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Table of Contents
Vol. 72, No. 3, 2005
Issue release date: May–June 2005
Respiration 2005;72:278–284
(DOI:10.1159/000085369)

Impact of Obstructive Sleep Apnea on Right Ventricular Global Function: Sleep Apnea and Myocardial Performance Index

Dursunoğlu N.a · Dursunoğlu D.b · Kılıç M.b
Departments of aChest Diseaseand bCardiology, Pamukkale University Medical Faculty, Denizli, Turkey
email Corresponding Author

Abstract

Background: Obstructive sleep apnea (OSA) is characterized by repetitive upper airway obstructions during sleep, and it might cause cardiovascular complications such as heart failure, arrhythmias, myocardial infarction, systemic and pulmonary hypertension. Objectives: To determine right ventricular diameters and myocardial performance index (MPI) reflecting ventricular global function in uncomplicated OSA patients. Methods: 49 subjects without hypertension, diabetes mellitus, or any cardiac or pulmonary disease referred for evaluation of OSA had overnight polysomnography and complete echocardiographic assessment. According to the apnea-hypopnea index (AHI), subjects were divided into three groups: group 1: control subjects (AHI <5, n = 20), group 2: patients with mild OSA (AHI: 5–14, n = 11), and group 3: moderate-severe OSA (AHI ≧15, n = 18). Right ventricular free wall diameter was measured by M mode, and right ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time)/pulmonary ejection time. Results: There were no differences of age, body mass index, heart rates, systolic and diastolic blood pressures among the groups (p > 0.05). Right ventricular end-diastolic and end-systolic diameters were not statistically different between the groups, and were within normal limits. Also, right ventricular free wall diameter was not significantly different between the groups of control, mild OSA and moderate-severe OSA (6.7 ± 0.9, 6.9 ± 1.0, 7.1 ± 1.1 mm, p > 0.05). Right ventricular diastolic dysfunction was shown only in group 3 patients. Right ventricular MPI was statistically higher in group 3 (0.62 ± 0.18) than in group 2 patients (0.50 ± 0.10), and group 1 patients (0.48 ± 0.08, p < 0.001). Conclusions: It wassuggested that patients with moderate-severe OSA had a right ventricular global dysfunction, in addition to the presence of a diastolic dysfunction.


 Outline


 goto top of outline Key Words

  • Obstructive sleep apnea
  • Myocardial performance index, right ventricular

 goto top of outline Abstract

Background: Obstructive sleep apnea (OSA) is characterized by repetitive upper airway obstructions during sleep, and it might cause cardiovascular complications such as heart failure, arrhythmias, myocardial infarction, systemic and pulmonary hypertension. Objectives: To determine right ventricular diameters and myocardial performance index (MPI) reflecting ventricular global function in uncomplicated OSA patients. Methods: 49 subjects without hypertension, diabetes mellitus, or any cardiac or pulmonary disease referred for evaluation of OSA had overnight polysomnography and complete echocardiographic assessment. According to the apnea-hypopnea index (AHI), subjects were divided into three groups: group 1: control subjects (AHI <5, n = 20), group 2: patients with mild OSA (AHI: 5–14, n = 11), and group 3: moderate-severe OSA (AHI ≥15, n = 18). Right ventricular free wall diameter was measured by M mode, and right ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time)/pulmonary ejection time. Results: There were no differences of age, body mass index, heart rates, systolic and diastolic blood pressures among the groups (p > 0.05). Right ventricular end-diastolic and end-systolic diameters were not statistically different between the groups, and were within normal limits. Also, right ventricular free wall diameter was not significantly different between the groups of control, mild OSA and moderate-severe OSA (6.7 ± 0.9, 6.9 ± 1.0, 7.1 ± 1.1 mm, p > 0.05). Right ventricular diastolic dysfunction was shown only in group 3 patients. Right ventricular MPI was statistically higher in group 3 (0.62 ± 0.18) than in group 2 patients (0.50 ± 0.10), and group 1 patients (0.48 ± 0.08, p < 0.001). Conclusions: It wassuggested that patients with moderate-severe OSA had a right ventricular global dysfunction, in addition to the presence of a diastolic dysfunction.

