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Continuous Positive Airway Pressure Therapy Reduces Right Ventricular Volume in Patients with Obstructive Sleep Apnea: A Cardiovascular Magnetic Resonance Study

2009; American Academy of Sleep Medicine; Volume: 05; Issue: 02 Linguagem: Inglês

10.5664/jcsm.27437

1550-9397

Ulysses J. Magalang, Kathryn E. Richards, Beth McCarthy, Ahmed Fathala, Meena Khan, Narasimham L. Parinandi, Subha V. Raman,

Congenital Heart Disease Studies

Free AccessCPAPContinuous Positive Airway Pressure Therapy Reduces Right Ventricular Volume in Patients with Obstructive Sleep Apnea: A Cardiovascular Magnetic Resonance Study Ulysses J. Magalang, M.D., Kathryn Richards, B.A., Beth McCarthy, R.T., Ahmed Fathala, M.D., Meena Khan, M.D., Narasimham Parinandi, Ph.D., Subha V. Raman, M.D., M.S.E.E. Ulysses J. Magalang, M.D. Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio , Kathryn Richards, B.A. Division of Cardiovascular Medicine , Beth McCarthy, R.T. Division of Cardiovascular Medicine Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio , Ahmed Fathala, M.D. Division of Cardiovascular Medicine Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio , Meena Khan, M.D. Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine , Narasimham Parinandi, Ph.D. Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio , Subha V. Raman, M.D., M.S.E.E. Address correspondence to: Subha V. Raman, MD, MSEE, Associate Professor of Internal Medicine, Division of Cardiovascular Medicine, The Ohio State University, 473 W. 12th Ave, Suite 200, Columbus, OH 43210614 293-8963 E-mail Address: [email protected] Division of Cardiovascular Medicine Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio Published Online:April 15, 2009https://doi.org/10.5664/jcsm.27437Cited by:19SectionsAbstractPDF ShareShare onFacebookTwitterLinkedInRedditEmail ToolsAdd to favoritesDownload CitationsTrack Citations AboutABSTRACTStudy Objectives.There are few data on the effects of continuous positive airway pressure (CPAP) therapy on the structural and functional characteristics of the right heart in patients with obstructive sleep apnea (OSA). We sought to leverage the advantages of cardiac magnetic resonance imaging (CMR) and hypothesized that CPAP treatment would improve right ventricular (RV) function in a group of patients with OSA who were free of other comorbid conditions.Methods.Patients with severe (apnea-hypopnea index ≥ 30/h) untreated OSA were prospectively enrolled. CMR included 3-dimensional measurement of biventricular size and function, and rest/stress myocardial perfusion and was performed at baseline and after 3 months of CPAP therapy.Results.Fifteen patients with mild to moderate desaturation were enrolled; 2 could not undergo CMR due to claustrophobia and obesity. There were significant decreases in the Epworth Sleepiness Scale score (p < 0.0001) and RV end-systolic and RV end-diastolic volumes (p < 0.05) with CPAP. There was a trend toward improvement in RV ejection fraction, but the improvement did not reach statistical significance. Other measures such as left ventricular volumes, left ventricular ejection fraction, myocardial perfusion reserve index, and thickness of the interventricular septum and ventricular free wall did not change significantly.Conclusions:This preliminary study found that CPAP treatment decreases RV volumes in patients with severe OSA who are otherwise healthy. CMR offers a novel technique to determine the effects of CPAP on ventricular structure and function in patients with OSA. A randomized controlled study is needed to confirm the results of our study.Citation:Magalang UJ; Richards K; McCarthy B; Fathala A; Khan M; Parinandi N; Raman SV. Continuous positive airway pressure therapy reduces right ventricular volume in patients with obstructive sleep apnea: a cardiovascular magnetic resonance study. J Clin Sleep Med 2009;5(2):110-114.INTRODUCTIONObstructive sleep apnea (OSA) is associated with increased cardiovascular