Impact of sleep-disordered breathing on myocardial salvage and infarct size in patients with acute myocardial infarction.

AIMS Sleep-disordered breathing (SDB) may be a risk factor for expansion of infarct size early after acute myocardial infarction (MI) by exposing the heart to repetitive oxygen desaturations and increased cardiac afterload. The objective of this study was to assess the impact of SDB on myocardial salvage and infarct size within 3 months after acute MI. METHODS AND RESULTS Patients with acute MI and percutaneous coronary intervention were enrolled in this prospective observational study. All patients underwent cardiovascular magnetic resonance (CMR) to define salvaged myocardium and infarct size within three to five days and at 3 months after acute MI. Patients were stratified according to apnoea-hypopnoea index (AHI) assessed by polysomnography at baseline into those with (AHI ≥ 15/h) and without (AHI < 15/h) SDB. Of the 56 patients included, 29 (52%) had SDB. The area at risk between both groups was similar (40 ± 12% vs. 40 ± 14%, P = 0.925). Patients with SDB had significantly less salvaged myocardium (myocardial salvage index 52% vs. 77%, P < 0.001), smaller reduction in infarct size (0.3% vs. 6.5%, P < 0.001) within 3 months after acute MI, a larger final infarct size (23% vs. 12%, P < 0.001), and a lower final left ventricular ejection fraction (48% vs. 54%, P = 0.023). In a multivariate analysis, including established risk factors for large MI, AHI was independently associated with less myocardial salvage and a larger infarct size 3 months after acute MI. CONCLUSIONS Sleep-disordered breathing was associated with less myocardial salvage and a smaller reduction in infarct size. These findings suggest a contribution of SDB to impaired healing of MI.

[1]  P. Lévy,et al.  Oxidative stress mediates cardiac infarction aggravation induced by intermittent hypoxia , 2013, Fundamental & clinical pharmacology.

[2]  M. Arzt,et al.  Natural course of sleep-disordered breathing after acute myocardial infarction , 2012, European Respiratory Journal.

[3]  Richard D. White,et al.  Prognostic Value of Routine Cardiac Magnetic Resonance Assessment of Left Ventricular Ejection Fraction and Myocardial Damage: An International, Multicenter Study , 2011, Circulation. Cardiovascular imaging.

[4]  J. Sandstede,et al.  Remodeling of the infarct territory in the time course of infarct healing in humans , 2011, Magnetic Resonance Materials in Physics, Biology and Medicine.

[5]  Stefan Neubauer,et al.  Dynamic Changes of Edema and Late Gadolinium Enhancement After Acute Myocardial Infarction and Their Relationship to Functional Recovery and Salvage Index , 2011, Circulation. Cardiovascular imaging.

[6]  Xuejiang Guo,et al.  Proteomic analysis of myocardial tissue from the border zone during early stage post‐infarct remodelling in rats , 2011, European journal of heart failure.

[7]  Ingo Eitel,et al.  T2-weighted cardiovascular magnetic resonance in acute cardiac disease , 2011, Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance.

[8]  H. Nakashima,et al.  Impact of obstructive sleep apnea on myocardial tissue perfusion in patients with ST-segment elevation myocardial infarction. , 2011, Circulation journal : official journal of the Japanese Circulation Society.

[9]  P. Pibarot,et al.  Predicting late myocardial recovery and outcomes in the early hours of ST-segment elevation myocardial infarction traditional measures compared with microvascular obstruction, salvaged myocardium, and necrosis characteristics by cardiovascular magnetic resonance. , 2010, Journal of the American College of Cardiology.

[10]  G. Schuler,et al.  Prognostic significance and determinants of myocardial salvage assessed by cardiovascular magnetic resonance in acute reperfused myocardial infarction. , 2010, Journal of the American College of Cardiology.

[11]  R. Kim,et al.  Cardiovascular magnetic resonance in patients with myocardial infarction: current and emerging applications. , 2009, Journal of the American College of Cardiology.

[12]  F. Burzotta,et al.  Myocardial no-reflow in humans. , 2009, Journal of the American College of Cardiology.

