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European Journal of Echocardiography Advance Access published online on October 8, 2008
European Journal of Echocardiography, doi:10.1093/ejechocard/jen257
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Effects of continuous positive airway pressure therapy on left ventricular function assessed by tissue Doppler imaging in patients with obstructive sleep apnoea syndrome

Nihal Akar Bayram1,*, Bulent Ciftci2, Tahir Durmaz1, Telat Keles1, Ekrem Yeter1, Murat Akcay1 and Engin Bozkurt1

1 Department of Cardiology, Ataturk Education and Research Hospital, Bilkent, Ankara, Turkey
2 Ataturk Chest Disease and Chest Surgery Center, Sleep Center, Ankara, Turkey

Received 29 April 2008; accepted after revision 12 September 2008.

* Corresponding author. Tel: +90 312 2912525; fax: +90 312 2912705. E-mail address: drnihkar{at}yahoo.co.uk


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Conclusion
 References
 
Aims: In this study, we aimed to assess left ventricular (LV) systolic and diastolic functions by tissue Doppler imaging (TDI) in patients with obstructive sleep apnoea syndrome (OSAS) and to investigate the effects of 6 month continuous positive airway pressure (CPAP) on LV systolic and diastolic functions.

Methods and results: We studied 28 new diagnosed moderate and severe OSAS patients (apnoea–hypopnoea index >15) and 18 control group. Exclusion criteria were the presence of structural heart disease, pulmonary disease, diabetes mellitus, dyslipidaemia, alcoholism, neuromuscular disease, renal failure, or malignancy. They were not previously considered or treated for OSA and were all free of drugs. Left ventricular lateral and septal wall early myocardial peak velocity (Em), late myocardial peak velocity (Am), Em to Am ratio, myocardial relaxation time (RTm), myocardial systolic wave (Sm) velocity, isovolumic acceleration (IVA), myocardial pre-contraction time (PCTm), contraction time (CTm), and PCTm to CTm ratio were measured. All echocardiographic parameters were calculated 6 months after CPAP therapy. No statistically significant difference was detected between the groups according to age, gender, body mass index, systolic and diastolic blood pressure, heart rate, fasting blood glucose, and serum lipid parameters. Left ventricular systolic parameters, such as LV septal and lateral wall IVA, CTm, and PCTm to CTm ratio, were significantly lower and Sm was similar in patients with the OSAS group compared with the controls. Left ventricular diastolic parameters, such as LV septal and lateral wall Em velocity and Em to Am ratio, were significantly lower; RTm was significantly prolonged; and Am velocity was similar in patients with OSAS compared with the controls. At the end of the treatment, 20 of 28 patients were compliant with CPAP therapy. Left ventricular septal and lateral wall Em velocity, Em to Am ratio, IVA and CTm, and PCTm to CTm increased significantly, PCTm, PCTm to CTm ratio, and RTm decreased significantly after the therapy, whereas Sm velocity and Am velocity did not change after CPAP therapy in compliant patients.

Conclusion: Left ventricular systolic and diastolic dysfunctions were determined in patients with OSAS, and it was demonstrated that LV systolic and diastolic dysfunctions improved with 6 month CPAP therapy.

Keywords: Obstructive sleep apnoea syndrome; Continuous positive airway pressure therapy; Left ventricle function; Tissue Doppler echocardiography


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Conclusion
 References
 
Obstructive sleep apnoea syndrome (OSAS) is a syndrome characterized by repeated episodes of upper respiratory track obstruction episodes during sleep and commonly a decrease in arterial oxygen saturation.1 Obstructive sleep apnoea syndrome is associated with numerous cardiovascular diseases (systemic arterial hypertension, coronary artery disease, congestive heart failure, cardiac arrhythmia, and pulmonary hypertension) and is an independent risk factor for cardiac mortality and morbidity.2–4

The relationship between OSAS and cardiovascular diseases is unclear, but cardiovascular risk can be declared to increase due to recurrent hypoxia, hypercapnia, acidosis, increased sympathetic activity, and impairment of the balance between myocardial oxygen demand and supply during sleep. Even though there is no underlying cardiovascular disease, left ventricular (LV) systolic and diastolic dysfunctions and LV hypertrophy (LVH) have been shown to be associated in patients with OSAS. Left ventricular systolic and diastolic dysfunctions and LVH are among the independent risk factors for morbidity and mortality of cardiovascular disease.5–10 To prevent development of cardiovascular disease, early diagnosis and treatment are recommended before clinical findings of LV dysfunction emerge. Tissue Doppler imaging (TDI) provides quantitative measurements of contraction and relaxation of selected myocardial segments11 and gives important information about the myocardial segment in cardiac diseases and in normal population. Despite conserved global function, TDI provides recognition of myocardial abnormality at an early stage.12,13