morbidity and mortality.1–3 Although the exact mechanism for this effect remains unclear, abnormalities of cardiac structure and function have been reported in patients with OSA.4–14 These latter studies have mainly examined the effects of OSA on left ventricular (LV) changes, with both systolic and diastolic dysfunctions reported. Indeed, even in patients with established congestive heart failure, continuous positive airway pressure (CPAP) improves LV systolic function.15,16There are few data on the structural and functional changes of the right heart in patients with OSA and the effects of CPAP therapy on right ventricular (RV) function.7,8,11,14 Most of the studies have employed echocardiography and suggested significant association of the severity of OSA, assessed by the apnea-hypopnea index, to RV dysfunction. One study examined the effects of CPAP treatment on the right heart, and these authors reported improvements in RV tissue Doppler systolic velocity after 6 months of therapy.14 However, the inherent challenges of echocardiography-based imaging of the right ventricle, further compounded by the frequently poor acoustic window in obese patients with OSA, may limit the reproducibility of these findings.The volumetric nature of cardiac magnetic resonance imaging (CMR), which is not affected by body habitus, has made this modality the current gold standard for quantifying ventricular size and function and the preferred modality for precise measurements in clinical trials.17,18 CMR provides an accurate and reproducible measurement of ventricular structure and function by assessment of volumes, ejection fraction, and mass17 and is particularly useful in evaluation of the right heart. Compared with other modalities, the improved precision of CMR reduces the sample size required in clinical studies.19 Furthermore, the superior spatial resolution of CMR affords recognition of subtle subendocardial perfusion abnormalities, not feasible with any other noninvasive modality.20 This is of particular interest, since subclinical atherosclerotic heart disease has been reported in patients with OSA.21 We sought to leverage these advantages of CMR in implementing a comprehensive evaluation of cardiac structure and function and myocardial perfusion reserve in patients with OSA. Specifically, we hypothesized that CPAP treatment will improve RV function even in a group of patients with OSA who were free of other comorbid conditions.METHODS AND MATERIALSPatient PopulationPatients referred for suspicion of OSA were initially evaluated by a sleep disorders specialist (UJM) and included in the study if they met the following inclusion criteria: apnea-hypopnea index greater than 30 by overnight polysomnography and Epworth Sleepiness Scale score greater than 10. The polysomnography methods and definition of respiratory events are described below. These characteristics identify a group of patients with severe OSA who likely would be compliant with CPAP treatment.22 Patients were excluded if they had any the following: known diabetes mellitus, heart failure, or coronary artery disease; use of illicit drugs or excessive alcohol consumption; active smoking; advanced lung disease; use of inhalers; prior treatment with CPAP; or any contraindication to MRI, such as ferromagnetic foreign body, orbital metal, cerebral aneurysm clip, pacemaker, defibrillator, neurostimulator, allergy to gadolinium-based contrast, or severe claustrophobia. Patients with hypertension were included only if their hypertension was well controlled (defined as a systolic blood pressure < 140 mm Hg and diastolic blood pressure < 90 mm Hg) and were on a stable dose of medications for at least a month. Written informed consent was obtained from all the subjects to participate in this Institutional Review Board-approved protocol. Venous blood samples were collected prior to baseline CMR imaging. After baseline CMR examination, all patients initiated CPAP treatment with an objective compliance card embedded