Copyright © 2005 S. Karger AG, Basel


goto top of outline Introduction

Obstructive sleep apnea (OSA) is characterized by a repetitive collapse of the upper airway during sleep [1]. The obstructive apneic event is associated with considerable breathing efforts against totally or partially occluded upper airways. The apnea is terminated by an arousal and heavy snoring as airflow is restored. The severity of OSA is described according to the total number of apneas and hypopneas per hour of sleep, which is named the apnea-hypopnea index (AHI).

Cardiovascular disturbances are the most serious complications of OSA. These complications include heart failure [2], acute myocardial infarction [3],noctur nal arrhythmias [4], stroke [5], and systemic [6, 7] and pulmonary hypertension [8]. All these cardiovascular complications increase morbidity and mortality of OSA. Nowadays, sleep apnea is accepted as one of the identifiable causes of hypertension in the JNC 7 report [9]. Also, OSA is closely associated withobesity [10] and aging [11].

The left ventricular systolic and diastolic functions are closely related to mortality and morbidity. Diastolic dysfunction precedes left ventricular systolic impairment and accounts alone for about 30–40% of patients with left ventricular failure [12, 13]. Early recognition and appropriate therapy of left ventricular diastolic dysfunction are advisable to prevent further progression to heart failure and death [12,13,14,15]. Arterial hypertension, evidence of left ventricular hypertrophy, and coronary artery disease are independent predictors of diastolic dysfunction. In addition to these factors, diastolic dysfunction is related to a high body mass index, high body fat mass, and diabetes mellitus [13,14,15,16,17,18].

Ventricular dysfunction could not be detected clinically, but could just be detected echocardiographically. The left ventricular myocardial performance index (MPI) reflects left ventricular both systolic and diastolic functions (global functions) [19, 20]. In the presence of global dysfunction of the ventricle, MPI increases in contrast to the ejection fraction of the ventricle. MPI is a reproducible, widely applicable and a simple noninvasive method for the estimation of the ventricular global function in the patients.

So, in this study, we aimed to estimate the left and right ventricular diameters and global function in uncomplicated OSA patients.

 

goto top of outline Methods

goto top of outline Study Population

49 subjects admitted to the sleep clinic with symptoms of nocturnal snoring and/or excessive daytime sleepiness were entered into the study. A detailed sleep and cardiovascular anamnesis of the patients was recorded. Sleep cycle, nutritional status, medications, alcohol usage and family anamnesis were also recorded. Epworth sleepiness scale [21] was established in all patients, and patients having high scores (Epworth sleepiness scale ≥10) were entered into the sleep study.

A physical examination was performed in all subjects. Systolic and diastolic blood pressure was measured in the sitting position on the right arm using a sphygmomanometer (Erka, Germany) after at least 5 min of rest. Hypertension was defined as blood pressure ≥140/90 mm Hg or the use of antihypertensive drugs. Heart rate per minute was measured in the sitting position, and body mass index of the patients was calculated as weight divided by height square (kg/m2).

Pulmonary function tests (Sensor medics 2400, The Netherlands) and arterial blood gas analysis (ABL 30, Copenhagen) were performed in all patients at rest. A 12-leadsurface ECG was taken from each subject, and all of them were in sinus rhythm. Also, all subjects underwent a treadmill exercise test, which was normal in all of them.

Symptoms of nocturnal snoring and/or excessive daytime sleepiness were accepted as inclusion criteria. Exclusion criteria of the study were the presence of (1) any known cardiac and lung disease, (2) hypertension, (3) diabetes mellitus, (4) angina pectoris, (5) atrial fibrillation or any arrhythmias, (6) chronic renal and hepatic diseases, and (7) serum electrolyte imbalances.

goto top of outline Polysomnography

Polysomnography [22] was applied to all subjects on the diagnostic night 0 (Medilog Replay, Oxford Medical), measuring the following: 1-channel EEG (electroencephalogram), 2-channel EOG (electrooculogram), 2-channel chin EMG (electromyogram), oronasal airflow, tracheal microphone, thoracal and abdominal movement sensor, 2 leg movement sensors and 1-channel ECG. Apneas, hypopneas and desaturations were recorded automatically by computer-based Medilog software.

