Article

PDF
Access to the PDF text
Advertising


Free Article !

Archives of cardiovascular diseases
Volume 101, n° 6
pages 391-397 (juin 2008)
Doi : 10.1016/j.acvd.2008.06.007
Received : 8 April 2008 ;  accepted : 9 June 2008
Is the aortic root dilated in obstructive sleep apnoea syndrome?
Dilatation aortique et syndrome d’apnée du sommeil
 

Catherine Meuleman a, Franck Boccara a, Xuan-Lan Nguyen b, Emanuele Di Angelantonio a, Stéphane Ederhy a, Sandra Janower a, Ghislaine Dufaitre a, Nabila Haddour a, Louise Boyer-Chatenet a, Dominique Rakotonanahary b, Bernard Fleury b, Ariel Cohen a,
a Department of Cardiology, Saint-Antoine University and Medical School, Université Pierre-et-Marie-Curie, 184, rue du Faubourg-Saint-Antoine, 75571 Paris cedex 12,France 
b Department of Respiratory Medicine, Saint-Antoine University and Medical School, université Pierre-et-Marie-Curie, Paris, France 

Corresponding author.
Summary
Background

Obstructive sleep apnoea syndrome (OSAS) is associated with an increased risk of arterial hypertension (AH), coronary artery disease, atrial arrhythmias, heart failure, stroke and death. Whether OSAS influences aortic root size has not been fully investigated. The aim of our study was to investigate aortic root diameter and aortic stiffness in OSAS.

Methods

Using transthoracic Doppler echocardiography, we evaluated 76 patients with OSAS (mean age 52.7±9.5 years, 70 men [92%]) with no overt cardiovascular disease. The following parameters were measured offline: aortic diameter at Valsalva sinuses, aortic regurgitation (AR) grade, left ventricular (LV) mass, LV ejection fraction (LVEF, Simpson rule), systolic pulmonary artery pressure (sPAP). Aortic stiffness (carotid-femoral pulse wave velocity, PWV) was measured non-invasively using SphygmoCor technology.

Results

Mean duration of OSAS was four years and 84% of patients were being treated with continuous positive airway pressure. AH was documented in 39 (51%) patients. The mean aortic root diameter was 35.3±3.8mm (26.9–44.6mm) and the prevalence of aortic root dilatation was 3.9% (3 of 76 patients). On univariate analysis, age and sex were significant predictors of aortic root dilatation whereas arterial hypertension was not.

Conclusions

The prevalence of aortic root enlargement was not increased in OSAS. Only age and sex and not arterial hypertension, were associated with aortic dilatation.

The full text of this article is available in PDF format.
Résumé
But de l’étude

Le syndrome d’apnée obstructive du sommeil (SAOS) est associé à une augmentation du risque d’hypertension artérielle, de maladie coronaire, de fibrillation auriculaire, d’insuffisance cardiaque, d’accident vasculaire cérébral et de décès. Une éventuelle relation entre le syndrome d’apnées du sommeil et la dilatation aortique n’a jamais été étudiée. Le but de cette étude était de mesurer les diamètres aortiques et la rigidité aortique chez des patients présentant un SAOS.

Méthodes

Une échocardiographie transthoracique a été réalisée chez 76 patients présentant un SAOS (âge moyen 52.7±9.5 years, 70 hommes [92 %]) sans antécédent cardiovasculaire connu. Les paramètres suivants ont été mesurés off-line  : diamètre aortique au niveau des sinus de Valsalva, insuffisance aortique (IA), masse ventriculaire gauche, rapport h/R, fraction d’éjection ventriculaire gauche (par la méthode de Simpson) et les pressions artérielles pulmonaires. La rigidité aortique a été évaluée par la mesure de la vitesse de l’onde de pouls carotido-fémorale (VOP).

Résultats

La durée moyenne du SAOS était de quatre années et 84 % des patients étaient traités par pression positive continue. Une hypertension artérielle (HTA) a été documentée chez 39 patients (51 %). Le diamètre aortique moyen était de 35.3±3.8mm (26.9–44.6mm) et la prévalence de la dilatation aortique était de 3.9 % (3/76 patients). En analyse univariée, l’âge et le sexe étaient des facteurs prédictifs significatifs de dilatation aortique mais non l’hypertension artérielle.