Continuous positive airway pressure (CPAP) therapy is the gold standard treatment for patients with obstructive sleep apnoea. Although there are studies in which the effects of CPAP therapy on LV functions were examined by conventional echocardiography,8–10 to our knowledge, there is only one study that evaluated by TDI.14 In that study, only mitral annulus tissue Doppler systolic velocity was evaluated, and no other LV systolic and diastolic parameters were examined by TDI. In our study, we aimed to assess LV systolic and diastolic functions in patients with moderate to severe OSAS, and to examine the effects of 6 month CPAP therapy on LV systolic and diastolic functions.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Conclusion
 References
 
Study population
The study population was recruited among the subjects investigated upon clinical suspicion of OSA in the Sleep Disorders Center of the Ataturk Chest Diseases and Chest Surgery Research and Training Hospital (Ankara, Turkey). The subjects with any of the followings were excluded: structural heart disease, pulmonary disease, diabetes mellitus, dyslipidaemia, alcoholism, neuromuscular disease, renal failure, or malignancy. They were not previously considered or treated for OSA and were all free of drugs. Subjects with total sleep time shorter than 240 min and those with signs of central sleep apnoea on polysomnography (PSG) recordings were not included.

The Ethics Committee of the local hospital approved the study protocol and informed consent was obtained from patients and controls.

Sleep study
All patients underwent a standard full night PSG, performed in a quiet, partially sound-proofed room with stable humidity and temperature. Polysomnography was performed with a computerized system (Compumedics® Voyager Digital Imaging E-series system, Melbourne, Victoria, Australia) and included the following variables: four electroencephalogram channels, two electro-oculograms, bipolar surface electromyograms of the submentalis, and bilateral anterior tibialis muscles and position sensors to record body position and movements. Respiratory monitoring consisted of nasal and oral airflow measures (oro-nasal cannula), tracheal microphone, thoracic and abdominal respiratory effort (Piezo belts), finger pulse oximetry, and an electrocardiogram as well as simultaneous video recording. Sleep stages were scored according to the standard criteria of American Academy of Sleep Medicine.15 Apnoea was defined as complete cessation of oro-nasal air flow for at least 10 s. Hypopnoea was defined as at least 50% reduction in airflow accompanied by ≥3% desaturation in the preceding 30 s and a reduction in chest wall movement and/or arousal. Arousal was defined as waking up while sleeping or to pass to a more superficial sleep phase. Apnoea–hypopnoea index (AHI) referred to the average number of apnoeas and hypopnoeas per sleep hour. Subjects with AHI <5–h were defined as OSA negative and included in the study as controls. The patients with AHI ≥15–h were regarded as OSA fulfilling the criteria for CPAP treatment.

Polysomnography recordings were repeated at the first night on CPAP treatment by auto-titrating CPAP devices (S8®, ResMed Ltd, Sydney, Australia or Respironics REMstar®, Plus M Series w/C-flexTM Respironics, Inc., Murrysville, PA, USA) according to the clinical routines with a nasal or full-face mask and humidifier by trained staff. All patients assigned to CPAP were instructed to use CPAP at home every night for at least 4 h, contacted by telephone after 1 week, and given a check-up in the clinic after 1, 3, and 6 months, respectively. Patients were considered to be CPAP compliant, if they used the CPAP (downloaded from CPAP system) for an average of 4 h or more per night and 5 days or more per week.16

Echocardiography
The patients underwent a standard two-dimensional and Doppler echocardiographic examinations using 2.5–3.5 MHz transducer interfaced to an echocardiographic imaging system (Vingmed System 7; Vivid 7 Pro; Horten, Norway). All measurements were performed with the subjects in the left lateral decubitus positing, according to the recommendations of American Society of Echocardiography.17 Three consecutive cycles were averaged for every parameter.

Left ventricular end-diastolic diameter (millimetre), LV end-systolic diameter (millimetre), interventricular septum diameter (IVSd; millimetre) at end-diastole, and posterior wall diameter (PWd; millimetre) at end-diastole were measured with the M Mode echocardiography. Left ventricular ejection fraction was calculated as (diastolic volume–systolic volume)/(diastolic volume) with Simpson's method.

