Asian Cardiovasc Thorac Ann 2007;15:e3-e6
© 2007 Asia Publishing EXchange Ltd
Severe Sleep Apnea Syndrome Diagnosed With Acute Myocardial Infarction
Nese Dursunoglu, MD,
Dursun Dursunoglu, MD1,
Sibel Özkurt, MD,
Halil Tanriverdi, MD1,
Harun Evrengül, MD1,
Göksel Kiter, MD
Department of Pulmonary Diseases
1 Department of Cardiology, Pamukkale University Medical Faculty, Denizli, Turkey
For reprint information contact: Nese Dursunoglu, MD Tel: 90 258 211 8585 Fax: 90 258 213 4922 Email: ndursunoglu{at}yahoo.com, Pamukkale Üniversitesi Tip Fak, Gö
üs Hastaliklari Anabilim Dali, Kinikli-20200, Denizli, Turkey.
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ABSTRACT
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A 55-year-old man with acute myocardial infarction and no heart failure, had episodes of severe oxygen desaturation and apnea, while his hemodynamic parameters were stable. Sleep recordings revealed severe sleep apnea, and pulmonary function tests showed bronchial obstruction. Apnea and desaturation resolved on bilevel positive airway pressure. Patients with acute myocardial infarction who have apnea and hypoxemia without evident heart failure should be evaluated for sleep disorders.
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INTRODUCTION
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Obstructive sleep apnea syndrome (OSAS) is associated with nocturnal intermittent hypoxia, repeated activation of the sympathetic nervous system, as well as fluctuations in cardiac output and total peripheral resistance. Obstructive sleep apnea syndrome has been suggested as an important factor in the prevalence of hypertension and overall cardiovascular risk.1 Acute myocardial infarction is one of the potentially fatal complications of OSAS.
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CASE REPORT
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A 55-year-old man was admitted to our coronary care unit with acute inferolateral myocardial infarction (MI). He had no dyspnea or loss of consciousness. There was no history of hypertension, diabetes mellitus, hyperlipidemia, or alcohol usage. He was a smoker with a 70 packs per year smoking history, and his body mass index was 32.5 kg·m–2. Physical examination showed a blood pressure of 120/65 mm Hg, pulse 80 beats·min–1, respiratory rate 20 breaths·min–1, and an axillary temperature of 36.5°C. Cardiac and pulmonary examinations were normal. An electrocardiogram revealed sinus rhythm, ST-segment elevation (2 mm) on inferolateral leads, and ST segment depression (4–5 mm) on anteroseptal leads (Figure 1
). Thrombolytic therapy (streptokinase) was administered within 1 hr of the onset of symptoms. Cardiac enzymes levels were elevated, and arterial blood gases in room air showed hypoxemia: pH was 7.46, PCO2 was 37 mm Hg, PO2 57 was mm Hg, SaO2 was 91%. Echocardiography revealed grade 2 left ventricular (LV) diastolic dysfunction, LV local wall motion defects, and LV ejection fraction of 55%. Medical treatment included aspirin, low dosages of a beta blocker and an angiotensin-converting enzyme inhibitor, nitroglycerin, and standard heparin infusions. Anteroseptal ST-segment depression normalized, but pathological Q waves appeared in leads DII, DIII, aVF, V6, and an RS pattern was seen in leads V1 and V2, indicating a posterior MI (Figure 2).
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Figure 1. The first electrocardiogram showed sinus rhythm, ST-segment elevation (2 mm) in inferolateral leads (DII, DIII, aVF, DI, V6) and ST-segment depression (4–5 mm) in anteroseptal leads (V1, V2, V3, V4).
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Figure 2. Electrocardiogram on the 16th day after acute myocardial infarction showed normalization of anteroseptal ST-segment depression, pathological Q waves in leads DII, DIII, aVF, V6, and an RS pattern in leads V1 and V2, indicating posterior myocardial infarction.