Conclusion

La prévalence de la dilatation aortique n’est pas augmentée dans le syndrome d’apnées du sommeil. Seuls l’âge et le sexe et non l’hypertension artérielle étaient associés à la dilatation aortique.

The full text of this article is available in PDF format.

Abbreviations : AH, AHI, AR, BMI, CPAP, LV, LVEDD, LVEF, OSAS, PWV, sPAP

Keywords : Obstructive sleep apnoea syndrome, Aortic root dilatation, Pulse wave velocity

Mots clés : Syndrome d’apnée obstructive du sommeil, Dilatation aortique, Vitesse de l’onde de pouls


Introduction

Obstructive sleep apnoea syndrome (OSAS) is a disordered breathing in which the upper airway closes repeatedly during sleep. These repetitive partial or complete cessations of airflow during sleep result in oxygen desaturation, sleep fragmentation and excessive daytime sleepiness. OSAS is common and affects up to 4% of middle-aged men and up to 2% of women [1]. It is associated with vascular risk factors and increased cardiovascular morbidity and mortality [2]. Several studies have reported that OSAS is independently associated with arterial hypertension [3], coronary artery disease [4, 5], heart failure [6, 7], stroke and death [8]. An association has also been demonstrated between OSAS and aortic stiffness [9] and an increased risk of aortic dissection [10]. Whether OSAS influences aortic root size has not yet been investigated. The aim of our study was to investigate aortic root diameter and aortic stiffness in patients with OSAS and to evaluate the influence of arterial hypertension.

Methods
Study population

We conducted an observational cohort study in patients with OSAS who were referred consecutively for a cardiovascular evaluation by the Saint-Antoine sleep disorders centre between March 2005 and March 2007. The study was performed in patients included in our outpatient clinic, with regular examinations that did not require the patient’s written consent. All information was, however, given to the patients.

Data on patient’s demographic characteristics, sleep and medical history, cardiovascular risk factors and medication use and habits were obtained during a consultation. Data on risk factors included a history of hypertension (defined as systolic blood pressure greater or equal to 140mmHg and/or diastolic blood pressure greater or equal to 90mmHg and/or use of antihypertensive medication, being measured with a standard sphygmomanometer on three different occasions with the subject in the supine position, or blood pressure greater than 125/80mmHg during 24-hour ambulatory blood pressure monitoring [11]), diabetes mellitus, hyperlipidaemia, and current or former smoking with an indication of the number of pack-years and coronary heredity. Metabolic syndrome was defined according to the National Cholesterol Education Program–Adult Treatment Panel III (NCEP ATP-III) guidelines [12]. The diagnosis required at least three of the following criteria: fasting glycaemia greater than 6.1mmol/L (1.1g/L), fasting triglycerides greater than 1.7mmol/L (1.5g/L), high-density lipoprotein cholesterol lesser than 1mmol/L (men) or 1.3mmol/L (women) (0.6 and 0.5g/L), blood pressure greater than 130/85mmHg, and waist circumference greater than 102cm (men) or greater than 88cm (women). Data regarding medications included the daily use of beta-blockers, angiotensin converting-enzyme inhibitors or angiotensin-receptor antagonists, diuretics, calcium-channel blockers, oral medications or insulin for the treatment of diabetes, and lipid-lowering medications. Each patient’s height and weight were recorded to determine their body mass index (BMI). Patients underwent a clinical examination, including biological samples (routine biochemical investigation, fasting glucose, insulin, lipids and high-sensitivity C-reactive protein), an electrocardiogram, a chest X-ray, ambulatory blood pressure monitoring, Holter monitoring, and transthoracic echocardiography. Aortic stiffness (carotid-femoral pulse wave velocity [PWV]) was measured non-invasively using SphygmoCor® technology.

Echocardiography

Transthoracic echocardiography was performed with a GE Vingmed Vivid 7 dimension with a 2.5-MHz transducer according to the recommendations of the American Society of Echocardiography [13]. All echocardiograms were reviewed and were excluded from the analysis if they had inadequate two-dimensional images for the assessment of ascending aorta dimensions. Aortic root diameter was measured according to Roman et al.’s [14] recommendations at end-diastole, in the parasternal long-axis view at four levels:

the annulus;
the sinuses of Valsalva;
the supra-aortic ridge;
the proximal ascending aorta.

