International Journal of Cardiology 187 (2015) 486–487
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Acute myocardial infarction and sleep apnea Tomoyuki Kawada ⁎ Department of Hygiene and Public Health, Nippon Medical School, Japan
a r t i c l e
i n f o
Article history: Received 24 March 2015 Accepted 27 March 2015 Available online 28 March 2015 Keywords: Sleep apnea Myocardial infarction Apnea–hypopnea index Day–night variation
To the Editor: I read the study by Ludka et al. with interest [1]. The authors investigated the prevalence of sleep apnea (SA) and examined the day– night variation of onset of myocardial infarction (MI) in 607 acute MI patients. Using the apnea–hypopnea index (AHI), patients were classified into 4 groups as 1) patients without SA (b5 events/h), 2) mild SA (5–15 events/h), 3) moderate SA (15–30 events/h), and 4) severe SA (≥ 30 events/h). Prevalence of mild SA, moderate SA and severe SA was 32.6%, 20.4% and 12.7%, respectively, and there was no difference of day–night variation in the onset of MI in SA patients and in non-SA patients. In addition, the frequency of MI was higher in both SA and non-SA patients from 6 AM to noon, as compared to the interval from midnight to 6 AM. I have some concerns on their study. Firstly, Ludka et al. assumed that the vast majority of their SA patients had obstructive sleep apnea (OSA) by quoting a reference [2]. In contrast, Shah et al. reported that patients with SA, defined as an AHI ≥5/h, were classified as 47 (35%) patients with OSA and 58 (43%) patients with central sleep apnea and/or Cheyne–Stokes respiration among 136 acute MI patients. Residual acute 31 MI patients were classified as non-SA patients [3]. As the use of portable monitoring of oxygen saturation and nasal airflow cannot differentiate patients with OSA and central SA, their study outcome should be limited in patients with SA.
⁎ Department of Hygiene and Public Health, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-Ku, Tokyo 113-8602, Japan. E-mail address: [email protected].
http://dx.doi.org/10.1016/j.ijcard.2015.03.389 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
Secondly, Ludka et al. quoted some references that acute IMI have a high likelihood of SA. Although the authors did not evaluate the association or causality between SA and acute MI by their study design, they reported that SA was present in 65.7% of patients after acute MI. Shah et al. demonstrated that patients with OSA, defined as an AHI ≥5/h, have less severe cardiac injury during an acute non-fatal MI, when compared to patients without OSA, by using highly sensitive troponin-T levels [3], and the cardio-protective role of sleep apnea during acute MI via ischemic preconditioning should be considered as further study. Thirdly, Ludka et al. quoted a reference of meta-analysis that the onset of MI is predominant between 6 AM and noon [4], and described in the last part of “Introduction” to investigate the potential effects of SA on the day–night variation of acute MI. Unfortunately, their study design cannot achieve their purpose. Instead, I recognize that four grades of SA including no SA have an advantage to know the trend of MI occurrence between 6 AM and noon in relation to the level of SA. I recommend the authors conducting Cochran–Armitage test for the trend of percentage, especially in men with enough number of patients. In addition, day–night variation of the onset of MI in OSA patients and in nonOSA patients can also be conducted by Cochran–Armitage test for the trend of percentage by setting 6-hour epochs of MI occurrence from 6 AM to noon, noon to 6 PM, 6 PM to midnight and midnight to 6 AM in this order. Finally, Marin et al. conducted a follow-up study to know the cardiovascular prognosis of male patients with OSA [5], and odds ratios (95% confidence intervals) of patients with untreated severe OSA against healthy participants for fatal and non-fatal cardiovascular events were 2.87 (1.17–7.51) and 3.17 (1.12–7.52), respectively. In addition, patients treated with continuous positive airway pressure reduced cardiovascular risk. I recommend Ludka et al. conducting survey on subsequent prognosis of acute MI in patients with SA. Conflict of interest The author reports no relationships that could be construed as a conflict of interest. Acknowledgments I wish to express my appreciation to the members of Hygiene and Public Health, Nippon Medical School, for the preparation of this study. The author of this manuscript has certified that he complies with the Principles of Ethical Publishing in the International Journal of Cardiology.
T. Kawada / International Journal of Cardiology 187 (2015) 486–487
References [1] O. Ludka, R. Stepanova, M. Vyskocilova, et al., Sleep apnea prevalence in acute myocardial infarction — the Sleep Apnea in Post-acute Myocardial Infarction Patients (SAPAMI) Study, Int. J. Cardiol. 176 (1) (2014) 13–19. [2] J. Hung, E.G. Whitford, R.W. Parsons, D.R. Hillman, Association of sleep apnoea with myocardial infarction in men, Lancet 336 (8710) (1990) 261–264. [3] N. Shah, S. Redline, H.K. Yaggi, et al., Obstructive sleep apnea and acute myocardial infarction severity: ischemic preconditioning? Sleep Breath. 17 (2) (2013) 819–826 (Erratum in Sleep Breath 2013;17(3):1119).
