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

Joshua D. Gottlieb, Alan R. Schwartz, Joanne Marshall, Pamela Ouyang, Linda Kern, Veena Shetty, Maria Trois, Naresh M. Punjabi, Cynthia Brown, Samer S. Najjar, Stephen S. Gottlieb

Research output: Contribution to journalArticle

49 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1706-1712
Number of pages7
JournalJournal of the American College of Cardiology
Volume54
Issue number18
DOIs
StatePublished - Oct 27 2009
Externally publishedYes

Fingerprint

Brain Natriuretic Peptide
Sleep Apnea Syndromes
Heart Failure
Hemodynamics
Sleep
Apnea
Arousal
Hypoxia
Oxygen
Oxidative Stress
Confidence Intervals

Keywords

  • brain natriuretic peptide
  • hypoxia
  • sleep apnea

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Hypoxia, Not the Frequency of Sleep Apnea, Induces Acute Hemodynamic Stress in Patients With Chronic Heart Failure. / Gottlieb, Joshua D.; Schwartz, Alan R.; Marshall, Joanne; Ouyang, Pamela; Kern, Linda; Shetty, Veena; Trois, Maria; Punjabi, Naresh M.; Brown, Cynthia; Najjar, Samer S.; Gottlieb, Stephen S.

In: Journal of the American College of Cardiology, Vol. 54, No. 18, 27.10.2009, p. 1706-1712.

Research output: Contribution to journalArticle

Gottlieb, JD, Schwartz, AR, Marshall, J, Ouyang, P, Kern, L, Shetty, V, Trois, M, Punjabi, NM, Brown, C, Najjar, SS & Gottlieb, SS 2009, 'Hypoxia, Not the Frequency of Sleep Apnea, Induces Acute Hemodynamic Stress in Patients With Chronic Heart Failure', Journal of the American College of Cardiology, vol. 54, no. 18, pp. 1706-1712. https://doi.org/10.1016/j.jacc.2009.08.016
Gottlieb, Joshua D. ; Schwartz, Alan R. ; Marshall, Joanne ; Ouyang, Pamela ; Kern, Linda ; Shetty, Veena ; Trois, Maria ; Punjabi, Naresh M. ; Brown, Cynthia ; Najjar, Samer S. ; Gottlieb, Stephen S. / Hypoxia, Not the Frequency of Sleep Apnea, Induces Acute Hemodynamic Stress in Patients With Chronic Heart Failure. In: Journal of the American College of Cardiology. 2009 ; Vol. 54, No. 18. pp. 1706-1712.
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abstract = "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.",
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T1 - Hypoxia, Not the Frequency of Sleep Apnea, Induces Acute Hemodynamic Stress in Patients With Chronic Heart Failure

AU - Gottlieb, Joshua D.

AU - Schwartz, Alan R.

AU - Marshall, Joanne

AU - Ouyang, Pamela

AU - Kern, Linda

AU - Shetty, Veena

AU - Trois, Maria

AU - Punjabi, Naresh M.

AU - Brown, Cynthia

AU - Najjar, Samer S.

AU - Gottlieb, Stephen S.

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Y1 - 2009/10/27

N2 - 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.

AB - 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.

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