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(Chest. 2002;122:1133-1138.)
© 2002 American College of Chest Physicians

Left Ventricular Systolic Dysfunction in Patients With Obstructive Sleep Apnea Syndrome*

Jean-Pierre Laaban, MD, FCCP; Sophie Pascal-Sebaoun, MD; Evelyne Bloch, MD; Elizabeth Orvoën-Frija, MD; Jean-Michel Oppert, MD and Gérard Huchon, MD, FCCP

* From the Departments of Pneumology (Drs. Laaban, Pascal-Sebaoun, Orvoën-Frija, and Huchon), Nuclear Medicine (Dr. Bloch), and Nutrition (Dr. Oppert), Hotel-Dieu Hospital, Paris, France.

Correspondence to: Jean-Pierre Laaban, MD, FCCP, Department of Pneumology, Hotel-Dieu Hospital, 1, place du Parvis Notre-Dame, 75181 Paris Cedex 04, France; e-mail: j-pierre.laaban{at}htd.ap-hop-paris.fr


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: Conflicting results have been reported regarding the effects of obstructive sleep apnea syndrome (OSAS) on daytime left ventricular (LV) systolic function. This study aimed to assess the prevalence and causes of LV systolic dysfunction, using radionuclide angiography, in a large group of patients with OSAS.

Design and setting: A prospective study in the pneumology department of a university medical center.

Patients: One hundred sixty-nine consecutive patients with OSAS diagnosed by polysomnography, hospitalized for the administration of nasal continuous positive airway pressure. Patients with a known cardiac disease were excluded.

Measurements: LV ejection fraction (LVEF) was measured in all patients, using radionuclide ventriculography with multiple-gated equilibrium cardiac imaging. Myocardial scintigraphy with a dipyridamole stress test and echocardiography were performed in those patients with LV systolic dysfunction, defined by a LVEF < 50%, to detect silent heart disease, especially coronary artery disease.

Results: LV systolic dysfunction was observed in 7.7% (13 of 169 patients). In these 13 patients, the mean ± SD LVEF was 42 ± 6%, the lowest value of LVEF was 32%, and no silent cardiac disease was revealed. Age, body mass index, apnea-hypopnea index, parameters of nocturnal oxyhemoglobin desaturation, and prevalence of systemic hypertension did not significantly differ between patients with LVEF < 50% and those with LVEF > 50%. In seven patients with LV dysfunction, LVEF was measured following treatment of OSAS and reached normal values.

Conclusion: OSAS may be a direct cause of daytime LV systolic dysfunction that can resolve following reversal of nocturnal apneas.

Key Words: left ventricular ejection fraction • left ventricular function • obstructive sleep apnea syndrome • positive airway pressure • radionuclide ventriculography


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Obstructive sleep apneas are associated with an acute increase in left ventricular (LV) afterload that can result in acute LV systolic dysfunction.1 2 3 However, conflicting results have been published regarding the effects of obstructive sleep apneas on daytime LV systolic function. In a canine model of obstructive sleep apnea syndrome (OSAS), a significant decrease in LV ejection fraction (LVEF) was demonstrated with two-dimensional echocardiography after a 1- to 3-month period of OSAS.1 Malone and coworkers4 showed, in patients with idiopathic dilated cardiomyopathy and severe OSAS, that daytime LVEF increased significantly after 4 weeks of nasal continuous positive airway pressure (CPAP) therapy. Yet several cross-sectional studies5 6 7 8 demonstrated that daytime LVEF was normal in patients with OSAS, and did not significantly differ between patients with OSAS and nonapneic control subjects.