Sleep stages were scored according to the atlas of Rechtschaffen and Kales [23] by a skilled pulmonary physician.

Apnea was defined as a total obstruction of oronasal airflow ≥10 s, an hypopnea was defined as a decrease of airflow by at least 50%, and desaturation was defined as a decrease of ≥4% in oxygen saturation [24]. Subjects with AHI ≥5 were diagnosed as OSA (n = 29) [25], and subjects with AHI ≤5 were defined as the control group (n = 20). Patients with OSA were divided into two groups according to AHI: patients with mild OSA (AHI = 5–14, n = 11) and patients with moderate-severe OSA (AHI ≥15, n = 18).

goto top of outline Echocardiographic Measurements

All measurements were performed with the subjects in the left lateral decubitus position with M mode, two-dimensional, and Doppler ultrasound echocardiography in the morning. The ultrasound equipment used was Contron Sigma Iris with a 2.5-MHz probe. The duration of the examination was at least 20 min. The ventricular diameters, volumes and functions were measured according to the recommendations of the American Society of Echocardiography [26]. Basic measurements of right and left ventricle dimensions in diastole, right ventricular free wall diameter, thickness of interventricular septum and posterior wall were measured with the M mode technique. Left ventricular ejection fraction with Simpson’s method was calculated as (diastolic volume – systolic volume)/(diastolic volume).

Early (E) and atrial (A) transmitral/transtricuspid maximal flow velocities, the ratio E/A and deceleration time of E were registered. Isovolumetric relaxation time was measured by the continuous wave Doppler technique. The velocity of mitral/tricuspid flow propagation was estimated using color Doppler M mode. The left/right ventricular MPI was calculated as (isovolumic contraction time of left/right ventricle + isovolumetric relaxation time of left/right ventricle)/aortic-pulmonary ejection time.

goto top of outline Statistical Analysis

Statistics were performed by Statistical Package for Social Sciences version 10.0 (SPSS-10.0) for windows statistic packet program. Results were given as mean ± standard deviation and the Kruskal-Wallis test was used. Also, the Mann-Whitney U test was used for comparison between the two groups. A p value <0.05 was considered significant.

 

goto top of outline Results

Basic characteristics of the patients with OSA and controls are shown in table 1. There were no significant differences between the controls, patients with mild OSA and patients with moderate-severe OSA according to age, body mass index, systolic and diastolic blood pressure and heart rate (p > 0.05).

TAB01

Table 1. Basic characteristics of controls and patients with OSA

Basic echocardiographic measurements of left ventricle in controls and patients with OSA are shown in table 2. Left ventricular diameters, systolic and diastolic functions did not differ significantly between the groups (p > 0.05), and were within normal limits. However, left ventricular MPI (global function) differed significantly between OSA patients and controls (p < 0.001), while it did not differ significantly between the OSA groups (p > 0.05).

TAB02

Table 2. Basic echocardiographic measurements of the left ventricle in controls and patients with OSA

Basic echocardiographic measurements of the right ventricle in controls and patients with OSA are shown in table 3. Right atrium, right ventricular free wall diameters, right ventricular end-diastolic and end-systolic diameters were not statistically different between the groups, and were within normal limits. Right ventricular diastolic dysfunction was shown in only moderate-severe OSA patients. Right ventricular MPI was statistically higher in moderate-severe OSA patients (0.62 ± 0.18) than in mild OSA patients (0.50 ± 0.10), and than in controls (0.48 ± 0.08, p < 0.001). MPI was not statistically different between group 1 (controls) and group 2 (mild OSA); it was significantly different between group 3 (moderate-severe OSA) and group 1 (p < 0.001), and was also significantly different between group 3 (moderate-severe OSA) and group 2 (p < 0.001).

