Effects of CPAP on right ventricular myocardial performance index in obstructive sleep apnea patients without hypertension
© Dursunoglu et al. 2006
Received: 22 November 2005
Accepted: 06 February 2006
Published: 06 February 2006
Obstructive sleep apnoea (OSA) might cause right ventricular dysfunction and pulmonary hypertension. We aimed to determine the effects of nasal continuous positive airway pressure (CPAP) therapy on right ventricular myocardial performance index (MPI) in OSA patients without hypertension.
49 subjects without hypertension, diabetes mellitus, any cardiac and pulmonary disease had overnight polysomnography and echocardiography. In 18 moderate-severe OSA (apnea-hypopnea index ≥ 15) patients, right ventricular free wall diameter (RVFWD) was measured by M-mode, and right ventricular MPI was calculated as (isovolumic contraction time+ isovolumic relaxation time) / pulmonary ejection time using Doppler at baseline and after 6 months CPAP therapy.
Mean age was 46.5 ± 4.9 year. Patients had high body mass index (BMI: 30.6 ± 4,0 kg/m2), but there was no change in either BMI or blood pressures after 6 months. Right ventricular end-diastolic and end-systolic diameters were in normal limits at baseline, and did not change after CPAP usage. Baseline RVFWD (7.1 ± 2.1 mm) significantly decreased after CPAP therapy (6.2 ± 1.7 mm, p < 0.001). 15 of patients (83%) had right ventricular diastolic dysfunction at baseline, and it was completely improved in 11 of them (73%) by CPAP usage. Right ventricular global dysfunction was shown in 11 patients (61%) with a high MPI (62.2 ± 9.3%) at baseline; and MPI was significantly decreased after CPAP therapy (47.3 ± 8.4%, p < 0.0001), and it was completely corrected in 4 of them (36%).
CPAP therapy significantly decreases RVFWD and improves right ventricular diastolic and global functions (MPI) in OSA patients without hypertension.
The obstructive apneic event is associated with considerable breathing efforts against totally or partially occluded upper airway. Obstructive sleep apnoea (OSA) might lead to cardiovascular complications such as heart failure, left/right ventricular dysfunction, myocardial infarction, arrhythmias, systemic and pulmonary hypertension, that all increase morbidity and mortality [1–10]. Early recognition and appropriate therapy of ventricular dysfunction is advisable to prevent further progression to heart failure and death [11, 12].
During an obstructive apnea, large negative intrathoracic pressures are generated during inspiratory efforts, which increase transmural pressures across the myocardium, thus increasing afterload. An increase in preload and pulmonary congestion may also occur due to increased venous return. The presence of hypoxemia decreases oxygen delivery to the myocardium, which may promote angina and arrhythmias. Also, frequent arousals from sleep lead to increase sympathetic activity. Other responsible mechanisms include impaired vagal activity, increased platelet aggregability, insulin resistance, and endothelial dysfunction with reduced endogenous nitric oxide production . Continuous positive airway pressure (CPAP) is known to maintain upperairway patency during sleep by increasing transmural pressure of upper airways, and treatment of OSA by CPAP improves cardiac function and quality of life [14–17].
Ventricular dysfunction could not be detected clinically, but could just be detected echocardiographically. Myocardial performance index (MPI) reflects both systolic and diastolic functions (global function) of the ventricle [18, 19]. In the presence of ventricular global dysfunction, MPI increases in contrast to ejection fraction (EF) of the ventricle. MPI is reproducible and a simple non-invasive method for the estimation of ventricular global function.
In the present study, we aimed to determine the effects of nasal CPAP after 6 months of therapy on right ventricular MPI in moderate-severe OSA patients without hypertension.
a) Study population
49 subjects admitted to sleep clinic with symptoms of nocturnal snoring and/or excessive day-time sleepiness taken into the study. A detailed sleep and cardiovascular anamnesis of the patients were recorded. Sleep cycle, nutritional status, medications, alcohol usage and family anamnesis were also questioned. Epworth sleepiness scale (ESS)  was questioned to all patients, and patients having high scores (ESS ≥ 10) were taken into the sleep study.
Physical examination was performed to all subjects at baseline and at 6 months. Systolic (SBP) and diastolic (DBP) blood pressures were measured in the sitting position on the right arm using a sphygmomanometer (Erka, Germany), after at least 5 min of rest. Hypertension was identified as blood pressure ≥ 140/90 mmHg or being used antihypertensive drugs. Heart rate per minute (HR) was measured in the sitting position, and body mass index (BMI) of the patients were calculated as weight divided to height square (kg/m2).