The relevance of these studies is hampered by several factors: the number of OSAS patients was small, ranging from 15 to 30 patients5 6 7 8 ; LV systolic function was assessed in most studies5 6 8 by echocardiography, which is associated with a high risk of technical failure in patients with severe obesity9 ; patients with systemic hypertension were excluded,5 8 although hypertension is a well-recognized complication of OSAS10 11 12 13 14 that may induce LV dysfunction; and patients with awake hypoxemia and/or hypercapnia were excluded,5 8 although these patients have been reported to have more profound nocturnal oxyhemoglobin desaturation and/or more severe obesity, which may theoretically affect LV function.15 The aim of this study was to assess the prevalence and potential causes of LV systolic dysfunction, using radionuclide angiography, in a large group of patients with OSAS with no associated cardiac diseases.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patients
The study population included patients with OSAS diagnosed by polysomnography (apnea-hypopnea index [AHI] > 10 events per hour) consecutively admitted to our Department of Pneumology over a 5-year period for the administration of nasal CPAP. In these patients, LVEF was systematically measured using radionuclide angiography as part of a routine evaluation.

Exclusion Criteria
Exclusion criteria were as follows: (1) central sleep apnea, defined as a central apnea index (AI) > 5/h associated with an obstructive AI < 5/h; (2) unstable cardiorespiratory status, defined as the occurrence of respiratory failure, bronchopulmonary infection, or congestive heart failure in the previous 2 months; (3) coronary artery disease, defined as a typical angina pectoris, a prior myocardial infarction, a positive exercise test result, positive myocardial scintigraphy or positive coronary angiography findings; (4) valvulopathy, permanent atrial fibrillation, congenital heart disease; and (5) chronic severe alcoholism.

Polysomnography
An overnight polygraphic sleep study was carried out in the sleep laboratory using standard recording techniques with the Alvar polygraphic recorder (Medical Equipment International; Lyon, France) and Nightingale software (Deltamed; Paris, France). Sleep was monitored with EEG, an electrooculogram, and chin electromyogram. Air-flow recording, by means of an oronasal thermistor-detected apnea, defined as cessation of air flow for at least 10 s. The AI was calculated as the number of apneas per hour of sleep. The type of apnea was defined by the analysis of thoracoabdominal movements, which were recorded by respiratory inductive plethysmography using a mercury strain gauge (Volucapt; Vickers; Bordeaux, France). The transducers were placed around the chest and abdomen.

Arterial oxyhemoglobin saturation (SaO2) was recorded by means of a pulse oximeter (Oxyshuttle; SensorMedics; Yorba Linda, CA). Hypopnea was defined as a decrease in ventilation > 50% associated with an SaO2 drop of >= 4% for at least 10 s. The AHI was calculated as the number of apneas and hypopneas per hour of sleep. Several parameters of oxyhemoglobin desaturation were computed: (1) minimal SaO2; (2) percentage of total sleep time (TST) spent at SaO2 < 90%; and (3) percentage of TST spent at SaO2 < 80%.

Radionuclide Ventriculography
Multiple-gated equilibrium cardiac imaging was performed following standard procedure: 1 gigabecquerel of technetium Tc 99m was injected after in vivo RBC labeling. Data were acquired in the left anterior oblique view, using a degree of obliquity that provided the best separation between both ventricles and the atria. Sixteen frames per cycle were obtained (minimum of 200,000 counts per frame, matrix 64 x 64, Tomo camera Elscint 609 or Elscint Helix; Elscint; Haifa, Israel) and processed with a special computer system (Elscint Apex SP 1; Elscint).

LVEF was calculated with both automatic and semiautomatic programs, after generation of Fournier phase and amplitude images, and a definition of end-diastolic and end-systolic left ventricular images. LV systolic dysfunction was defined by a LVEF of < 50%. The physician who interpreted the radionuclide scans was aware that the patient had sleep apnea syndrome, but he had no knowledge of polysomnographic data.

Evaluation of Cardiovascular Risk Factors
Body weight was measured to the nearest 0.1 kg with subjects in indoor clothing and no shoes. Height was measured to the nearest 0.5 cm with a wall-mounted stadiometer, in the same conditions. Body mass index (BMI) was calculated as weight divided by height squared. Obesity was defined as a BMI > 30, and massive obesity was defined as BMI > 40.