Aortic root dilatation was identified when aortic root diameter at the sinus of Valsalva was greater than two standard deviations (SD) above the regression line with body surface area in a previously studied reference population [14]. Aortic regurgitation was semiquantified as mild, moderate, or severe, based on other flow mapping and usual indices [15].

Left ventricular end-diastolic diameter and end-systolic diameter were measured by M-mode echocardiography from two-dimensional echocardiography according to the recommendations of the American Society of Echocardiography [16]. The left ventricular mass index was calculated according to Devereux et al. [17]. LVEF was estimated visually. sPAP was calculated using the modified Bernoulli equation on tricuspid regurgitation [18]. Measurements were made in three cardiac cycles, and the average was calculated for subsequent analyses. All Doppler and echocardiographic recordings were stored on optical disks and were analysed off-line by a single experienced investigator blinded to the patient’s status and treatment.

PWV measurement

Aortic stiffness (carotid-femoral PWV) was measured non-invasively using SphygmoCor® technology. All arterial measurements were carried out during the consultation in a central core laboratory. Measurements were performed in a controlled environment at 22±1°C after 15minutes of rest. Transcutaneous Doppler flow recordings were carried out simultaneously at the carotid and femoral arteries. PWV was calculated as the distance between recording sites measured over the surface of the body divided by the time travelled by the reflected wave. The time delay was averaged over 10 to 15 cardiac cycles [19].

Polysomnography

All participants underwent attended overnight polysomnography with the use of the Cidelec® system (Angers, France). The recordings included a two-channel electroencephalogram, electromyogram, electrocardiogram, electro-oculogram, body position, chest and abdominal excursions, naso-oral airflow assessed by a nasal cannula, and oxyhaemoglobin saturation (finger pulse oximetry). A single, attended polysomnographic study conducted during an entire night was used to establish the presence of sleep apnoea [20].

Total cessation of airflow at the nose and mouth for at least 10 seconds was classified as apnoea (as obstructive if respiratory effort was present and as central apnoea if respiratory efforts were absent). Partial airway closure resulting in a diminution of airflow by greater than 30% for greater or equal to 10 seconds associated with oxygen desaturation greater or equal to 4% was classified as hypopnoea [21]. Calculated polysomnographic variables included the apnoea-hypopnoea index (AHI) and the percentage of total sleep time during which the oxygen saturation was lesser than 90% (SaO2 <90%). Sleep history data included a validated measure of daytime sleepiness (Epworth sleepiness scale) [22]. Sleep studies were performed in the sleep laboratory and were supervised throughout by an experienced technician.

Statistical analysis

Data are expressed as means±SD or medians with interquartile ranges. Pearson’s correlation analysis was used to assess the possible relation between aortic dimensions and demographic or echocardiographic parameters, with significance at a critical level of five per cent or lower. A probability value less than 0.05 was considered statistically significant. All statistical analysis was performed using STATA 9 statistical software.

Results

Table 1 summarizes the baseline characteristics of the 76 patients included in the study. The mean age was 52.7±9.6 years, 70 (92%) were men, and the mean BMI was 31.5±5.8kg/m2. Thirty-nine (51%) patients had evidence of hypertension at baseline examination. Of these, 25 (64%) patients had a history of hypertension with a mean duration of 6.4±4.7 years and 14 (36%) were newly diagnosed during the cardiovascular evaluation or by ambulatory blood pressure monitoring. A history of hypercholesterolaemia was present in 39 (51%) patients of whom 17 (44%) were being treated with statins or fibrates. Thirteen (17%) patients had diabetes mellitus, two of whom were being treated with insulin and four with oral hypoglycaemic drugs, and the others with diet. Metabolic syndrome was present in 37 (49%) patients. None of these patients had a history of cardiovascular disease (myocardial infarction, heart failure, atrial fibrillation, stroke, or aortic disease). No patient had a previous diagnosis of Marfan syndrome or related disease.