TAB03

Table 3. Echocardiographic assessment of the right ventricle in controls and patients with OSA

Right ventricular MPI showed a positive correlation with AHI reflecting the severity of OSA (p < 0.001, r = 0.847). The correlation between MPI and AHI in OSA patients is shown in figure 1.

FIG01

Fig. 1. Correlation between MPI and AHI in OSA patients (r = 0.847; p < 0.001).

 

goto top of outline Discussion

OSA might cause cardiovascular complications such as heart failure, myocardial infarction, arrhythmias, and systemic and pulmonary hypertension. Since the left ventricular function was closely related to mortality and morbidity, we aimed to estimate the MPI reflecting ventricular global function in uncomplicated OSA patients. In our study, systemic hypertension, diabetes mellitus and coronary artery disease were excluded, and there were no significant differences in age, body mass index and arterial blood pressures of the subjects. Thus, we assessed the ventricular function (MPI) in uncomplicated (isolated) OSA patients.

Left ventricular systolic and/or diastolic functions provide prognostic information in patients. In our study, although left ventricular diameters and both systolic and diastolic functions of all subjects were within normal limits, left ventricular MPI (global function) significantly differed between OSA patients (0.51 ± 0.10 in mild OSA group and 0.53 ± 0.14 in moderate-severe OSA group) and controls (0.36 ± 0.09, p < 0.001), while it was not significantly different between the OSA groups (p > 0.05). However, right ventricular MPI was statistically higher in moderate-severe OSA patients (0.62 ± 0.18) than in mild OSA patients (0.50 ± 0.10) and in controls (0.48 ± 0.08, p < 0.001). On the other hand, right ventricular diastolic dysfunction was shown in only moderate-severe OSA patients. Also, right ventricular MPI showed a positive correlation with AHI reflecting the severity of OSA (p < 0.001, r = 0.847).

The relation of sleep apnea to right heart structure and function is controversial. The prevalence of right ventricular hypertrophy by echocardiography in sleep apnea ranged from 0 to 71% [27]. It has been argued that concomitantchronic pulmonary disorders are required for sleep apnea to causeright heart failure [28,29,30,31,32]. However, Sanneret al. [33] demonstrated that sleep apnea was independentlyassociated with depressed right ventricular ejection fraction by radionuclideventriculography after adjusting for lung function, age, bodymass index, sex, blood gas analysis, pulmonary artery pressure,and left ventricular ejection fraction. Hanly et al. [34] found no difference in right or left ventricular dimensions betweennonapneic snorers and subjects with OSA.

The reasons for the disparate conclusions of the prior studies examining right ventricular hypertrophy, systolic function, and right ventricular enlargementare not certain. In a study [35], right atrial and ventricular dimensions, and right ventricular systolicfunction were not found to be significantly different betweensubjects with sleep-disordered breathing and the low respiratory disturbance index subjects, but this study indicated that sleep-disordered breathing was associated with increased right ventricular wall thickness in a general population [35].

Our study does not clarify the reason of right and left ventricular both diastolic and global dysfunctions in OSA patients compared with controls. In these patients intermittent nocturnal hypoxemia might have caused right ventricular dysfunction. It is well-known that the risk of developing systemic hypertension increases depending on the severity of OSA [36, 37]. Hedner et al. [38] showed that nocturnal hypoxemia increases sympathetic stimulation and this might cause systemic hypertension. On the other hand, Arabi et al. [39] proved that systemic hypertension developed in a hypoxic situation in normotensive cases, and furthermore they showed a decrease in the adrenergic mediators in patients having continuous positive airway pressure therapy for OSA.

Right ventricular diastolic filling is a complex event that is influenced by several factors, such as right ventricular relaxation, right ventricular compliance, right atrium contraction force and pulmonary artery resistance. Thus, right ventricular dysfunction might be the result of a variety of these impairments.

Since the systolic and diastolic dysfunction frequently coexist, it was shown that a combined measure of left ventricular performance with a calculation of MPI might be more reflective of overall cardiac dysfunction than systolic or diastolic measures alone. MPI is a reproducible, widely applicable and a simple noninvasive method for the estimation of left ventricular global function in patients with OSA.