Pulmonary function tests (Sensor medics 2400, Netherlands), arterial blood gas analysis (ABL 30, Kopenhagen) were performed to all patients at rest. A 12-leadsurface ECG was taken from every subject, and all of them were in sinus rhythm. Also, all of subjects underwent treadmill exercise test and, the test was normal for each subject.
Symptoms of nocturnal snoring and/or excessive day-time 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, 7- serum electrolytes imbalances.
b) Polysomnography (PSG)
All patients underwent an entire night of diagnostic PSG while breathing room air, followed a second night of PSG with nasal CPAP titration . The portable, limited sleep study performed with the Emblettadevice , consisted of the following: 1) nasal pressure detectorusing nasal cannulae/pressure transducer system, recording thesquare root of pressure as an index of flow; 2) thoraco-abdominalmovement detection through two piezoelectric belts; 3) fingerpulse oximeter; and 4) body position detection.
Apnea was defined as total obstruction of oronasal airflow ≥ 10 seconds, an hypopnea was defined as decrease of airflow at least 50%, and desaturation was accepted as a decrease of ≥ 4% in oxygen saturation . Desaturation index (DI) was identified as number of oxygen desaturation events per hour of sleep. In this study, 21 non-hypertensive subjects with AHI ≥ 15 were diagnosed as moderate-severe OSA .
c) Nasal continuous positive airway pressure (CPAP)
Patients with severe OSA were prescribed nasal CPAP (Remstarplus, Respironics Corporation; Murrysville, Pennsylvania, USA), including use of a heated humidifier. The CPAP machines were equipped with compliance monitors that measured CPAP use, in order to observe CPAP usage/compliance at home. Routine troubleshooting took place in an effort to maximize compliance with nasal CPAP. Patients were considered to be CPAP compliant if they used CPAP an average ≥ 3.5 h per night at the 6-month follow-up.
d) Echocardiographic measurements
Echocardiograms were obtained following the diagnosis of OSA and prior to initiation of CPAP, and at 6 months. All measurements were performed with the subjects in the left lateral decubitus position by M mode, two dimensional (2D), 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 minutes. The ventricular diameters, volumes and functions were measured according to the recommendations of the American Society of Echocardiography . Basic measurements of left/right ventricular dimensions in diastole and systole, thickness of interventricular septum (IVS), left ventricular posterior wall (LVPW) and right ventricular free wall diameter (RVFWD) were measured by M-mode technique.
Early (E) and atrial (A) trans-mitral/tricuspid maximal flow velocities, the ratio (E/A) and deceleration time (DT) of E was registered. Isovolumetric relaxation time (IVRT) was measured by the continuous wave Doppler technique. The velocity of mitral/tricuspid flow propagation (VPR) was estimated using color Doppler M-mode. The left/right ventricular MPI was calculated as (isovolumic contraction time of left/right ventricle + IVRT of left/right ventricle) / (aortic/pulmonary ejection time) by Doppler.
e) Statistical analysis
Measurements are expressed as mean ± SD. A Wilcoxon test for related measurements was used to compare primary outcome variables of both IVS, LVPW, RVFWD and ventricular functions (LVEF, MPI) at baseline and 6 months. Also, Mc Nemar chi-square test was used for comparison of number of obstructive sleep apnea patients without hypertension according to right ventricular hypertrophy and diastolic or global dysfunctions at baseline (before treatment) and after 6 months of CPAP usage. A p value of < 0.05 was regarded as significant.
Baseline characteristics of obstructive sleep apnea patients without hypertension at pre-treatment of continuous positive airway pressure (CPAP).
Mean age yrs
46.5 ± 4.9
Male n, (%)
Female n, (%)
30.6 ± 4,0
120.3 ± 10.1
82.0 ± 4.1
82.4 ± 13.4
AHI per h
50.1 ± 11.6
DI per h
37.8 ± 18.0
73.8 ± 18.9
80.1 ± 2.6
*Sleep duration %
CPAP usage h/night
5.6 ± 1.7
CPAP pressure cmH2O
11.3 ± 2.5
Basic characteristics and left ventricular structure and function indices in overall obstructive sleep apnoea patients before and after 6 months of continuous positive airway pressure (CPAP) treatment.