The median duration of OSAS was four years and 84% were treated with continuous positive airway pressure (CPAP). The median AHI was 56.5/h (minimum 11.8, maximum 188), with a median time spent with SaO2 <90% of 12.2%. The median Epworth Sleepiness Scale score was 10 (minimum 1, maximum 16) (Table 2).

Echocardiographic characteristics are shown in Table 3. No patients had left ventricular dysfunction or pulmonary arterial hypertension. The mean aortic root diameter was 35.3±3.8mm (26.9–44.6mm). According to the definition by Roman et al. [14], only three (3.9%) patients had aortic dilatation defined by aortic root diameter at the sinus of Valsalva greater than two SD above the regression line with body surface area. Mild aortic regurgitation was present in 13 (17%) patients. No moderate or severe aortic regurgitation was diagnosed. The mean PWV was 9.8±1.7m/s.

The main results are presented according to tertile of aortic diameter. Aortic root diameter was positively and significantly associated with age and male sex, and to a lesser extent with left ventricular end-diastolic diameter and left ventricular mass (although not statistically significant). No significant correlation was found between aortic root diameter and arterial hypertension, PWV or OSAS (Table 4).

Discussion

To our knowledge, this is the first evaluation of aortic root diameter in a large cohort of patients with OSAS. We found that the prevalence of aortic root dilatation was 3.9% and that the aortic root diameter was not increased in individuals with OSAS.

Determinants of aortic root dilatation

The relation between anthropometric variables and aortic dimensions have been recognized and confirmed in echocardiographic studies of the aortic root [14, 23, 24]. Age-related dilation of the aortic root has been discussed in autopsy series and in clinical studies. Whereas an age-related increase was evident in some studies [14, 22], it was not in others [25]. Generally, aortic root dimensions are smaller in women than in men [14]. Height is suggested to be the most important determinant of aortic root size compared with body surface area or weight [23]. In some studies, correlations with systolic [23] and diastolic [26] blood pressure have been reported whereas in others there were no significant correlations with either systolic or diastolic pressure [14].

Roman et al. [14] reported that two-dimensional echocardiographic aortic root dimensions were influenced by age and body size but not by blood pressure. The authors proposed normograms presenting aortic diameter according to age and body surface area in both children and adults. Vasan et al. [24] showed that age, height, weight, and sex were the principal determinants of aortic root dimensions in the Framingham Heart study, which included 1849 men and 2152 women. Our study confirmed a relation between age, sex, and aortic dilatation but showed that arterial hypertension was not a predictor of aortic root dilatation.

Aortic disease in patients with OSAS

In one study, patients with aortic dissection presented a high prevalence of previously undiagnosed and frequently severe OSAS [10]. A higher mean AHI was found in these patients compared with a control group of hypertensive patients. Arterial hypertension, marked increase in sympathetic activity, and increased transmural pressure of the aorta wall during apnoeas are suggested mechanisms that could explain aortic dissection in OSAS [10]. These mechanisms have been previously described in Marfan’s syndrome, in which a high prevalence of OSAS was detected [27]. OSAS treatment with nasal CPAP was associated with attenuation of aortic root dilatation [28, 29]. This treatment has also been shown to alleviate daytime sleepiness, improve quality of life, decrease the occurrence of new cardiovascular events in patients with coronary artery disease [30], and may reduce cardiovascular morbidity and mortality [31, 32, 33].

PWV and OSAS

PWV is an indicator of arterial stiffness [34, 35]. Nagahama et al. [36] have shown that brachial-ankle PWV was significantly higher in patients with OSAS than in controls even when the degree of risk factors was equal or in the absence of risk factors. Tanriverdi et al. [37] reported that the elastic properties of the aorta were deteriorated in patients with OSAS, characterized by increased aortic stiffness and lower distensibility. Increased aortic stiffness might be responsible for the alteration of left ventricular systolic and diastolic function reported in OSAS syndrome [36]. In our study, mean PWV was 9.8±1.7m/s, and no significant correlation was found between aortic root diameter and PWV.

Limitations

The main limitation of this study was the absence of controls (BMI and age-matched control patients). Moreover, its retrospective design and the absence of follow-up do not allow us to draw definite conclusions. To extend these preliminary results, it is necessary to undertake a case-control study and a longitudinal follow-up to evaluate the determinants of cardiovascular events.