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[4] M.C. Cohen, K.M. Rohtla, C.E. Lavery, J.E. Muller, M.A. Mittleman, Meta-analysis of the morning excess of acute myocardial infarction and sudden cardiac death, Am. J. Cardiol. 79 (11) (1997) 1512–1516 (Erratum in Am J Cardiol 1998;81(2):260). [5] J.M. Marin, S.J. Carrizo, E. Vicente, A.G. Agusti, Long-term cardiovascular outcomes in men with obstructive sleep apnoea–hypopnoea with or without treatment with continuous positive airway pressure: an observational study, Lancet 365 (9464) (2005) 1046–1053.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Acute myocardial infarction and sleep apnea Tomoyuki Kawada ⁎ Department of Hygiene and Public Health, Nippon Medical School, Japan
a r t i c l e
i n f o
Article history: Received 24 March 2015 Accepted 27 March 2015 Available online 28 March 2015 Keywords: Sleep apnea Myocardial infarction Apnea–hypopnea index Day–night variation
To the Editor: I read the study by Ludka et al. with interest [1]. The authors investigated the prevalence of sleep apnea (SA) and examined the day– night variation of onset of myocardial infarction (MI) in 607 acute MI patients. Using the apnea–hypopnea index (AHI), patients were classified into 4 groups as 1) patients without SA (b5 events/h), 2) mild SA (5–15 events/h), 3) moderate SA (15–30 events/h), and 4) severe SA (≥ 30 events/h). Prevalence of mild SA, moderate SA and severe SA was 32.6%, 20.4% and 12.7%, respectively, and there was no difference of day–night variation in the onset of MI in SA patients and in non-SA patients. In addition, the frequency of MI was higher in both SA and non-SA patients from 6 AM to noon, as compared to the interval from midnight to 6 AM. I have some concerns on their study. Firstly, Ludka et al. assumed that the vast majority of their SA patients had obstructive sleep apnea (OSA) by quoting a reference [2]. In contrast, Shah et al. reported that patients with SA, defined as an AHI ≥5/h, were classified as 47 (35%) patients with OSA and 58 (43%) patients with central sleep apnea and/or Cheyne–Stokes respiration among 136 acute MI patients. Residual acute 31 MI patients were classified as non-SA patients [3]. As the use of portable monitoring of oxygen saturation and nasal airflow cannot differentiate patients with OSA and central SA, their study outcome should be limited in patients with SA.
⁎ Department of Hygiene and Public Health, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-Ku, Tokyo 113-8602, Japan. E-mail address: [email protected].
http://dx.doi.org/10.1016/j.ijcard.2015.03.389 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
Secondly, Ludka et al. quoted some references that acute IMI have a high likelihood of SA. Although the authors did not evaluate the association or causality between SA and acute MI by their study design, they reported that SA was present in 65.7% of patients after acute MI. Shah et al. demonstrated that patients with OSA, defined as an AHI ≥5/h, have less severe cardiac injury during an acute non-fatal MI, when compared to patients without OSA, by using highly sensitive troponin-T levels [3], and the cardio-protective role of sleep apnea during acute MI via ischemic preconditioning should be considered as further study. Thirdly, Ludka et al. quoted a reference of meta-analysis that the onset of MI is predominant between 6 AM and noon [4], and described in the last part of “Introduction” to investigate the potential effects of SA on the day–night variation of acute MI. Unfortunately, their study design cannot achieve their purpose. Instead, I recognize that four grades of SA including no SA have an advantage to know the trend of MI occurrence between 6 AM and noon in relation to the level of SA. I recommend the authors conducting Cochran–Armitage test for the trend of percentage, especially in men with enough number of patients. In addition, day–night variation of the onset of MI in OSA patients and in nonOSA patients can also be conducted by Cochran–Armitage test for the trend of percentage by setting 6-hour epochs of MI occurrence from 6 AM to noon, noon to 6 PM, 6 PM to midnight and midnight to 6 AM in this order. Finally, Marin et al. conducted a follow-up study to know the cardiovascular prognosis of male patients with OSA [5], and odds ratios (95% confidence intervals) of patients with untreated severe OSA against healthy participants for fatal and non-fatal cardiovascular events were 2.87 (1.17–7.51) and 3.17 (1.12–7.52), respectively. In addition, patients treated with continuous positive airway pressure reduced cardiovascular risk. I recommend Ludka et al. conducting survey on subsequent prognosis of acute MI in patients with SA. Conflict of interest The author reports no relationships that could be construed as a conflict of interest. Acknowledgments I wish to express my appreciation to the members of Hygiene and Public Health, Nippon Medical School, for the preparation of this study. The author of this manuscript has certified that he complies with the Principles of Ethical Publishing in the International Journal of Cardiology.
T. Kawada / International Journal of Cardiology 187 (2015) 486–487
References [1] O. Ludka, R. Stepanova, M. Vyskocilova, et al., Sleep apnea prevalence in acute myocardial infarction — the Sleep Apnea in Post-acute Myocardial Infarction Patients (SAPAMI) Study, Int. J. Cardiol. 176 (1) (2014) 13–19. [2] J. Hung, E.G. Whitford, R.W. Parsons, D.R. Hillman, Association of sleep apnoea with myocardial infarction in men, Lancet 336 (8710) (1990) 261–264. [3] N. Shah, S. Redline, H.K. Yaggi, et al., Obstructive sleep apnea and acute myocardial infarction severity: ischemic preconditioning? Sleep Breath. 17 (2) (2013) 819–826 (Erratum in Sleep Breath 2013;17(3):1119).
487
[4] M.C. Cohen, K.M. Rohtla, C.E. Lavery, J.E. Muller, M.A. Mittleman, Meta-analysis of the morning excess of acute myocardial infarction and sudden cardiac death, Am. J. Cardiol. 79 (11) (1997) 1512–1516 (Erratum in Am J Cardiol 1998;81(2):260). [5] J.M. Marin, S.J. Carrizo, E. Vicente, A.G. Agusti, Long-term cardiovascular outcomes in men with obstructive sleep apnoea–hypopnoea with or without treatment with continuous positive airway pressure: an observational study, Lancet 365 (9464) (2005) 1046–1053.