The transmitral flow velocities were performed in the apical four-chamber view using pulsed Doppler echocardiography with the sample volume sited at the tip of mitral leaflet. The peak early diastole (E; metre per second) and late diastole (A; metre per second) transmitral flow velocities, deceleration time of E (DT; milliseconds), and isovolumetric relaxation time (IVRT; milliseconds) were measured. Pulsed Doppler study of LV outflow was obtained by placing the sample just below the aortic valve in the five-chamber apical view. Ejection period (EP; milliseconds; between onset and cessation of the LV outflow) and pre-ejection period (PEP; milliseconds; from the onset of electrocardiogram QRS to the beginning of EP) were calculated.

For the acquisition of tissue Doppler velocities, LV images were obtained from apical four-chamber view, and a 3 mm pulsed Doppler sample volume was placed at the level of septal mitral annulus and lateral mitral annulus. The peak systolic velocity (Sm; centimetre per second), early diastolic myocardial peak velocity (Em; centimetre per second), late diastolic myocardial peak velocity (Am; centimetre per second), isovolumic acceleration (IVA; meter per second squared; precedes Sm and was calculated by dividing myocardial peak velocity during isovolumic contraction by the time interval from the onset of this wave to the time at peak velocity), myocardial pre-contraction time (PCTm; milliseconds; time interval between the onset of electrocardiograms QRS and onset of Sm), myocardial contraction time (CTm; milliseconds; between onset and cessation of the Sm), and myocardial relaxation time (RTm; milliseconds; from the end of Sm to the onset of Em) were calculated.

Sm velocity, PCTm, PCTm/CTm, IVA, PEP, and PEP/EP were classified as LV systolic function parameters. E velocity, A velocity, DT, IVRT, E to A ratio, Em velocity, Am velocity, E to Em ratio, and RTm were determined as parameters of LV diastolic function.

All measurements were assessed by two independent cardiologists blinded to the sleep recordings of the subjects and the average values were taken.

Statistical analysis
All analyses were performed using a SPSS 13.0 packet program (SPSS Inc., Chicago, IL, USA). Descriptive statistics were provided for the numeric and categorical variables using mean, median, range, standard deviation, and per cent distributions where necessary. Two group differences were analysed using Student's t-test or Mann–Whitney U-test for normal and non-normal distributed continuous variables. For two paired comparisons of continuous variables, paired sample t-test was used when normally distributed; otherwise, Wilcoxon test was used. Categorical variables were analysed using crosstab statistics, especially {chi}2 tests and for 2 x 2 tables Fisher's test. Correlations were analysed using the Pearson or Spearman rank correlation test. A P-value of <0.05 was used as the cut-off for statistical significance.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Conclusion
 References
 
Baseline characteristics of the patients with OSAS and controls were listed in Table 1. There were no significant differences regarding age, body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate, fasting glucose levels, total cholesterol, low-density lipoprotein (LDL)-cholesterol, high-density lipoprotein (HDL)-cholesterol, and triglyceride.


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  		Table 1 Clinical characteristics of the patients with the OSAS and control groups

 
The results of baseline echocardiographic examination are shown in Table 2. In patients with OSAS, IVSd, and PWd were larger; DT, PEP, IVRT were significantly prolonged; EP and PEP to EP ratio were significantly lower; LV septal and lateral wall IVA, Em, Em to Am ratio, CTm, and PCTm to CTm ratio were lower; and PCTm and RTm were longer than controls. No significant differences were detected between the groups for EF, mitral E and A velocities, Sml, Sms, Aml, and Ams values.


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  		Table 2 Left ventricle echocardiographic measurements of patients with obstructive sleep apnoea syndrome and the control group

 
Correlation analysis showed that AHI was found to increase parallel to severity of LV dysfunction. Significant negative correlations were found between AHI and Eml velocity (r = –55, P < 0.001), Ems velocity (r = –0.56, P < 0.001), Eml to Aml ratio (r = –0.63, P < 0.001), Ems to Ams ratio (r = –0.58, P < 0.001), IVAl (r = –0.45, P = 0.000), IVAs (r = –0.43, P = 0.003), CTml (r = –0.59, P < 0.001), and CTms (r = –0.59, P < 0.001), but there were no correlations between AHI and Aml, Ams, Sml, Sms velocities, PCTml, and PCTms (P > 0.05).