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While the patient’s hemodynamic parameters and general health status were stable, severe oxygen desaturation and apnea were noticed by a nurse. As there was no manifest LV dysfunction causing hypoxemia and apnea, a detailed sleep history was obtained, which revealed habitual snoring, witnessed apnea, and excessive daytime sleepiness for many years. Polysomnography recordings showed severe sleep apnea: in a sleep period of 7 hr, there were 73 episodes of apnea and 97 of hypopnea; the apnea-hypopnea index was 31/hr, the oxygen desaturation index was 89.2, minimum nocturnal oxygen saturation was 77%, and mean nocturnal oxygen saturation was 89%. Therefore, continuous positive airway pressure was applied the following night. Even with a pressure of 15 cm H2O, the patient still had episodes of apnea and severe oxygen desaturation. As his pulmonary function tests showed bronchial obstruction: forced vital capacity was 2,680 mL (67%), forced expiratory volume in 1 sec was 1,700 mL (51%); he was diagnosed as having an overlap of chronic obstructive pulmonary disease and sleep apnea. Bilevel positive airway pressure (Respironics Inc; Murrysville, PA, USA) was applied with pressures of 12/6 cm H2O, and his apnea and desaturation resolved. Bronchodilator treatment was added to his therapy, and arterial blood gases in room air came within normal limits: pH 7.40, PCO2 36 mm Hg, PO2 80 mm Hg, SaO2 95%. A left coronary angiogram showed severe stenosis in the proximal circumflex artery, and a non-significant lesion in the left anterior descending artery (Figure 3A). A right coronary angiogram (Figure 4A) showed severe stenosis in the proximal right coronary artery. Left ventricular function was normal. A stent was successfully implanted into the circumflex artery without pre-dilation of the lesion (Figure 3B). Another stent was implanted into the right coronary artery 4 weeks later (Figure 4B). The patient was discharged home with bilevel positive airway pressure and medical therapy for chronic obstructive pulmonary disease and coronary artery disease (CAD).
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Figure 3. (A) Left coronary angiogram revealed severe stenosis in the proximal circumflex artery, and a non-significant lesion in the left anterior descending artery. (B) Left coronary angiogram after successful stent implantation into the circumflex artery.
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Figure 4. (A) Right coronary angiogram revealed severe stenosis in the proximal right coronary artery; (B) Right coronary angiogram after successful stent implantation into the right coronary artery.
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DISCUSSION
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Cardiovascular disturbances are the most serious complications of OSAS. They include heart failure, acute MI, arrhythmias, stroke, systemic and pulmonary hypertension1–4. Nowadays, sleep apnea is accepted as one of the identifiable causes of hypertension.1 Obstructive sleep apnea syndrome is closely associated with obesity and aging. We diagnosed an overlap syndrome of obstructive sleep apnea and chronic obstructive pulmonary disease in this patient. Overlap syndrome was first described by Flenley,5 and the prevalence was found to be 11%. Sleep hypoxemia and cardiovascular complications are more frequent and more severe in overlap syndrome than in sleep apnea or chronic obstructive pulmonary disease alone, requiring aggressive treatment.5 Diagnosis is based on a sleep study showing the typical saw-tooth pattern of desaturation.
In a recent study on 386 subjects from a sleep clinic, CAD was present in 24% of untreated patients with OSAS, and the percentage of patients with CAD was high among those with moderate to severe OSAS.6 De Olazabal and colleagues7 were the first to report breathing disorders and hypoxia during sleep in CAD patients. Schafer and colleagues8 found OSAS in 30% of 223 male patients with angiographically verified CAD compared with 20% of 66 controls without CAD.
Therefore, we suggest that acute MI patients, especially if they have apnea and hypoxemia without evident heart failure, should be evaluated for sleep disorders. Conversely, as OSAS patients commonly have coronary risk factors such as hypertension and obesity, they should be investigated for CAD.
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REFERENCES
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- Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003;289:2560–72.[Abstract/Free Full Text]
- Dursunoglu N, Dursunoglu D, Kiliç M. Impact of obstructive sleep apnea on right ventricular global function: sleep apnea and myocardial performance index. Respiration 2005;72:278–84.[Medline]
- Dursunoglu D, Dursunoglu N, Evrengul H, Ozkurt S, Kilic M, Fisekci F, et al. QT interval dispersion in obstructive sleep apnoea syndrome patients without hypertension. Eur Respir J 2005;25:677–81.[Abstract/Free Full Text]
- Dursunoglu N, Dursunoglu D, Cuhadaroglu C, Kilicaslan Z. Acute effects of automated continuous positive airway pressure on blood pressure in patients with sleep apnea and hypertension. Respiration 2005;72:150–5.[Medline]
- Flenley DC. Sleep in chronic obstructive lung disease. Clin Chest Med 1985;6:651–61.[Medline]
- Maekawa M, Shiomi T, Usui K, Sasanabe R, Kobayashi T. Prevalence of ischemic heart disease among patients with sleep apnea syndrome. Psychiatry Clin Neurosci 1998;52:219–20.[Medline]
- De Olazabal JR, Miller MJ, Cook WR, Mithoefer JC. Disordered breathing and hypoxia during sleep in coronary artery disease. Chest 1982;82:548–52.[Medline]
- Schafer H, Koehler U, Ewig S, Hasper E, Tasci S, Luderitz B. Obstructive sleep apnea as a risk marker in coronary artery disease. Cardiology 1999;92:79–84.[Medline]
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ABSTRACT
INTRODUCTION