in the machine and returned for monthly visits with the sleep disorders specialist for CPAP therapy optimization followed by repeat CMR at 3-month follow-up. The prescribed CPAP pressure was based on a CPAP titration study that eliminated respiratory events and improved oxyhemoglobin saturation during sleep.PolysomnographyAll patients underwent standard diagnostic overnight polysomnography. Airflow was measured by monitoring of nasal pressure via a nasal cannula. Sleep stages were scored in 30-second epochs using standard criteria.23 Each epoch was analyzed for the number of apneas, hypopneas, and electroencephalographic arousals and oxyhemoglobin desaturation. Apnea was defined as the absence of airflow for at least 10 seconds. Hypopnea was defined as a visible reduction in airflow lasting at least 10 seconds associated with at least a 4% decrease in arterial oxyhemoglobin saturation.24 The apnea-hypopnea index was defined as the number of apneas and hypopneas per hour of sleep.Cardiac MRIAll subjects underwent identical CMR examination completed on a 1.5-Tesla clinical magnetic resonance scanner (MAGNETOM Avanto, Siemens Medical Solutions, Inc., Erlangen, Germany) using a 12-element cardiac-phased array coil. The CMR protocol included (1) cine acquisitions in standard planes, including contiguous short-axis slices to measure RV and LV free-wall thickness, end-diastolic volumes, end-systolic volumes, and ejection fractions; (2) first-pass myocardial perfusion imaging during intravenous administration of 140 mcg/kg adenosine using 0.1-mmol/kg gadolinium-DTPA contrast and rest perfusion imaging 15 minutes after stress; and (3) late post-gadolinium acquisitions in standard planes for myocardial scar visualization 5 to 10 minutes after rest perfusion imaging was completed. Standard 12-lead electrocardiography was performed prior to and after each CMR examination.Image AnalysisLV and RV volumes and ejection fractions were computed from short-axis cine images (Figure 1) using standardized semiautomated segmentation software (Argus, Siemens Medical Solutions). Briefly, endocardial contours at end-systole and end-diastole delineated the left and right ventricle in each slice; using the Simpson rule, the volumes from each short-axis slice (area × slice thickness) were summed to obtain ventricular volumes. Ejection fraction was computed as the stroke volume (end-diastolic volume – end-systolic volume) divided by end-diastolic volume. Quantification of myocardial perfusion was performed using semiautomatic delineation of endocardial and epicardial LV borders throughout the phases of first-pass perfusion, with respiratory-motion correction as needed (CMRTools, London, UK). Rest and stress myocardial perfusion slopes were derived using Fermi-fitting of signal intensity versus time and normalized to the LV blood pool slope as well as heart rate. A myocardial perfusion reserve index, calculated for each subject, was defined as the ratio of stress to rest normalized myocardial perfusion slope. Thickness of the interventricular septum was measured at the midventricular level from an end-diastolic long-axis image. All image analysis was performed blinded to subject history.Figure 1 Representative cardiac magnetic resonance imaging (MRI) midventricular short-axis slice in 1 patient with obstructive sleep apnea shown at end diastole (left) and end systole (right). The contours indicate semiautomated delineation of endocardial and epicardial contours around the left ventricular (LV) myocardium and endocardial contours delineating the inner surface of the right ventricular (RV) myocardium. Knowing the areas of these contours and the thickness of the slice allows calculation of the volume in each slice; summing over the slices that cover the heart yields total ventricular volumes.Download FigureStatistical AnalysisAll continuous variables are expressed as mean ± SD. Volumes are reported normalized to body surface area (mL/m2). Stata/SE 8.1 (Stata Corp., College Station, TX) was