[13]  P. Lévy,et al.  Major role for hypoxia inducible factor-1 and the endothelin system in promoting myocardial infarction and hypertension in an animal model of obstructive sleep apnea. , 2009, Journal of the American College of Cardiology.

[14]  A. Walker,et al.  Coronary blood flow becomes uncoupled from myocardial work during obstructive sleep apnea in the presence of endothelial dysfunction. , 2008, Sleep.

[15]  Daniel C. Lee,et al.  Infarct size by contrast enhanced cardiac magnetic resonance is a stronger predictor of outcomes than left ventricular ejection fraction or end-systolic volume index: prospective cohort study , 2007, Heart.

[16]  G. Adam,et al.  Prediction of left ventricular remodeling and analysis of infarct resorption in patients with reperfused myocardial infarcts by using contrast-enhanced MR imaging. , 2007, Radiology.

[17]  Sebastian Kelle,et al.  Comparison of myocardial infarct size assessed with contrast-enhanced magnetic resonance imaging and left ventricular function and volumes to predict mortality in patients with healed myocardial infarction. , 2007, The American journal of cardiology.

[18]  Jianguo Li,et al.  Chronic intermittent hypoxia induces atherosclerosis. , 2007, American journal of respiratory and critical care medicine.

[19]  A. Chesson,et al.  The American Academy of Sleep Medicine (AASM) Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications , 2007 .

[20]  A. Chesson,et al.  The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology, and Techinical Specifications , 2007 .

[21]  H. Nakashima,et al.  Obstructive sleep apnoea inhibits the recovery of left ventricular function in patients with acute myocardial infarction. , 2006, European heart journal.

[22]  P. Lévy,et al.  Functional assessment of vascular reactivity after chronic intermittent hypoxia in the rat , 2006, Respiratory Physiology & Neurobiology.

[23]  Richard D. White,et al.  Tracking and Analysis of Cine-Delayed Enhancement MR , 2005, MICCAI.

[24]  C. Balke,et al.  Oxidative stress and left ventricular function with chronic intermittent hypoxia in rats. , 2005, American journal of respiratory and critical care medicine.

[25]  T. Borg,et al.  Structure and mechanics of healing myocardial infarcts. , 2005, Annual review of biomedical engineering.

[26]  P. Lévy,et al.  Chronic intermittent hypoxia increases infarction in the isolated rat heart. , 2005, Journal of applied physiology.

[27]  Stefan Frantz,et al.  Healing after myocardial infarction. , 2005, Cardiovascular research.

[28]  N. Oldridge,et al.  Health-related quality of life in patients with coronary artery disease treated for angina: Validity and reliability of German translations of two specific questionnaires , 2003, Quality of Life Research.

[29]  C. Julien,et al.  Vascular reactivity to norepinephrine and acetylcholine after chronic intermittent hypoxia in mice , 2003, Respiratory Physiology & Neurobiology.

[30]  S. Ando,et al.  Hemodynamic effects of simulated obstructive apneas in humans with and without heart failure. , 2001, Chest.

[31]  Daniel J Buysse,et al.  Sleep–Related Breathing Disorders in Adults: Recommendations for Syndrome Definition and Measurement Techniques in Clinical Research , 2000 .

[32]  Daniel J Buysse,et al.  Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force. , 1999, Sleep.

[33]  J. Floras,et al.  Effects of continuous positive airway pressure on obstructive sleep apnea and left ventricular afterload in patients with heart failure. , 1998, Circulation.

[34]  K. Franklin,et al.  Sleep apnoea and nocturnal angina , 1995, The Lancet.

[35]  R A Deyo,et al.  Development and evaluation of the Seattle Angina Questionnaire: a new functional status measure for coronary artery disease. , 1995, Journal of the American College of Cardiology.

[36]  D. Garcia-Dorado,et al.  Myocardial oedema: a preventable cause of reperfusion injury? , 1993, Cardiovascular research.

[37]  R. Gibbons,et al.  Determinants of Infarct Size in Reperfusion Therapy for Acute Myocardial Infarction , 1992, Circulation.

[38]  D. Hillman,et al.  Association of sleep apnoea with myocardial infarction in men , 1990, The Lancet.