Conclusion

These results suggest that aortic root enlargement is not increased in individuals with OSAS. Aortic root dilatation in patients with OSAS was associated with age and sex, but not with arterial hypertension.

Conflicts of interest

None.

References

Young T., Palta M., Dempsey J., and al. The occurrence of sleep-disordered breathing among middle-aged adults N Engl J Med 1993 ;  328 : 1230-1235 [cross-ref]
Young T., Peppard P.E., Gottlieb D.J. Epidemiology of obstructive sleep apnea: a population health perspective Am J Respir Crit Care Med 2002 ;  165 : 1217-1239 [cross-ref]
Peppard P.E., Young T., Palta M., Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension N Engl J Med 2000 ;  342 : 1378-1384 [cross-ref]
Mooe T., Rabben T., Wiklund U., and al. Sleep-disordered breathing in men with coronary artery disease Chest 1996 ;  109 : 659-663 [cross-ref]
Schafer H., Koehler U., Ewig S., and al. Obstructive sleep apnea as a risk marker in coronary heart disease Cardiology 1999 ;  92 : 79-84 [cross-ref]
Cormican L.J., Williams A. Sleep disordered breathing and its treatment in congestive in heart failure Heart 2005 ;  91 : 1265-1270 [cross-ref]
Laaban J.P., Pascal-Sebaoun S., Bolch E., and al. Left ventricular dysfunction in patients with obstructive sleep apnea Chest 2002 ;  122 : 1133-1138 [cross-ref]
Yaggi Klar, Concato J., Kernan W., and al. Obstructive sleep apnea as a risk factor for stroke and death N Engl J Med 2005 ;  353 : 2034-2041
Phillips C., Hedner J., Berend N., and al. Diurnal and obstructive sleep apnea influences on arterial stiffness and central blood pressure in men Sleep 2005 ;  28 : 604-609 [cross-ref]
Sampol G., Romero O., Salas A., and al. Obstructive sleep apnea and thoracic aortic dissection Am J Resp Crit Care Med 2003 ;  168 : 1528-1531 [cross-ref]
Mansia G, De Backer G, Dominiczak A et al.; European Society of Hypertension; European Society of Cardiology 2007 ESH-ESC Guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Blood Press. 2007; 16(3):135-232.
Hanley A.J., Wagenknecht L.E., D’Agostino R.B., Zinman B., Haffner S.M. Identification of subjects with insulin resistance and beta-cell dysfunction using alternative definitions of the metabolic syndrome Diabetes 2003 ;  52 : 2740-2747 [cross-ref]
Sahn D.J., De Maria A., Kisslo J., and al. The committee on M-mode standardization of the American society of echocardiography; recommendations regarding quantification in M-mode echocardiography: results of a survey of echocardiographics measurements Circulation 1978 ;  58 : 1072-1081 [cross-ref]
Roman M.J., Devereux R.B., Kramer-Fox R., and al. Two-dimensional echocardiographic aortic root dimensions in normal children and adults Am J Cardiol 1989 ;  64 : 507-512 [cross-ref]
Zoghbi W.A., Enriquez-Sarano M., Foster E., and al. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography J Am Soc Echocardiogr 2003 ;  16 : 777-802 [inter-ref]
Schiller N.B., Shah P.M., crawford M., and al. Recommendations for quantification of the left ventricle by two-dimensional echocardiography: American Society of Echocardiography by committee on standards, Subcommittee on quantification of two-dimensional Echoacrdiograms J Am Soc Echocardiogr 1989 ;  2 : 358-367 [cross-ref]
Devereux R.B., Alonso D.R., Lutas E.M., and al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings Am J Cardiol 1986 ;  57 : 450-458 [cross-ref]
Berger M., Haimowitz A., Van Tosh A., and al. Quantitative assessment of pulmonary hypertension in patients with tricuspid regurgitation using continuous wave doppler ultrasound J Am Coll Cardiol 1985 ;  6 : 359-365 [cross-ref]
Laurent S., Boutourye P., Asmar E., and al. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients Hypertension 2001 ;  37 : 1236-1241 [cross-ref]