used for statistical analysis. The Mann-Whitney Rank Sum 2-sample test was used to compare values pre-CPAP and post-CPAP therapy. A p value of less than 0.05 was considered significant.RESULTSFifteen patients aged 27 to 66 years were enrolled; 2 could not complete CMR examination, 1 due to claustrophobia and another due to morbid obesity. The average body mass index was 35.3 ± 7.6 kg/m2. All subjects had severe OSA, with apnea-hypopnea index ranging from 30 to 102 events per hour, associated with mild to moderate oxyhemoglobin desaturations during sleep, with a nadir of 80% ± 6%. Oxyhemoglobin saturation by pulse oximetry during wakefulness was greater than 95% in all patients. Only 5 of the 13 patients (38%) were on antihypertensive medications, and these patients all had good blood-pressure control during the study period. None of the patients had an elevated B-type natriuretic peptide level. Except for 3 patients (34, 36, and 51 pg/mL), all patients had B-type natriuretic peptide levels of less than 30 pg/mL, which is the lower limit of detection in our laboratory. The clinical characteristics are summarized in Table 1 There was no significant change in body weight from baseline to after 3 months of CPAP treatment (baseline: 110.0 ± 21 versus 3-month: 112.0 ± 22.6 kg, p = NS), and no changes in medications occurred during this time period. Patients were compliant with CPAP therapy, with an average use of 5.3 ± 1.6 hours per night (time at effective pressure) throughout the study period. Subjective sleepiness measured by the Epworth Sleepiness Scale score significantly decreased with CPAP treatment (baseline: 15 ± 3 vs 3-month: 6 ± 3, p < 0. 0001).Table 1 Patient Characteristics at BaselinePatients (N = 13)Men (%)9 (69)Age, y48.8 ± 10.8BMI, kg/m235.3 ± 7.6Systolic blood pressure, mm Hg121 ± 12Diastolic blood pressure, mm Hg71 ± 8Epworth Sleepiness Scale score15.0 ± 3.0AHI, events/h60.2 ± 23.7Obstructive apneas, % of total events48.4 ± 27.3Central apneas, % of total events1.9 ± 1.6Hypopneas, % of total events49.7 ± 28.2SpO2 during wakefulness, %97 ± 1SpO2 nadir during sleep, %80 ± 6CT90, min8.3 ± 6.3Fasting blood glucose, mg/dL92 ± 8Total cholesterol, mg/dL 162 ± 37Data are presented as mean ± SD. BMI refers to body mass index; AHI, apnea-hypopnea index, SpO2, oxyhemoglobin saturation by pulse oximetry; CT90, cumulative time with an oxyhemoglobin saturation index below 90% during sleepPatients' RV volumes were significantly reduced with CPAP therapy (Figures 2 and 3): RV end-diastolic volume index decreased from 57.6 ± 11.4 mL/m2 to 47.8 ± 14.4 mL/m2 (p < 0. 05), and RV end-systolic volume index decreased from 30.0 ± 7.7 mL/m2 to 22.2 ± 5.5 mL/m2 (p < 0.05). There was a trend toward improved RV ejection fraction with CPAP therapy that did not achieve statistical significance (47.5% ± 12.1% vs 52.5% ± 8.6%, p = 0.33,Figure 4). There was also no significant change in the RV free-wall thickness (p = 0.53). In this cohort, CPAP did not produce any significant change in LV volumes, ejection fraction, or free-wall thickness. Similarly, myocardial perfusion index did not change significantly (0.94 ± 0.14 vs 0.83 ± 0.63, p = 0.14). No patient with OSA had LV hypertrophy; thickness of the interventricular septum was normal at baseline and did not change significantly at 3-month follow-up (7.9 ± 2.2 mm vs 8.0 ± 2.4 mm, p = NS, Table 2).Figure 2 Right ventricular end-diastolic volume indexed to body surface area (RVEDVI, mL/m2) decreased significantly after 3 months of continuous positive airway pressure (CPAP) treatment (p < 0. 05) in patients with obstructive sleep apnea (OSA). Box plots of the RVEDVI are shown. The lower and upper bars represent the lowest and highest values, respectively; the lower and upper boundaries of the box represent the first and third quartiles, whereas the line within the box represents the median value.Download FigureFigure 3 Right ventricular end-systolic volume indexed to body surface area (RVESVI, mL/m2) decreased significantly after 3 months of continuous positive airway pressure (CPAP) therapy (p < 0. 