Overall (n = 18)
BMI kg*m-2 (<30)*
30.6 ± 4,0
31,0 ± 3,5
SBP mmHg (<140)*
120.3 ± 10.1
119,1 ± 10,2
DBP mmHg (<90)*
82.0 ± 4.1
81.2 ± 3,8
Left ventricular structure
Left atrium mm (19–40)*
35.1 ± 3.2
36.0 ± 3.0
IVS thickness mm (6–11)*
10.3 ± 1.1
10,4 ± 1,0
LVPW thickness mm (6–11)*
10.1 ± 0.8
10,0 ± 0,9
LVEDD mm (37–56)*
47.1 ± 4.1
46.1 ± 4.3
LVESD mm (19–40)*
32.2 ± 4.8
31.8 ± 4.7
E/A ratio (>1)*
1.6 ± 0.1
1.6 ± 0.2
IVRT ms (<100)*
80.0 ± 12.0
81.1 ± 12.6
DT ms (<220)*
180.2 ± 16.5
179.5 ± 16.8
VPR cm*s-1 (>55)*
89.2 ± 10.6
88.6 ± 10.3
LVEF % (55–75)*
64.0 ± 4.9
64,1 ± 4,7
MPI % (39 ± 5)*
37.2 ± 6.0
36.8 ± 5.8
Compliance of CPAP
The major reasons for noncompliance were mask discomfort or pressure intolerance. All subjects were offered heated humidity, and efforts were made in all subjects to improve comfort and compliance with therapy. Average CPAP pressure after 6 months of therapy did not change from the initial CPAP pressure that was prescribed (11.3 ± 2.5 cmH2O and 11.0 ± 2,3 cmH2O).
Echocardiographic findings before and after CPAP therapy
Baseline characteristics and left ventricular structure and function indices in OSA patients before and after 6 months of CPAP treatment were shown in table 2. All echocardiographic left ventricular structural (e.g. IVS, LVPW diameters) and functional (e.g. E/A ratio, LVEF and MPI) parameters were in normal limits, and all of them did not significantly change after 6 months of CPAP therapy in OSA patients without hypertension.
Right ventricular structure and function indices in overall obstructive sleep apnoea patients before and after 6 months of continuous positive airway pressure (CPAP) treatment.
Overall (n = 18)
Right atrium mm
23.9 ± 3.0
23.7 ± 3.2
RVFWD mm (5–8)
7.1 ± 2.1
6.2 ± 1.7
RVEDD mm (9–26)
25.4 ± 3.6
25.0 ± 3.3
0.4 ± 0.1
0.6 ± 0.1
0.6 ± 0.13
0.5 ± 0.9
E/A ratio (>1)*
0,7 ± 0.1
1.2 ± 0.2
IVRT ms (<100)*
106.9 ± 24.0
91.1 ± 18.6
DT ms (<220)*
245.5 ± 61.0
210.2 ± 46.8
VPR cm*s-1 (>55)*
41.1 ± 9.9
60.9 ± 10.2
MPI % (39 ± 5)*
62.2 ± 9.3
47.3 ± 8.4
Although patients had right ventricular diastolic dysfunction with an increased mean value of diastolic function parameters such as E/A ratio, IVRT, DT and VPR at baseline; average value of all those parameters significantly decreased by CPAP therapy. Also, right ventricular MPI (62.2 ± 9.3%) was significantly decreased after 6 months of CPAP usage (47.3 ± 8.4%, p < 0.0001), but it did not come to the normal limits, and it still reflected right ventricular global dysfunction (see table 3).
Comparison of number of obstructive sleep apnea patients without hypertension according to right ventricular hypertrophy (RVH) and diastolic or global dysfunctions at baseline (before treatment) and after 6 months of continuous positive airway pressure (CPAP) usage.
Overall (n = 18)
Patients with RVH n (%)
Diastolic dysfunction n (%)
Global dysfuntion n (%)
In our previous studies, we showed right and left ventricular global dysfunctions in OSA patients with an increased MPI [3, 4]. Arterial hypertension, obesity, diabetes mellitus and coronary artery disease which often have coexistince with OSA are independent predictors of ventricular dysfunction. On the other hand, it's well known that OSA might cause cardiovascular complications such as heart failure, myocardial infarction, arryhthmias, systemic and pulmonary hypertension which all increase mortality and morbidity [1–10]. Continuous positive airway pressure is known to maintain upperairway patency during sleep by increasing transmural pressure of upper airways, and treatment of OSA by CPAP improves cardiac function and quality of life [14–17]. In the present study, we aimed to determine the effects of nasal CPAP after 6 months of therapy on right ventricular structure and global function (MPI) in moderate-severe OSA patients without hypertension.