 

goto top of outline Conclusions

The present study demonstrates that increased AHI in the patientswith OSA may result in biventricular (especially right ventricular) dysfunction.Since diastolic dysfunction might be combined with systolic dysfunction, especially severe OSA patients having diastolic dysfunction might have an increased risk of heart failure. In this study, a significant positive correlation between MPI and the severity of OSA was also shown. It will be important to resolve whether the ventricular dysfunction may be corrected by continuous positive airway pressure treatment.

goto top of outline Study Limitations

Our sleep clinic population may not reflect the findings in the general community because of the small number of patients. Since the ventricular systolic and/or diastolic functions provide prognostic information as regards the patients, our results should be further confirmed with several longitudinal studies.


 goto top of outline References
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  2. Malone S, Liu PP, Holloway R, Rutherford R, Xie A, Bradley TD: Obstructive sleep apnea in patients with dilated cardiomyopathy: Effects of CPAP. Lancet 1991;338:1480–1484.
  3. Hung J, Whitford EG, Parsons RW, Hillman DR: Association of sleep apnoea with myocardial infarction in men. Lancet 1990;336:261–264.
  4. Guilleminault C, Connoly S, Winkle RA: Cardiac arrhythmia and conduction disturbances during sleep in 400 patients with sleep apnea syndrome. Am J Cardiol 1983;52:490–494.
  5. Palomaki H, Partinen M, Erkinjuntti I, Kaste M: Snoring, sleep apnea syndrome and stroke. Neurology 1992;42:75–82.
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  29. Weitzenblum E, Krieger J, Apprill M, Vallee E, Ehrhart M, Ratomaharo J, Oswald M, Kurtz D: Daytime pulmonary hypertension in patients with obstructive sleep apnea syndrome. Am Rev Respir Dis 1988;138:345–349.
  30. Chaouat A, Weitzenblum E, Krieger J, Oswald M, Kessler R: Pulmonary hemodynamics in the obstructive sleep apnea syndrome. Results in 220 consecutive patients (see comments). Chest 1996;109:380–386.
  31. Bradley TD: Right and left ventricular functional impairment and sleep apnea. Clin Chest Med 1992;13:459–479.
  32. Weiss JW, Remsburg S, Garpestad E, Ringler J, Sparrow D, Parker JA: Hemodynamic consequences of obstructive sleep apnea. Sleep 1996;19:388–397.
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  34. Hanly P, Sasson Z, Zuberi N, Alderson M: Ventricular function in snorers and patients with obstructive sleep apnea. Chest 1992;102:100–105.
  35. Guidry UC, Mendes LA, Evans JC, Levy D, O’Connor GT, Larson MG, Gottlieb DJ, Benjamin EJ: Echocardiographic features of the right heart in sleep-disordered breathing: The Framingham Heart Study. Am J Respir Crit Care Med 2001;164:933–938.
  36. Otsuka K: Hypertension and altered cardiovascular variability associated with obstructive sleep apnea. Nippon Rinsho 2000;58:1711–1716.
  37. Lavie P, Yoffe N, Berger T, Peled R: The relationship between the severity of sleep apnea syndrome and 24-h blood pressure values in patients with obstructive sleep apnea. Chest 1993;103:717–721.
  38. Hedner J, Ejnell H, Sellgren J, Hedner T, Wallin G: Is high and fluctuating muscle nerve sympathetic activity in the sleep apnoea syndrome of pathogenetic importance for the development of hypertension? J Hypertens 1988;6:529–531.
  39. Arabi Y, Morgan BJ, Goodman B, Puleo DS, Xie A, Skatrud JB: Daytime blood pressure elevation after nocturnal hypoxia. J Appl Physiol 1999;87:689–698.