At the end of the study, 20 OSA patients were found to be compliant and 8 OSA patients were non-compliant with CPAP therapy. Compliant patients used CPAP for a mean of 6.4 ± 2.2 h per night and their mean CPAP pressure was 10.9 ± 2.8 cm H2O. Non-compliant patients used CPAP for a mean of 2.1 ± 0.9 h per night and their mean CPAP pressure was 8.4 ± 2.9 cm H2O. With CPAP treatment, a decrease in AHI levels (62.3 ± 21.6 vs. 3.3 ± 1.8; P = <0.001), an increase in mean and lowest arterial oxygen saturations, and a decrease in the duration of oxygen saturation below 90% were seen in patients with OSAS (Table 3).


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  		Table 3 Changes in polysomnographic data of the compliant patients with obstructive sleep apnoea syndrome after 6 month continuous positive airway pressure treatment

 
In compliant patients, thickness of IVSd and PWd, DT, PEP to EP ratio, IVRT, lateral and septal wall PCTm, PCTm to CTm ratio, and RTm at baseline were significantly decreased, whereas E to A ratio, EP, IVAml, IVAms, Eml, Ems, Eml to Aml ratio, Ems to Ams ratio, CTml, and CTms were significantly increased after 6 month CPAP therapy. Ejection fraction, E and A velocities, PEP, and lateral and septal wall Sm and Am velocities were similar before and after CPAP therapy (Table 4).


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  		Table 4 Effects of 6 month continuous positive airway pressure treatment on left ventricle echocardiographic parameters in compliant patients with obstructive sleep apnoea syndrome

 
Changes in baseline LV echocardiographic parameters in non-compliant patients with OSAS are shown in Table 5. Left ventricular echocardiographic parameters did not change in non-compliant patients with OSAS in the 6th month control.


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  		Table 5 Effects of 6 month continuous positive airway pressure treatment on left ventricle echocardiographic parameters in non-compliant patients with obstructive sleep apnoea syndrome

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Conclusion
 References
 
Cardiovascular complications are the most serious complications of patients with OSAS. These complications include hypertension, coronary artery disease, cardiac failure, left/right ventricular dysfunction, cardiac arrhythmia, and pulmonary hypertension.2–4 Although the mechanism of impairment in myocardial contraction and relaxation seen in patients with OSAS has not been fully understood, OSAS may increase cardiac risk due to impairment of relation between myocardial oxygen demand and supply as a result of hypoxia, hypercapnia, increased sympathetic activation occurring during apnoea and oxygen desaturation associated with apnoea triggered by myocardial ischaemia at night.18,19

Obstructive sleep apnoea syndrome contributes to development of LVH, and as severity of OSAS increases the incidence of LVH increases.20,21 Left ventricular hypertrophy is one of the independent risk factors for development of morbidity and mortality from cardiovascular disease.22,23 Diseases, such as hypertension, obesity, and diabetes mellitus, which often accompany OSAS, also contribute to development of LVH.24,25 In the study by Hedner et al.,20 LVH was seen more in 61 male patients with OSAS than in the control group. In this study, 50% of the patients had hypertension, and when the normotensive group was evaluated, LVH incidence in normotensive patients with OSAS was found 15% higher than normotensive control group. In our study, IVSd and PWd in patients with OSAS were significantly thicker than the control group, and no other cardiovascular disease was accompanying with the study group.

Left ventricular diastolic dysfunction leads to development of LV systolic dysfunction, and accounts for 30–40% of LV failure, alone.26,27 In a study by Dursunoglu et al.,10 in which LV diastolic functions were assessed in patients with OSAS, although LVEF was conserved in patients with moderate–severe OSAS, it was found that there were LV diastolic dysfunction and LV global dysfunction. To prevent progress to heart failure and death, early diagnosis and treatment of LV diastolic dysfunction is recommended. Before the clinical signs of LV dysfunction appear, it is difficult to detect the changes occurring in the heart with conventional two-dimensional echocardiography. Tissue Doppler imaging provides quantitative measurements of contraction and relaxation of selected myocardial segments.11,12 Tissue Doppler imaging gives important information about the myocardial segment in normal people and cardiac diseases. Diastolic filling patterns measured by conventional echocardiography are affected by preload and afterload. On the contrary, with analyses of signals with high amplitude and low frequency, TDI measures wall motion velocities relatively irrespective of volume.12,13 There are studies comparing TDI findings of patients with OSAS with the control group. In the study by Kasikcioglu et al.28 in patients with OSAS who had normal LV functions, septal Sm and Em velocities, and Em/Am ratio were found lower than the control group, and myocardial abnormality was detected at an early stage. Otto et al.29 evaluated LV functions conserved obese patients with and without OSAS, and demonstrated that LV diastolic function impaired in patients with OSAS. In our study, in patients with OSAS, among the diastolic parameters, Em velocity of LV septal and lateral wall and Em/Am ratio were found low; RTm long, and Am velocities were detected similar; among the systolic parameters, septal and lateral wall IVA, CTm, and PCTm to CTm ratio were found significantly low; and Sm velocities were found similar.