Diabetes mellitus was defined by a fasting blood glucose level >= 7.7 mmol/L, a postprandial blood glucose >= 11 mmol/L, or a history of regular treatment for previously known diabetes. Systemic arterial hypertension was defined as systolic BP >= 160 mm Hg or diastolic BP >= 95 mm Hg, observed over at least three recordings. Patients with a history of regular antihypertensive medication for known systemic arterial hypertension were also considered as hypertensive.

Myocardial Scintigraphy and Echocardiography
Myocardial scintigraphy and echocardiography were performed only in those patients in whom radionuclide angiography showed LV systolic dysfunction. The aim of the myocardial scintigraphy was to exclude a silent myocardial ischemia, related to coronary artery disease. Echocardiography was undertaken to exclude significant valvulopathy that could have been missed on clinical examination, ECG, and chest radiography.

Single-photon emission CT myocardial study with a dipyridamole stress test was performed, using an IV infusion of dipyridamole, 0.6 mg/kg. An IV injection of 111 megabecquerel thallous chloride Tl 201, or 296 to 740 megabecquerel 99mTc-labelled methoxy-isobutyl-isonotrile (depending on the patient’s weight) was followed by single-photon emission CT acquisition: 30 frames on a 180° arc extending from 45° right anterior oblique to 45° left posterior oblique position (30 s per frame, matrix 64 x 64). Horizontal long-axis, short-axis, and vertical long-axis slices were reconstructed using filtered backprojection. Myocardial segment activity was assessed on a short-axis sliced bull’s eye, where the maximum count per pixel of each cut was normalized to a value of 100%. A new acquisition using the same procedure was performed following a rest injection, 240 min later for thallium delayed imaging, 2 days later for methoxy-isobutyl-isonotrile rest imaging. Myocardial ischemia was defined as the presence of a myocardial perfusion defect on the dipyridamole images, which disappeared or markedly decreased on the rest images. Doppler echocardiography was performed (Model 77020-CF; Hewlett-Packard; Andover, MA).

Statistical Analysis
The results are presented as mean (SD) values and as percentages. Quantitative data were compared in patients with LV systolic dysfunction and in those with normal LV systolic function using the Student t test, and the percentages were compared in the two groups using the {chi}2 test.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
The main characteristics of the patients are summarized in Table 1 . The study population included 169 OSAS patients with a mean AHI of 47/h. The AHI was > 30/h in 71% of the patients, and > 50/h in 41%. Seventy-nine percent of the patients were obese, with massive obesity in 37%.


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  		Table 1. Characteristics of the Study Population (n = 169)*

 
Radionuclide angiography could be performed in all patients without any technical failure. LV systolic dysfunction was present in 7.7% (13 of 169 patients) of the study population, and these patients had a mean LVEF of 42 ± 6%, while the mean LVEF was 63 ± 6% in the 156 patients with normal LV systolic function. The LVEF ranged from 40 to 50% in nine patients, and from 30 to 40% in four patients. The lowest LVEF value was 32%. The alteration in LV function was diffuse in all these 13 patients, without segmental akinesis or hypokinesis.

Myocardial scintigraphy with a dipyridamole stress test was performed in the 13 patients with LV systolic dysfunction and did not disclose a pattern of myocardial ischemia in any of these patients. Doppler echocardiography was also performed in the 13 patients with LV systolic dysfunction, and was technically satisfactory in 10 of these patients. None of these patients had significant valvulopathy or segmental wall motion abnormalities of the left ventricle.

The polysomnographic data are shown in Table 2 . The AHI, the AI, and the parameters of nocturnal oxyhemoglobin desaturation did not significantly differ between patients with LV systolic dysfunction and those with normal LV function. Age, sex ratio, body weight, BMI, and the percentages of patients with obesity, hypertension, diabetes mellitus, or history of smoking did not significantly differ between patients with LV systolic dysfunction and those with normal LV function (Table 3 ). The percentages of patients with a history of regular use of ß-blockers, angiotensin-converting enzyme (ACE) inhibitors, or diltiazem did not significantly differ between the two groups (Table 3) .