05) in patients with obstructive sleep apnea (OSA).Download FigureFigure 4 Right ventricular ejection fraction (RVEF, %) shows a trend toward improvement after 3 months of continuous positive airway pressure (CPAP) therapy in patients with obstructive sleep apnea (OSA).Download FigureTable 2 CMR Baseline and Follow-Up MeasurementsBaselineAfter 3 Monthsof CPAPLVEDVI, mL/m254.2 ± 19.550.4 ± 8.1LVESVI, mL/m222.4 ± 9.020.5 ± 3.5">LV free wall, mm8.0 ± 1.18.0 ± 1.1LVEF, %58.5 ± 8.258.9 ± 5.4RVEDVI, mL/m257.6 ± 11.447.8 ± 14.4aRVESVI, mL/m2*30.0 ± 7.722.2 ± 5.5aRVEF, %47.5 ± 12.152.5 ± 8.6RV free wall, mm4.4 ± 1.34.2 ± 1.2IVS, mm7.9 ± 2.28.0 ± 2.4MPRI0.94 ± 0.140.83 ± 0.63Data are presented as mean + SD. CMR refers to cardiac magnetic resonance imaging; CPAP, continuous positive airway pressure; LVEDVI, left ventricular end-diastolic volume index; LVESVI, left ventricular end-systolic volume index; RVEDVI, right ventricular end-diastolic volume index; RVESVI, right ventricular end-systolic volume index; RVEF, right ventricular ejection fraction; RV, right ventricular; interventricular septum; MPRI, myocardial perfusion reserve index.ap < 0. 05 compared with baseline measurements.DISCUSSIONIn a cohort of patients with severe OSA, we found mild improvements in RV volumes and a trend toward improved RV ejection fraction with short-term CPAP treatment. No significant change was seen in LV volumes, LV ejection fraction, myocardial perfusion reserve index, or thickness of the interventricular septum, RV free wall, or LV free wall in this study population. By excluding patients with any history of tobacco use, diabetes, atherosclerotic heart disease, or heart failure, we studied a group of subjects with OSA whose cardiac parameters were close to normal at baseline. Still, we found improvements in RV volumes with CPAP treatment. This suggests that, prior to the development of overt cardiovascular disease and prior to demonstrable LV dysfunction, the right heart is the first to undergo adverse remodeling due to OSA.This is the first study that has utilized CMR in assessing the effects of CPAP on cardiac structure and function. A prior small study involving 5 patients with OSA used CMR, but imaging was not performed after CPAP therapy.25 We have shown that, in our current study of obese subjects, excellent-quality images can be obtained for a precise and comprehensive noninvasive assessment of cardiac structure and function. Prior studies examining the effects of CPAP treatment have uniformly employed echocardiography, with its inherent limitations in obtaining adequate images in predominantly obese subjects. In addition, the CMR also allows assessment of rest and stress myocardial perfusion in the same examination. This, as well as the small sample-size requirement afforded by the higher reproducibility of CMR, would be important in future studies examining the effects of CPAP treatment in patients with OSA with preexisting cardiovascular disease or in patients with OSA who are at increased cardiovascular risk due to diabetes and hypertension.RV remodeling in OSA may result from repetitive nocturnal elevations in pulmonary artery pressure that results in intermittent RV pressure overload26,27 and also by increased sympathetic discharges during apneic episodes.5 CPAP treatment for 3 months has been shown to decrease pulmonary artery systolic pressure.28 Our patients had mild to moderate oxyhemoglobin desaturations during sleep prior to treatment and, despite the absence of clinical symptoms of RV dysfunction, had improvements in their RV volume after a relatively short period of CPAP therapy. We speculate that our findings may, in part, be due to the reduction in sympathetic nervous system activity that is known to occur with CPAP treatment. It is possible that we could have seen more improvements in RV function if our patient population had included subjects with more severe oxyhemoglobin