Continuous positive airway pressure therapy is the gold standard treatment for patients with obstructive sleep apnoea. By increasing transmural pressure of upper respiratory tract, CPAP therapy maintains upper respiratory tract flow during sleep. AHI and arousal diminish, oxygen saturation normalizes, excessive platelet activation decreases, sympathetic activity reduces, and myocardial oxygen transport improves and LV transmural pressure and afterload decrease.30–32

There are studies of conventional echocardiography, which examined effects of CPAP therapy on LV functions. Cloward et al.8 found in their study that LVH regressed with 6 month CPAP therapy in 25 patients with severe OSAS. Arias et al. demonstrated that there was an increase in E/A ratio and a decrease in DT and IVRT among the diastolic parameters with a 12 week CPAP therapy in patients with OSAS without another concomitant disease. Yet similarly, in another study, in which the effects of 6 month CPAP therapy was examined,33 an increase in E/A ratio and a decrease in DT and IVRT were seen with compliant CPAP therapy.

To date, there is only one study that evaluated the effects of CPAP therapy on LV functions in patients with OSAS by TDI, and in that study,14 the group with severe OSAS and without concomitant cardiac disease and pulmonary disease was compared with the control group, and LV functions were re-evaluated after 6 month CPAP therapy. Only mitral Sm velocity was examined by TDI. It was shown that mitral Sm velocity in patients with OSAS was low, and that it increased with 6 month OSAS therapy. In our study, we aimed to assess LV systolic and diastolic functions in patients with moderate to severe OSAS, and to examine the effects of 6 month CPAP therapy on LV systolic and diastolic functions. In this study, blood pressures, resting heart rates, and BMI in patients with OSAS were higher than the control group, whereas in our study, there was no difference in blood pressure, heart rate, and BMI between the OSAS and the control groups. Distinctly in our study, LV lateral and septal wall Sm velocities were similar, and no changes were detected after CPAP therapy. Furthermore, IVA, one of the parameters of LV systolic function, which was not previously evaluated in patients with OSAS, was examined in our study. Isovolumic acceleration was detected low in patients with OSAS, and was observed to increase with CPAP therapy. Isovolumic acceleration is one of the parameters recently used in the assessment of LV contractile functions, is more sensitive than Sm, and is not affected by preload and afterload.34,35 Emergence of LV dysfunction is a long process, and impairment is seen in distinct parameters in different stages. Isovolumic acceleration seems to be one of the parameters that can be used in early detection of LV systolic dysfunction. In our study, the effects of CPAP therapy on LV diastolic functions were also evaluated by TDI, and an increase in LV septal and lateral wall Em velocity and Em/Am ratio and a decrease in RTm were detected.

Study limitations
Number of patients in our study is relatively small, and larger randomized studies are needed.


   Conclusion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
References
 
Consequently, in our study, where LV functions were assessed using TDI, compared with the control group, LV systolic and diastolic dysfunctions were determined in patients with OSAS, and improved LV systolic and diastolic functions were observed with 6 month CPAP therapy. Isovolumic acceleration is considered to be one of the parameters that can be used in early detection of LV systolic dysfunction in patients with OSAS with normal LV functions.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
 References
 

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N. Haruki, M. Takeuchi, H. Nakai, Y. Kanazawa, N. Tsubota, R. Shintome, R. M. Lang, and Y. Otsuji
Overnight sleeping induced daily repetitive left ventricular systolic and diastolic dysfunction in obstructive sleep apnoea: quantitative assessment using tissue Doppler imaging
Eur J Echocardiogr, August 1, 2009; 10(6): 769 - 775.
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