 goto top of outline Author Contacts

Dr. Dursun Dursunoğlu
Yunus Emre Mah. Prof. Huseyin Yilmaz cad., No: 14/4, Kınıklı
TR–20200 Denizli (Turkey)
Tel. +90 258 213 67 62/+90 532 273 74 84, Fax +90 258 213 49 22
E-Mail ddursunoglu@tnn.net


 goto top of outline Article Information

Received: April 13, 2004
Accepted after revision: September 1, 2004
Number of Print Pages : 7
Number of Figures : 1, Number of Tables : 3, Number of References : 39


 goto top of outline Publication Details

Respiration (International Journal of Thoracic Medicine)

Vol. 72, No. 3, Year 2005 (Cover Date: May-June 2005)

Journal Editor: Bolliger, C.T. (Cape Town)
ISSN: 0025–7931 (print), 1423–0356 (Online)

For additional information: http://www.karger.com/res


Copyright / Drug Dosage / Disclaimer

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

Abstract

Background: Obstructive sleep apnea (OSA) is characterized by repetitive upper airway obstructions during sleep, and it might cause cardiovascular complications such as heart failure, arrhythmias, myocardial infarction, systemic and pulmonary hypertension. Objectives: To determine right ventricular diameters and myocardial performance index (MPI) reflecting ventricular global function in uncomplicated OSA patients. Methods: 49 subjects without hypertension, diabetes mellitus, or any cardiac or pulmonary disease referred for evaluation of OSA had overnight polysomnography and complete echocardiographic assessment. According to the apnea-hypopnea index (AHI), subjects were divided into three groups: group 1: control subjects (AHI <5, n = 20), group 2: patients with mild OSA (AHI: 5–14, n = 11), and group 3: moderate-severe OSA (AHI ≧15, n = 18). Right ventricular free wall diameter was measured by M mode, and right ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time)/pulmonary ejection time. Results: There were no differences of age, body mass index, heart rates, systolic and diastolic blood pressures among the groups (p > 0.05). Right ventricular end-diastolic and end-systolic diameters were not statistically different between the groups, and were within normal limits. Also, right ventricular free wall diameter was not significantly different between the groups of control, mild OSA and moderate-severe OSA (6.7 ± 0.9, 6.9 ± 1.0, 7.1 ± 1.1 mm, p > 0.05). Right ventricular diastolic dysfunction was shown only in group 3 patients. Right ventricular MPI was statistically higher in group 3 (0.62 ± 0.18) than in group 2 patients (0.50 ± 0.10), and group 1 patients (0.48 ± 0.08, p < 0.001). Conclusions: It wassuggested that patients with moderate-severe OSA had a right ventricular global dysfunction, in addition to the presence of a diastolic dysfunction.



 goto top of outline Author Contacts

Dr. Dursun Dursunoğlu
Yunus Emre Mah. Prof. Huseyin Yilmaz cad., No: 14/4, Kınıklı
TR–20200 Denizli (Turkey)
Tel. +90 258 213 67 62/+90 532 273 74 84, Fax +90 258 213 49 22
E-Mail ddursunoglu@tnn.net


 goto top of outline Article Information

Received: April 13, 2004
Accepted after revision: September 1, 2004
Number of Print Pages : 7
Number of Figures : 1, Number of Tables : 3, Number of References : 39


 goto top of outline Publication Details

Respiration (International Journal of Thoracic Medicine)

Vol. 72, No. 3, Year 2005 (Cover Date: May-June 2005)

Journal Editor: Bolliger, C.T. (Cape Town)
ISSN: 0025–7931 (print), 1423–0356 (Online)

For additional information: http://www.karger.com/res


Copyright / Drug Dosage

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

References

  1. Guilleminault C, Tilkian A, Dement WC: The sleep apnea syndromes. Annu Rev Med 1976;27:465–484.
  2. Malone S, Liu PP, Holloway R, Rutherford R, Xie A, Bradley TD: Obstructive sleep apnea in patients with dilated cardiomyopathy: Effects of CPAP. Lancet 1991;338:1480–1484.
  3. Hung J, Whitford EG, Parsons RW, Hillman DR: Association of sleep apnoea with myocardial infarction in men. Lancet 1990;336:261–264.
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