In our study, we excluded systemic hypertension, diabetes mellitus, coronary artery disease and any pulmonary diseases including chronic obstructive pulmonary disease, and there were no significant differences in BMI or BPs after 6 months of therapy. Thus, we assessed the ventricular structure and functions (MPI) in uncomplicated (isolated) OSA patients.
Left ventricular systolic and/or diastolic functions provide prognostic information in the patients. In our study, left ventricular diameters and both systolic and diastolic functions of all subjects were in normal limits and did not significantly change after CPAP therapy. However, right ventricular free wall diameter significantly decreased after CPAP usage. Eleven of 15 patients having diastolic dysfunction (73%) and 4 of 11 patients having right ventricular global dysfunction (36%) completely improved by CPAP therapy.
The relation of OSA to right heart structure and function is controversial. The prevalence of RVH by echocardiography in sleep apnea was ranged from 0 to 71% . In the present study, 3 of 18 patients (17%) had RVH, and it was significantly improved by CPAP usage inspite of any change in the number of patients having RVH. It has been argued that concomitantchronic pulmonary disorders are required for sleep apnea to causeright heart failure [27–31]. However, Sannerand colleagues 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 and colleagues 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 RVH, systolic function, and right ventricular enlargementare not certain. In a study, 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 . Right atrial and ventricular diameters of our patients without hypertension were in normal limits at baseline, and none of them significantly have changed by CPAP usage.
Doherty LS, et all. performed a long-term follow-up study of 168 patients with OSA who had begun receiving CPAP therapy at least 5 years previously, most of whom had been prospectively followed up, having been the subject of an earlier report on cardiovascular risk factors in OSA patients with the average follow-up period 7.5 years . They compared the cardiovascular outcomes of those patients who were intolerant of CPAP (untreated group, 61 patients) with those continuing CPAP therapy (107 patients). Deaths from cardiovascular disease were more common in the untreated group than in the CPAP-treated group during follow-up (14.8% vs 1.9%, respectively; p < 0.009), but no significant differences were found in the development of new cases of hypertension, cardiac disorder, or stroke. Total cardiovascular events (ie, death and new cardiovascular disease combined) were more common in the untreated group than in the CPAP-treated group (31% vs 18%, respectively; p < 0.05). They concluded that their results support a protective effect of CPAP therapy against death from cardiovascular disease in patients with OSA.
Since the systolic and diastolic dysfunction frequently coexist, it was shown that a combined measure of ventricular performance with calculation of MPI might be more reflective of overall cardiac dysfunction than systolic or diastolic measures alone. MPI is a simple and reproducible non-invasive method for diagnosis of ventricular global dysfunction in patients with OSA.
In the present study, a very noticeable finding is the improvement of right ventricular free wall dimension and global dysfunction with a significantly decreased MPI by CPAP therapy, even if 6 months usage.
OSA patients, especially having diastolic dysfunction, is in an increased risk of heart failure, since the systolic and diastolic dysfunction frequently coexist. A combined measure of ventricular performance with the calculation of MPI might be more reflective of overall cardiac dysfunction than systolic or diastolic measures alone. CPAP therapy significantly decreases right ventricular free wall thickness and improves global dysfunction with a significantly decreased MPI even if 6 months of CPAP usage. We consider that much longer-term usage of CPAP therapy may achieve complete improvement of right ventricular global dysfunction in patients with OSA.
Small number of patients in our study population is an important study limitation to determine the effects of CPAP on RVH and right ventricular dysfunction. Also, our sleep clinic population may not reflect the findings in the general community. A larger population of study subjects would be helpful to determine the effects of CPAP on right ventricular structure and function.
