Sleep and Breathing

, Volume 17, Issue 2, pp 819–826 | Cite as

Obstructive sleep apnea and acute myocardial infarction severity: ischemic preconditioning?

  • Neomi Shah
  • Susan Redline
  • H. Klar Yaggi
  • Richard Wu
  • C. George Zhao
  • Robert Ostfeld
  • Mark Menegus
  • Daniel Tracy
  • Elizabeth Brush
  • W. David Appel
  • Robert C. Kaplan
Original Article

Abstract

Background

Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia (IH). In animal models, IH has been shown to protect the myocardium during periods of ischemia by reducing infarct size. However, this phenomenon of “ischemic preconditioning” has not been investigated among OSA patients with acute myocardial infarction (MI). This study investigates the role of OSA on MI severity as measured by cardiac enzymes, specifically troponin-T, among patients with an acute MI.

Methods

This is an observational cohort study of patients ≥18 years of age who were hospitalized with an acute MI. Each participant underwent portable sleep monitoring (Apnea Link Plus); OSA was defined as an apnea–hypopnea index ≥5/h. Multivariable regression analysis was conducted to assess the relationship between OSA and highly sensitive troponin-T levels.

Results

In our entire cohort of acute MI patients (n = 136), 77 % of the sample had evidence of sleep disordered breathing, with 35 % of the sample having OSA (i.e., an AHI >5). Higher AHI was associated with lower peak troponin-T levels in partially adjusted models (β = −0.0320, p = 0.0074, adjusted for age, gender, and race) and fully adjusted models (β = −0.0322, p = 0.0085) (additionally adjusted for smoking, hypertension, hyperlipidemia, body mass index, history of prior cardiovascular or cerebrovascular disease, diabetes and baseline admission creatinine levels). The mean value of the log-transformed peak troponin-T variable was used to dichotomize the outcome variable. In both partially (OR 0.949, CI 0.905–0.995, p = 0.03) and fully adjusted (OR 0.918, CI 0.856–0.984, p = 0.0151) logistic regression models, the OR for AHI suggests a protective effect on high troponin-T level.

Conclusions

Our study demonstrates that patients with OSA have less severe cardiac injury during an acute non-fatal MI when compared to patients without OSA. This may suggest a cardioprotective role of sleep apnea during acute MI via ischemic preconditioning.

Keywords

Obstructive sleep apnea Myocardial infarction Intermittent hypoxemia Cardiac enzymes Ischemic preconditioning 