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  		Table 2. Polysomnographic Data in Patients With LV Systolic Dysfunction vs Those With Normal LV Systolic Function*

 

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  		Table 3. Anthropometric Data, Cardiovascular Risk Factors, and Cardiac Medications in Patients With LV Systolic Dysfunction vs Those with Normal LV Systolic Function*

 
LVEF was measured using radionuclide angiography following a reversal of OSAS in 7 of the 13 patients with LV systolic dysfunction. Six patients were treated with nasal CPAP, and one patient underwent uvulopalatopharyngoplasty. The mean delay between the two measurements of LVEF was 12 ± 5 months. The LVEF increased significantly from 44 ± 3% before treatment to 62 ± 4% after treatment (Table 4 ). All seven patients had normal LVEF (> 50%) following treatment. The body weight did not significantly vary between the two measurements of LVEF. Of those seven patients, cardiac medications were used in three patients with systemic hypertension, which had been treated with a combination of ACE inhibitor and diuretic for several years, but these medications remained unchanged during the follow-up period. In the six other patients with LV dysfunction, a second LVEF measurement was not performed because two patients refused nasal CPAP therapy, two patients received nasal CPAP < 3 h per night, and two patients were unavailable for follow-up.


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  		Table 4. Evaluation of LV Systolic Function Before and After Treatment of OSAS With Nasal CPAP (n = 6) or Pharyngoplasty (n = 1)*

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
This study showed that left ventricular systolic dysfunction, diagnosed by radionuclide angiography, was observed in 7.7% (13 of 169 patients) with OSAS requiring nasal CPAP, and with no associated cardiac disease. LV function impairment was moderate, as the lowest value of LVEF was 32%. In the seven patients with LV dysfunction in whom a second measurement of LVEF could be obtained following efficient treatment of OSAS, LVEF improved significantly and reached normal values in all of them.

This LV systolic dysfunction was observed in a study population in whom an associated cardiac disease had been excluded. It has been demonstrated that OSAS patients have a high prevalence of cardiovascular risk factors.16 A coexisting coronary artery disease would be a major confounding factor in the interpretation of LVEF measurements in patients with OSAS. Therefore, the study population did not include patients with a previously diagnosed coronary artery disease. Moreover, in those patients with OSAS with LV dysfunction, myocardial scintigraphy with dipyridamole stress test was systematically performed and did not reveal signs of myocardial ischemia. Segmental LV wall motion disturbances were not demonstrated in any of these patients by radionuclide angiography or echocardiography. Therefore, it is very unlikely that the LV systolic dysfunction observed in our patients with OSAS could be related to a silent coronary artery disease. Valvulopathy and congenital heart disease were excluded in these patients by echocardiography. Systemic hypertension was observed in 54% of the patients with LV dysfunction and could theoretically have affected LV function. Unlike other authors,5 8 we did not exclude patients with systemic hypertension, since it has been clearly demonstrated that OSAS is a risk factor for daytime systemic hypertension.10 11 12 13 14 However, in our study, the prevalence of systemic hypertension did not significantly differ between patients with and without LV dysfunction.

The prevalence of obesity was high (69%) in our OSAS patients with LV dysfunction, and this might be a confounding factor in assessing the effects of OSAS on LV function, since obesity in itself is a well-known cause of LV systolic dysfunction.17 18 Decreased LVEF in obese subjects is influenced, among other factors, by the degree of obesity.19 Nevertheless, epidemiologic data have shown that obesity is strongly associated with OSAS, so that the majority of OSAS patients are usually obese.20 21 In our study, the BMI was not significantly greater in the patients with LV dysfunction when compared to those with normal LV function. Thus, it is likely that the daytime LV systolic dysfunction observed in our OSAS patients was primarily related to nocturnal apneas and hypopneas because it could not be explained by an associated cardiac disease, a higher prevalence or degree of obesity, or a higher prevalence of systemic hypertension. Nonetheless, these results need to be confirmed by prospective studies comparing LV function in OSAS patients and in OSAS-free control subjects who should be matched in terms of BMI, age, and gender.