- Dursunoglu N, Dursunoglu D: Obstructive sleep apnea syndrome, endothelial dysfunction and coronary atherosclerosis. Tuberk Toraks 2005,53(3):299–306.PubMedGoogle Scholar
- Dursunoglu N, Dursunoglu D: The effects of obstructive sleep apnea hypopnea syndrome on cardiovascular system. Anadolu Kardiyol Derg 2005, 5:41–5.PubMedGoogle Scholar
- Dursunoglu D, Dursunoglu N, Evrengül H, Özkurt S, Kuru Ö, Kılıç M, Fişekçi F: Impact of obstructive sleep apnea on left ventricular mass and global function. Eur Respir J 2005, 26:283–8.View ArticlePubMedGoogle Scholar
- Dursunoglu N, Dursunoglu D, Kılıç M: Impact Of Obstructive Sleep apnea on right ventricular global function: sleep apnea and myocardial performance index. Respiration 2005, 72:278–84.View ArticlePubMedGoogle Scholar
- Dursunoglu N, Dursunoglu D, Özkurt S, Tanriverdi H, Evrengül H, Kiter G: Severe Sleep Apnea Syndrome Diagnosed With Acute Myocardial Infarction. Asian Cardiovasc Thorac Ann 2006, in press.Google Scholar
- Guilleminault C, Connoly S, Winkle RA: Cardiac arrhythmia and conduction disturbances during sleep in 400 patients with sleep apnea syndrome. Am J Cardiol 1983, 52:490–4.View ArticlePubMedGoogle Scholar
- Dursunoglu D, Dursunoglu N, Evrengül H, Özkurt S, Kılıç M, Fişekçi F, Kuru Ö, Delen Ö: QT interval dispersion in obstructive sleep apnea syndrome patients without hypertension. Eur Respir J 2005, 25:677–681.View ArticlePubMedGoogle Scholar
- Hedner J, Ejnell H, Caidahl K: Left ventricular hypertrophy independent of hypertension in patients with obstructive sleep apnea. J Hypertens 1990, 8:941–6.View ArticlePubMedGoogle Scholar
- Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, Jones DW, Materson BJ, Oparil S, Wright JT Jr, Roccella EJ: National Heart, Lung, and Blood Institute Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure and National High Blood Pressure Education Program Coordinating Committee. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003, 289:2560–72.View ArticlePubMedGoogle Scholar
- Peker Y, Hedner J, Norum J, Kraiczi H, Carlson J: Increased Incidence of Cardiovascular Disease in Middle-aged Men with Obstructive Sleep Apnea: A 7-Year Follow-up. Am J Respir Crit Care Med 2002, 166:159–165.View ArticlePubMedGoogle Scholar
- Bonow RO, Udelson JE: Left ventricular diastolic dysfunction as a cause of congestive heart failure. Mechanisms and management. Ann Intern Med 1992, 117:502–10.View ArticlePubMedGoogle Scholar
- Petrie MC, Caruana L, Berry C, McMurray JJ: "Diastolic heart failure" or heart failure caused by subtle left ventricular systolic dysfunction? Heart 2002, 87:29–31.View ArticlePubMedPubMed CentralGoogle Scholar
- Naughton MT: The link between obstructive sleep apnea and heart failure: underappreciated opportunity for treatment. Curr Cardiol Rep 2005,7(3):211–5.View ArticlePubMedGoogle Scholar
- Sullivan CE, Issa FG, Berthon-Jones M, Eves L: Reversal of obstructive sleep apnea by continuous positive airway pressure applied through the nares. Lancet 1981, 1:862–865.View ArticlePubMedGoogle Scholar
- Rapoport DM, Sorkin B, Garay SM, Goldring RM: Reversal of "pickwickian syndrome" by long term use of nocturnal airway pressure. N Engl J Med 1982, 307:931–933.View ArticlePubMedGoogle Scholar
- Sanders MH, Moore SE, Eveselage J: CPAP via nasal mask: a treatment for occlusive sleep apnea. Chest 1983, 83:144–145.View ArticlePubMedGoogle Scholar
- Dursunoglu N, Dursunoglu D, Çuhadaroğlu Ç, Kılıçaslan Z: Acute effects of automated CPAP on blood pressure in the patients with sleep apnea and hypertension. Respiration 2005, 72:150–155.View ArticlePubMedGoogle Scholar
- Tei C, Ling LH, Hodge DO, Bailey KR, Oh JK, Rodeheffer RJ, Tajik AJ, Seward JB: New index combined systolic and diastolic myocardial performance: a simple and reproducible measure of cardiac function: a study in normals and dilated cardiomyopathy. J Cardiol 1995, 26:357–66.PubMedGoogle Scholar
- Tei C: New non-invasive index for combined systolic and diastolic function. J Cardiol 1995, 26:396–404.Google Scholar
- Johns MW: A new method for measuring daytime sleepiness. Sleep 1991, 14:540–5.PubMedGoogle Scholar
- Indications for Polysomnography Task Force, American Sleep Disorders Association Standards of Practice Committee. Practice parameters for the indications for polysomnography and related proceduresSleep 1997, 20:406–22.