References

  1. 1.
    Collinson PO (2011) Biochemical estimation of infarct size. Heart 97:169–170PubMedCrossRefGoogle Scholar
  2. 2.
    Gozal D, Lipton AJ, Jones KL (2002) Circulating vascular endothelial growth factor levels in patients with obstructive sleep apnea. Sleep 25:59–65PubMedGoogle Scholar
  3. 3.
    Imagawa S, Yamaguchi Y, Higuchi M, Neichi T, Hasegawa Y, Mukai HY, Suzuki N, Yamamoto M, Nagasawa T (2001) Levels of vascular endothelial growth factor are elevated in patients with obstructive sleep apnea—hypopnea syndrome. Blood 98:1255–1257PubMedCrossRefGoogle Scholar
  4. 4.
    Lavie L, Kraiczi H, Hefetz A, Ghandour H, Perelman A, Hedner J, Lavie P (2002) Plasma vascular endothelial growth factor in sleep apnea syndrome: effects of nasal continuous positive air pressure treatment. Am J Respir Crit Care Med 165:1624–1628PubMedCrossRefGoogle Scholar
  5. 5.
    Ma J, Xu Y, Zhang Z, Liu H, Xiong W, Xu S (2007) Serum level of vascular endothelial growth factor in patients with obstructive sleep apnea hypopnea syndrome. J Huazhong Univ Sci Technol Med Sci 27:157–160PubMedCrossRefGoogle Scholar
  6. 6.
    Martinez D, da Silva RP, Klein C, Fiori CZ, Massierer D, Cassol CM, Bos AJ, Gus M (2012) High risk for sleep apnea in the Berlin questionnaire and coronary artery disease. Sleep Breath 16(1):89–94PubMedCrossRefGoogle Scholar
  7. 7.
    Martinez D, Klein C, Rahmeier L, da Silva RP, Fiori CZ, Cassol CM, Goncalves SC, Bos AJ (2012) Sleep apnea is a stronger predictor for coronary heart disease than traditional risk factors. Sleep Breath 16(3):695–701PubMedCrossRefGoogle Scholar
  8. 8.
    Mayr A, Mair J, Klug G, Schocke M, Pedarnig K, Trieb T, Pachinger O, Jaschke W, Metzler B (2011) Cardiac troponin T and creatine kinase predict mid-term infarct size and left ventricular function after acute myocardial infarction: a cardiac MR study. J Magn Reson Imaging 33:847–854PubMedCrossRefGoogle Scholar
  9. 9.
    Metzler B, Hammerer-Lercher A, Jehle J, Dietrich H, Pachinger O, Xu Q, Mair J (2002) Plasma cardiac troponin T closely correlates with infarct size in a mouse model of acute myocardial infarction. Clin Chim Acta 325:87–90PubMedCrossRefGoogle Scholar
  10. 10.
    Murry CE, Jennings RB, Reimer KA (1986) Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation: 1124-1136Google Scholar
  11. 11.
    Neckar J, Ostadal B, Kolar F (2004) Myocardial infarct size-limiting effect of chronic hypoxia persists for five weeks of normoxic recovery. Physiol Res 53:621–628PubMedGoogle Scholar
  12. 12.
    Peker Y, Carlson J, Hedner J (2006) Increased incidence of coronary artery disease in sleep apnoea: a long-term follow-up. Eur Respir J 28:596–602PubMedCrossRefGoogle Scholar
  13. 13.
    Reichlin T, Hochholzer W, Bassetti S, Steuer S, Stelzig C, Hartwiger S, Biedert S, Schaub N, Buerge C, Potocki M, Noveanu M, Breidthardt T, Twerenbold R, Winkler K, Bingisser R, Mueller C (2009) Early diagnosis of myocardial infarction with sensitive cardiac troponin assays. N Engl J Med 361(9):858–867PubMedCrossRefGoogle Scholar
  14. 14.
    Shah NA, Yaggi HK, Concato J, Mohsenin V (2010) Obstructive sleep apnea as a risk factor for coronary events or cardiovascular death. Sleep Breath 14:131–136PubMedCrossRefGoogle Scholar
  15. 15.
    Steiner S, Schueller PO, Schulze V, Strauer BE (2010) Occurrence of coronary collateral vessels in patients with sleep apnea and total coronary occlusion. Chest 137:516–520PubMedCrossRefGoogle Scholar
  16. 16.
    Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD, Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction (2012) Third universal definition of myocardial infarction. Circulation 50:2173–2195Google Scholar
  17. 17.
    Tsukamoto K, Ohara A (2006) Temporal worsening of sleep-disordered breathing in the acute phase of myocardial infarction. Circ J 70:1553–1556PubMedCrossRefGoogle Scholar
  18. 18.
    Valipour A, Litschauer B, Mittermayer F, Rauscher H, Burghuber OC, Wolzt M (2004) Circulating plasma levels of vascular endothelial growth factor in patients with sleep disordered breathing. Respir Med 98:1180–1186PubMedCrossRefGoogle Scholar
  19. 19.
    Weinreich G, Armitstead J, Topfer V, Wang YM, Wang Y, Teschler H (2009) Validation of ApneaLink as screening device for Cheyne–Stokes respiration. Sleep 32:553–557PubMedGoogle Scholar
  20. 20.
    Xu WQ, Yu Z, Xie Y, Huang GQ, Shu XH, Zhu Y, Zhou ZN, Yang HT (2011) Therapeutic effect of intermittent hypobaric hypoxia on myocardial infarction in rats. Basic Res Cardiol 106:329–342PubMedCrossRefGoogle Scholar
  21. 21.
    Younger JF, Plein S, Barth J, Ridgway JP, Ball SG, Greenwood JP (2007) troponin-I concentration 72 h after myocardial infarction correlates with infarct size and presence of microvascular obstruction. Heart 93(12):1547–1551PubMedCrossRefGoogle Scholar
  22. 22.
    Zong P, Setty S, Sun W, Martinez R, Tune JD, Ehrenburg IV, Tkatchouk EN, Mallet RT, Downey HF (2004) Intermittent hypoxic training protects canine myocardium from infarction. Exp Biol Med (Maywood) 229:806–812Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2012

Authors and Affiliations

  • Neomi Shah
    • 1
    • 2
  • Susan Redline
    • 3
  • H. Klar Yaggi
    • 4
  • Richard Wu
    • 1
  • C. George Zhao
    • 1
  • Robert Ostfeld
    • 1
  • Mark Menegus
    • 1
  • Daniel Tracy
    • 2
  • Elizabeth Brush
    • 1
  • W. David Appel
    • 1
  • Robert C. Kaplan
    • 2
  1. 1.Pulmonary Division, Department of MedicineMontefiore Medical CenterBronxUSA
  2. 2.Department of Epidemiology and Population HealthAlbert Einstein College of MedicineBronxUSA
  3. 3.Brigham and Women’s Hospital and Beth Israel Deaconess Medical CenterHarvard Medical SchoolBostonUSA
  4. 4.Section of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal MedicineYale University School of MedicineNew HavenUSA

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