The hypothesis of a direct link between OSAS and daytime LV dysfunction is strengthened by the fact that we observed normalization of LV systolic function following treatment of OSAS in all the seven patients in whom a second determination of LVEF was performed. In these patients, there was no confounding factor during the follow-up period, such as a decrease in body weight or a change in cardiac medications that could modify LV function. Malone and coworkers4 have shown, in eight patients with severe OSAS and congestive heart failure secondary to idiopathic dilated cardiomyopathy, that LVEF increased significantly from 37 ± 4% pretreatment to 49 ± 5% after 4 weeks of nasal CPAP therapy. In 28 patients with severe OSAS and no overt ischemic heart disease, Krieger and coworkers22 reported a significant increase in LVEF from 59 ± 1% to 63 ± 1% after 1 year of treatment with nasal CPAP, but the interest of this study is limited by the fact that only two patients had a pretherapeutic LVEF < 50%. A rise of > 10% in LVEF was documented in 5 of 11 children with OSAS after adenotonsillectomy, of whom 3 children had a low LVEF before surgery.23

Patients with OSAS have recurrent increases in LV afterload during sleep that result from large negative intrathoracic pressure swings, hypoxemia, and arousals from sleep.24 In patients with OSAS and congestive heart failure secondary to idiopathic dilated cardiomyopathy or coronary artery disease, the nocturnal increase in LV afterload results primarily from surges in systolic BP, with reductions in intrathoracic pressure playing a minor role.25 Apnea-related hypoxemia and arousals from sleep increase sympathetic nervous system activity that results in systemic vasoconstriction.26 Recurrent LV strain over several hours of apnea may cumulatively lead to chronic daytime LV dysfunction. Hypoxemia related to apnea can also impair LV myocardial contractility.27 The improvement in LV systolic function following a reversal of OSAS by nasal CPAP is mainly related to a reduction in nocturnal LV afterload,25 but may also be explained by a down-regulation of sympathetic adrenergic activity and an improvement in myocardial contractility.4 In our study, the patients with LV systolic dysfunction did not demonstrate more severe OSAS in terms of AHI or nocturnal SaO2, but one cannot exclude that these patients actually had a more important increase in nocturnal systemic BP and/or a higher sympathetic nervous system activity. Unfortunately we did not perform monitoring of nocturnal BP, nor measurements of plasma or urinary noradrenaline concentrations.

LV systolic dysfunction is a rare complication of OSAS as was observed in < 10% of the patients in our study. Other types of LV involvement have been described in patients with OSAS. Hedner and coworkers5 showed that LV hypertrophy is a common phenomenon in OSAS patients without daytime systemic hypertension. However, in a recent study,28 the increase in LV mass that was observed in OSAS patients was found to be influenced by BMI, age, and the presence of hypertension, but was not correlated with the severity of OSAS. Alchanatis and coworkers8 demonstrated that patients with severe OSAS had LV diastolic dysfunction that improved significantly following nasal CPAP therapy.

In conclusion, the results of this study suggest that OSAS may be a direct cause of LV systolic dysfunction that can resolve following reversal of nocturnal apneas. Further studies are needed to evaluate the prevalence of LV systolic dysfunction in patients with less severe OSAS, and to clarify the mechanisms underlying the links between nocturnal apneas and daytime LV systolic dysfunction.


   Footnotes
 
Abbreviations: ACE = angiotensin-converting enzyme; AHI = apnea-hypopnea index; AI = apnea index; BMI = body mass index; CPAP = continuous positive airway pressure; LV = left ventricular; LVEF = left ventricular ejection fraction; OSAS = obstructive sleep apnea syndrome; SaO2 = arterial oxyhemoglobin saturation; TST = total sleep time

Received for publication July 26, 2001. Accepted for publication April 8, 2002.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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Left ventricular dysfunction and sleep apnea syndrome: cause or consequence?
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