- Dingli K, Coleman EL, Vennelle M, Finch SP, Wraith PK, Machay TW, Douglas NJ: Evaluation of a portable device for diagnosing the sleep apnoea/hypopnoea syndrome. Eur Respir J 2003, 21:253–9.View ArticlePubMedGoogle Scholar
- American Sleep Disorders Association. The Atlas Task Force, Bonnet M, Carley D, Carskadom M, et al.: EEG arousals: scoring rules and examples. Sleep 1994, 15:173–4.Google Scholar
- American Academy of Sleep Medicine Task Force: Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. Sleep 1999, 22:667–89.Google Scholar
- American Society of Echocardiography Committee on standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms, Schiller NB, Shah PM, Crawford M, et al.: Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr 1989, 2:358–367.View ArticleGoogle Scholar
- Berman EJ, DiBenedetto RJ, Causey DE, Mims T, Conneff M, Goodman LS, Rollings RC: Right ventricular hypertrophy detected by echocardiography in patients with newly diagnosed obstructive sleep apnea. Chest 1991, 100:347–50.View ArticlePubMedGoogle Scholar
- Bradley TD, Rutherford R, Grossman RF, Lue F, Zamel N, Moldofsky H, Phillipson EA: Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome. Am Rev Respir Dis 1985, 131:835–9.PubMedGoogle Scholar
- 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, 138:345–9.View ArticlePubMedGoogle Scholar
- 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, 109:380–6.View ArticlePubMedGoogle Scholar
- Bradley TD: Right and left ventricular functional impairment and sleep apnea. Clin Chest Med 1992, 13:459–79.PubMedGoogle Scholar
- Weiss JW, Remsburg S, Garpestad E, Ringler J, Sparrow D, Parker JA: Hemodynamic consequences of obstructive sleep apnea. Sleep 1996, 19:388–97.PubMedGoogle Scholar
- Sanner BM, Konermann M, Sturm A, Muller HJ, Zidek W: Right ventricular dysfunction in patients with obstructive sleep apnoea syndrome. Eur Respir J 1997, 10:2079–83.View ArticlePubMedGoogle Scholar
- Hanly P, Sasson Z, Zuberi N, Alderson M: Ventricular function in snorers and patients with obstructive sleep apnea. Chest 1992, 102:100–5.View ArticlePubMedGoogle Scholar
- 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, 164:933–8.View ArticlePubMedGoogle Scholar
- Bradley TD, Floras JS: Pathophysiologic and therapeutic implications of sleep apnea in congestive heart failure. J Card Fail 1996, 2:223–240.View ArticlePubMedGoogle Scholar
- Javaheri S: Central sleep apnea-hypopnea syndrome in heart failure: prevalence, impact and treatment. Sleep 1996, 19:229–231.Google Scholar
- Fung JW, Li TST, Choy DKL, Yip GW, Ko FW, Sanderson JE, Hui DS: Severe obstructive sleep apnea is associated with left ventricular diastolic dysfunction. Chest 2002, 121:422–429.View ArticlePubMedGoogle Scholar
- Arabi Y, Morgan BJ, Goodman B, Puleo DS, Xie A, Skatrud JB: Daytime blood pressure elevation after nocturnal hypoxia. J Appl Physiol 1999, 87:689–98.PubMedGoogle Scholar
- Cloward TV, Walker JM, Farney RJ, Anderson JL: Left ventricular hypertrophy is a common echocardiographic abnormality in severe obstructive sleep apnea and reverses with nasal continuous positive airway pressure. Chest 2003,124(2):594–601.View ArticlePubMedGoogle Scholar
- Dimsdale JE, Loredo JS, Profant J: Effect of continuous positive airway pressure on blood pressure: a placebo trial. Hypertension 2000, 35:144–7.View ArticlePubMedGoogle Scholar
- Faccenda JF, Mackay TW, Boon NA, et al.: Randomized placebo-controlled trial of continuous positive airway pressure on blood pressure in the sleep apnea-hypopnea syndrome. Am J Respir Crit Care Med 2002,163(2):344–8.View ArticleGoogle Scholar
- Becker HF, Jerrentrup A, Ploch T, Grote L, Penzel T, Sullivan CE, Peter JH: Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation 2003,107(1):68–73.View ArticlePubMedGoogle Scholar
- Doherty LS, Kiely JL, Swan V, McNicholas WT: Long-term effects of nasal continuous positive airway pressure therapy on cardiovascular outcomes in sleep apnea syndrome. Chest 2005,127(6):2076–84.View ArticlePubMedGoogle Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.