Parker, MD; Laura Wexler, MD; Scott E. Michaels, PhD; Elizabeth Stanberry, PhD; Hiroshi Nishyama, MD; and Gary A. Roselle, MD
[+] Article and Author Information

From the Department of Veterans Affairs Medical Center and the University of Cincinnati College of Medicine, Cincinnati, Ohio. Requests for Reprints: Shahrokh Javaheri, MD, Sleep Disorders Laboratory, Pulmonary Section (111F), Veterans Affairs Medical Center, 3200 Vine Street, Cincinnati, OH 45220. Grant Support: By Merit Review Grants from the Department of Veterans Affairs.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1995;122(7):487-492. doi:10.7326/0003-4819-122-7-199504010-00002
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Objective: To determine the prevalence and effect of sleep-disordered breathing in ambulatory patients with stable, optimally treated congestive heart failure.

Design: A prospective, longitudinal study.

Setting: Referral sleep laboratory of a Department of Veterans Affairs medical center.

Patients: 42 of the 48 eligible patients with stable congestive heart failure and left ventricular systolic dysfunction (left ventricular ejection fraction ≤ 45%).

Measurements: After an adaptation night, polysomnography and Holter monitoring were done in the sleep laboratory. Arterial blood gases and pH were measured, and cardiac radionuclide ventriculography and pulmonary, renal, and thyroid function tests were done.

Results: Patients were divided into two groups. Group I (n = 23) had an hourly rate of apnea and hypopnea (apnea–hypopnea index) of 20 episodes per hour or less; group II (n = 19 [45%; CI, 30% to 60%]) had an index of more than 20 episodes per hour. In group II, the index varied from 26.5 to 82.2 episodes per hour (mean ±SD, 44 ±13 episodes per hour; CI, 38 to 51 episodes per hour). Group II had significantly more arousals (24 ±12 compared with 3 ±3 in group I) that were directly attributable to episodes of apnea and hypopnea, longer periods of time with an arterial oxyhemoglobin saturation of less than 90% (23% ±24% of total sleep time compared with 2% ±4%), lower arterial oxyhemoglobin saturation during sleep (74% ±13% compared with 87% ±4%), lower left ventricular ejection fraction (22% ±9% compared with 30% ±10%), and a significantly increased number of episodes of nocturnal ventricular arrhythmias. Multiple regression analyses showed that left ventricular systolic dysfunction was an independent risk factor for sleep apnea in patients with congestive heart failure.

Conclusions: The prevalence of severe occult sleep-disordered breathing is high in ambulatory patients with stable, optimally treated chronic congestive heart failure. The breathing episodes are associated with severe nocturnal arterial blood oxyhemoglobin desaturation and excessive arousals. Severe untreated sleep-disordered breathing may adversely affect left ventricular function, resulting in a vicious cycle that could contribute to death in patients with congestive heart failure. Prospective, longitudinal studies on survival are needed.

Figures

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Figure 1.
Frequency distribution of the apnea–hypopnea index in 10-unit intervals in 42 patients with stable, optimally treated congestive heart failure.
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Figure 2.
Sleep-disordered breathing episodes and arterial oxyhemoglobin saturation in the two groups.

AH I = apnea–hypopnea index; CA I = central apnea index; OAH I = obstructive apnea–hypopnea index; Ar I DB = arousal index associated with disordered breathing; BASE SAT = baseline arterial oxyhemoglobin saturation in supine position before sleep onset; LOW SAT = lowest arterial oxyhemoglobin saturation during sleep; SAT < 90%, min = time in sleep (in minutes) when arterial oxyhemoblobin saturation was less than 90%; SAT < 90%, TST = percentage of total sleep time when arterial oxyhemoglobin saturation was less than 90%. Values are expressed as mean ±SD.

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