Sleep-related breathing disorders in adults: recommandations for syndrome definition and measurement techniques in clinical research:th ereport of an American Academy of sleep Medicine Task Force. Sleep 1999; 22:667-89.
Meoli A.L., Casey K.R., Clark R.W., and al. Hypopnea in sleep-disordered breathing in adults Sleep 2001 ;  24 : 469-470
Johns M.W. Daytime sleepiness, snoring and obstructive sleep apnea: the Epworth Sleepiness Scale Chest 1993 ;  103 : 30-36 [cross-ref]
Reed C.M., Richey P.A., Pulliam D.A., Somes G.W. Aortic dimensions in tall men and women Am J Cardiol 1993 ;  71 : 608-610 [cross-ref]
Vasan R.S., Larson M.G., Levy D. Determinants of echocardiographic aortic root size. The Framingham Heart Study Circulation 1995 ;  91 : 734-740 [cross-ref]
Valdez R.S., Motta J.A., London E., and al. Evaluation of the echocardiogram as an epidemiologic tool in an asymptomatic population Circulation 1979 ;  60 : 921-929 [cross-ref]
Tell G.S., Rutan G.H., Kronmal R.A., and al. Correlates of blood pressure in community-dwelling older adults Hypertension 1994 ;  23 : 59-67 [cross-ref]
Cistulli P.A., Sullivan C.E. Sleep-disordered breathing in Marfan’s syndrome Am Rev Respir Dis 1993 ;  147 : 645-648 [cross-ref]
Cistulli P., Wilcox I., Jeremy R., and al. Aortic root dilatation in Marfan’s syndrome. A contribution from obstructive sleep apnea? Chest 1997 ;  111 : 1763-1766 [cross-ref]
Verbraecken J., Paelinck B., Willemen M., and al. Aortic root diameter and nasal intermittent positive airway pressure treatment in Marfan’s syndrome Clin Genet 2003 ;  63 : 131 [cross-ref]
Milleron O., Pilliere R., Foucher A., and al. Benefits of obstructive sleep apneoa treatment in coronary artery disease: a long –term follow-up study Eur Heart J 2004 ;  25 : 728-734 [cross-ref]
Partinen M., Jamieson A., Guilleminault C. Long-term outcome for obstructive sleep apnea syndrome patients. Mortality Chest 1988 ;  94 : 1200-1204 [cross-ref]
Marin J.M., Carrizo S.J., Vicente E., and al. Long-term cardiovascular outcomes in men with obstructive sleep apnea-hypopnea syndrome with or without treatment with continuous positive airway presure: an observationnal study Lancet 2005 ;  365 : 1046-1053 [cross-ref]
Doherty L.S., Kiely J.L., Swan V., and al. Long-term effects of nasal continuous positive airway pressure therapy on cardiovascular outcomes in sleep apnea syndrome Chest 2005 ;  127 : 2076-2084 [cross-ref]
Lehmann E.D. Clinical value of aortic pulse wave velocity measurement Lancet 1999 ;  164 : 528-529 [cross-ref]
Asmar R., Benetos A., Topouchian J., and al. Assessment of arterial distensibility by automatic pulse wave velocity measurement: validation and clinical applications studies Hypertension 1995 ;  26 : 485-490 [cross-ref]
Nagahama H., Soejima M., Uenomachi H., and al. Pulse wave velocity as an indicator of atherosclerosis in obstructive sleep apnea syndrome Intern Med 2004 ;  43 : 184-188 [cross-ref]
Tanriverdi H., Evrengul H., Kaftan A., and al. Effect of obstructive sleep apnea on aortic elastic parameters – relationship to left ventricular mass and function Circ J 2006 ;  70 : 737-743 [cross-ref]



© 2008  Published by Elsevier Masson SAS.
EM-CONSULTE.COM is registrered at the CNIL, déclaration n° 1286925.
As per the Law relating to information storage and personal integrity, you have the right to oppose (art 26 of that law), access (art 34 of that law) and rectify (art 36 of that law) your personal data. You may thus request that your data, should it be inaccurate, incomplete, unclear, outdated, not be used or stored, be corrected, clarified, updated or deleted.
Personal information regarding our website's visitors, including their identity, is confidential.
The owners of this website hereby guarantee to respect the legal confidentiality conditions, applicable in France, and not to disclose this data to third parties.
Close
Article Outline