desaturations during sleep prior to treatment.We did not find any significant changes in LV structure and function with CPAP treatment. LV abnormalities have been associated with OSA in some,29 but not all, studies.30,31 Differences in the results of these studies, including ours, may in part be due to the fact that other studied populations may have had more significant hypertension, which is known to adversely affect LV structure and function. We specifically enrolled patients either without hypertension or whose blood pressure was well controlled and had been on a stable dose of medications.Our study has several limitations. Our sample size was relatively small, but we were able to show significant differences in RV end-diastolic volume index and RV end-systolic volume index after 3 months of CPAP therapy. It is not known whether a larger sample size would allow for the noted trend of an increase in RV ejection fraction to be statistically significant. We did not include a group of patients with untreated OSA. Therefore, we cannot totally exclude that unknown confounding factors such as regression to the mean could potentially explain our findings. Given our results, a randomized controlled trial would be appropriate to assess ventricular structure and function using CMR in patients with OSA. Finally, we included only a group of patients without co-existing comorbidities such as atherosclerotic heart disease or LV dysfunction. Further studies are required using CMR to determine the effects of CPAP on ventricular structure and function in patients with OSA with LV dysfunction, atherosclerotic heart disease, or both.In conclusion, patients with severe untreated OSA without cardiovascular disease have shown modest but significant improvements in RV structure after initiation of CPAP therapy. We have shown that, in this group of obese subjects with OSA, high-quality images using CMR can be obtained for a precise and comprehensive noninvasive assessment of cardiac structure and function. Ongoing longer-term follow-up and comparison to patients with OSA with more significant cardiac dysfunction may yield additional insights into the relationship between OSA and cardiovascular disease.ABBREVIATIONSCMRcardiac magnetic resonanceCPAPcontinuous positive airway pressureLVleft ventricleOSAobstructive sleep apneaRVright ventricleDISCLOSURE STATEMENTThis was not an industry supported study. Dr. Raman and Ohio State University have an unrestricted research agreement with Siemens that provided workstations for analysis of the imaging data acquired for this study. Siemens did not sponsor or have any other involvement in the study. The other authors have indicated no financial conflicts of interest.REFERENCES1 Young T, Peppard PE, Gottlieb DJEpidemiology of obstructive sleep apnea: a population health perspectiveAm J Respir Crit Care Med2002165121739, 11991871 CrossrefGoogle Scholar2 Shahar E, Whitney CW, Redline S, et al.Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health StudyAm J Respir Crit Care Med20011631925, 11208620 CrossrefGoogle Scholar3 Marin JM, Carrizo SJ, Vicente E, et al.Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational studyLancet2005365104653, 15781100 CrossrefGoogle Scholar4 Alchanatis M, Paradellis G, Pini H, et al.Left ventricular function in patients with obstructive sleep apnoea syndrome before and after treatment with nasal continuous positive airway pressureRespiration20006736771, 10940788 CrossrefGoogle Scholar5 Arias MA, Garcia-Rio F, Alonso-Fernandez A, et al.Obstructive sleep apnea syndrome affects left ventricular diastolic function: effects of nasal continuous positive airway pressure in menCirculation200511237583, 16009798 CrossrefGoogle Scholar6 Dursunoglu N, Dursunoglu D, Kilic MImpact of obstructive sleep apnea on right ventricular global function: sleep apnea and myocardial performance indexRespiration20057227884, 15942297 CrossrefGoogle Scholar7 Dursunoglu N, Dursunoglu D, Ozkurt S, et al.Effects of CPAP on right