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QUARTERLY FOCUS ISSUE: HEART FAILURE: CLINICAL RESEARCH

Hypoxia, Not the Frequency of Sleep Apnea, Induces Acute Hemodynamic Stress in Patients With Chronic Heart Failure

Joshua D. Gottlieb, AM^_*, Alan R. Schwartz, MD, Joanne Marshall, Pamela Ouyang, MBBS, Linda Kern, Veena Shetty, MPH, Maria Trois, Naresh M. Punjabi, MD, PhD, Cynthia Brown, MD^||, Samer S. Najjar, MD^¶ and Stephen S. Gottlieb, MD^,_*

^_* Harvard University, Cambridge, Massachusetts
Johns Hopkins Bayview Medical Center, Baltimore, Maryland
University of Maryland School of Medicine, Baltimore, Maryland
Medstar Research Institute, Baltimore, Maryland
^|| University of Virginia, Charlottesville, Virginia
^¶ National Institute on Aging, National Institutes of Health, Baltimore, Maryland

Manuscript received June 26, 2009; revised manuscript received August 26, 2009, accepted August 30, 2009.

^_* Reprint requests and correspondence: Dr. Stephen S. Gottlieb, University of Maryland, 22 South Greene Street, Baltimore, Maryland 21201 (Email: sgottlie{at}medicine.umaryland.edu).

Objectives: This study was conducted to evaluate whether brain (B-type) natriuretic peptide (BNP) changes during sleep are associated with the frequency and severity of apneic/hypopneic episodes, intermittent arousals, and hypoxia.

Background: Sleep apnea is strongly associated with heart failure (HF) and could conceivably worsen HF through increased sympathetic activity, hemodynamic stress, hypoxemia, and oxidative stress. If apneic activity does cause acute stress in HF, it should increase BNP.

Methods: Sixty-four HF patients with New York Heart Association functional class II and III HF and ejection fraction <40% underwent a baseline sleep study. Five patients with no sleep apnea and 12 with severe sleep apnea underwent repeat sleep studies, during which blood was collected every 20 min for the measurement of BNP. Patients with severe sleep apnea also underwent a third sleep study with frequent BNP measurements while they were administered oxygen. This provided 643 observations with which to relate apnea to BNP. The association of log BNP with each of 6 markers of apnea severity was evaluated with repeated measures regression models.

Results: There was no relationship between BNP and the number of apneic/hypopneic episodes or the number of arousals. However, the burden of hypoxemia (the time spent with oxygen saturation <90%) significantly predicted BNP concentrations; each 10% increase in duration of hypoxemia increased BNP by 9.6% (95% confidence interval: 1.5% to 17.7%, p = 0.02).

Conclusions: Hypoxemia appears to be an important factor that underlies the impact of sleep abnormalities on hemodynamic stress in patients with HF. Prevention of hypoxia might be especially important for these patients.

Key Words: brain natriuretic peptide • sleep apnea • hypoxia

Abbreviations and Acronyms   AHI = apnea-hypopnea index   BNP = brain (B-type) natriuretic peptide   CSA = central sleep apnea   HF = heart failure   OSA = obstructive sleep apnea   SaO2 = oxygen saturation   t90 = percentage of time spent during each epoch at oxygen saturation levels <90%

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