ventricular myocardial performance index in obstructive sleep apnea patients without hypertensionRespir Res2006722, 16460564 CrossrefGoogle Scholar8 Dursunoglu N, Dursunoglu D, Ozkurt S, et al.Effects of CPAP on left ventricular structure and myocardial performance index in male patients with obstructive sleep apnoeaSleep Med20078519, 17023210 CrossrefGoogle Scholar9 Fung JW, Li TS, Choy DK, et al.Severe obstructive sleep apnea is associated with left ventricular diastolic dysfunctionChest20021214229, 11834652 CrossrefGoogle Scholar10 Noda A, Okada T, Yasuma F, et al.Cardiac hypertrophy in obstructive sleep apnea syndromeChest1995107153844, 7781343 CrossrefGoogle Scholar11 Romero-Corral A, Somers VK, Pellikka PA, et al.Decreased Right and Left Ventricular Myocardial Performance in Obstructive Sleep ApneaChest2007132186370, 17908706 CrossrefGoogle Scholar12 Otto ME, Belohlavek M, Romero-Corral A, et al.Comparison of cardiac structural and functional changes in obese otherwise healthy adults with versus without obstructive sleep apneaAm J Cardiol20079912981302, 17478161 CrossrefGoogle Scholar13 Sanner BM, Konermann M, Sturm A, et al.Right ventricular dysfunction in patients with obstructive sleep apnoea syndromeEur Respir J199710207983, 9311506 CrossrefGoogle Scholar14 Shivalkar B, Van de Heyning C, Kerremans M, et al.Obstructive sleep apnea syndrome: more insights on structural and functional cardiac alterations, and the effects of treatment with continuous positive airway pressureJ Am Coll Cardiol20064714339, 16580533 CrossrefGoogle Scholar15 Kaneko Y, Floras JS, Usui K, et al.Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apneaN Engl J Med2003348123341, 12660387 CrossrefGoogle Scholar16 Mansfield DR, Gollogly NC, Kaye DM, et al.Controlled trial of continuous positive airway pressure in obstructive sleep apnea and heart failureAm J Respir Crit Care Med20041693616, 14597482 CrossrefGoogle Scholar17 Grothues F, Smith GC, Moon JC, et al.Comparison of interstudy reproducibility of cardiovascular magnetic resonance with two-dimensional echocardiography in normal subjects and in patients with heart failure or left ventricular hypertrophyAm J Cardiol2002902934, 12088775 CrossrefGoogle Scholar18 Grothues F, Moon JC, Bellenger NG, et al.Interstudy reproducibility of right ventricular volumes, function, and mass with cardiovascular magnetic resonanceAm Heart J200414721823, 14760316 CrossrefGoogle Scholar19 Bellenger NG, Davies LC, Francis JM, et al.Reduction in sample size for studies of remodeling in heart failure by the use of cardiovascular magnetic resonanceJ Cardiovasc Magn Reson200022718, 11545126 CrossrefGoogle Scholar20 Panting JR, Gatehouse PD, Yang GZ, et al.Abnormal subendocardial perfusion in cardiac syndrome X detected by cardiovascular magnetic resonance imagingN Engl J Med200234619481953, 12075055 CrossrefGoogle Scholar21 Sorajja D, Gami AS, Somers VK, et al.Independent association between obstructive sleep apnea and subclinical coronary artery diseaseChest200813392733, 18263678 CrossrefGoogle Scholar22 Weaver TEAdherence to positive airway pressure therapyCurr Opin Pulm Med20061240913, 17053489 CrossrefGoogle Scholar23 Rechtschaffen A, Kales AUniversity of California Los Angeles. 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CPAP increases exercise tolerance in obese subjects with obstructive sleep apneaPendharkar S, Tsai W, Eves N, Ford G and Davidson W Respiratory Medicine, 10.1016/j.rmed.2011.06.007, Vol. 105, No. 10, (1565-1571), Online publication date: 1-Oct-2011. Volume 05 • Issue 02 • April 15, 2009ISSN (print): 1550-9389ISSN (online): 1550-9397Frequency: Monthly Metrics History Submitted for publicationSeptember 1, 2008Submitted in final revised formNovember 1, 2008Accepted for publicationNovember 1, 2008Published onlineApril 15, 2009 Information© 2009 American Academy of Sleep MedicineKeywordsright ventricleheart function testscontinuous positive airway pressuremagnetic resonance imagingObstructive sleep apneaPDF download