0
Original Research: SLEEP DISORDERS |

Obstructive Sleep ApneaSleep Apnea and Cardiovascular Remodeling: Effects of Continuous Positive Airway Pressure on Cardiac Remodeling as Assessed by Cardiac Biomarkers, Echocardiography, and Cardiac MRI FREE TO VIEW

Jane Colish, BSc; Jonathan R. Walker, MSc; Nader Elmayergi, MD; Saleh Almutairi, MD; Fawaz Alharbi, MD; Matthew Lytwyn, BSc; Andrew Francis, BSc; Sheena Bohonis, BSc; Matthew Zeglinski, BSc; Iain D. C. Kirkpatrick, MD; Sat Sharma, MD, FCCP; Davinder S. Jassal, MD
Author and Funding Information

From the Institute of Cardiovascular Sciences (Mss Colish and Bohonis; Messrs Walker, Lytwyn, Francis, and Zeglinski; and Dr Jassal), St. Boniface General Hospital; Section of Cardiology (Drs Elmayergi and Jassal) and Section of Respiratory Medicine (Drs Almutairi, Alharbi, and Sharma), Department of Internal Medicine; and Department of Radiology (Drs Kirkpatrick and Jassal), University of Manitoba, Winnipeg, MB, Canada.

Correspondence to: Davinder S. Jassal, MD, Rm Y3010, Bergen Cardiac Care Centre, Section of Cardiology, Department of Internal Medicine, St Boniface General Hospital, 409 Taché Ave, Winnipeg, Manitoba R2H 2A6, Canada; e-mail: djassal@sbgh.mb.ca


For editorial comment see page 580

Funding/Support: The present study was supported by the St. Boniface General Hospital and Research Foundation and the Manitoba Medical Services Foundation.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2012 American College of Chest Physicians


Chest. 2012;141(3):674-681. doi:10.1378/chest.11-0615
Text Size: A A A
Published online

Background:  Obstructive sleep apnea (OSA) is associated with an increased risk of cardiovascular morbidity and mortality. Although previous echocardiographic studies have demonstrated short-term improvement in cardiovascular remodeling in patients with OSA receiving continuous positive airway pressure (CPAP) therapy, a long-term study incorporating cardiac biomarkers, echocardiography, and cardiac MRI (CMR) has not been performed to date.

Methods:  A prospective study of 47 patients with OSA was performed between 2007 and 2010. Cardiac biomarkers, including C-reactive protein (CRP), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and troponin T (TnT), were measured at baseline and serially over 1 year. All patients underwent baseline and serial transthoracic echocardiography (TTE) and CMR to assess cardiac remodeling.

Results:  Following 12 months of CPAP therapy, levels of CRP, NT-proBNP, and TnT did not change significantly from normal baseline values. As early as 3 months after initiation of CPAP, TTE revealed an improvement in right ventricular end-diastolic diameter, left atrial volume index, right atrial volume index, and degree of pulmonary hypertension, which continued to improve over 1 year of follow-up. Finally, left ventricular mass, as determined by CMR, decreased from 159 ± 12 g/m2 to 141 ± 8 g/m2 as early as 6 months into CPAP therapy and continued to improve until completion of the study at 1 year.

Conclusion:  Both systolic and diastolic abnormalities in patients with OSA can be reversed as early as 3 months into CPAP therapy, with progressive improvement in cardiovascular remodeling over 1 year as assessed by both TTE and CMR.

Figures in this Article

Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder that affects 2% to 10% of the general North American population and is associated with an increased risk of cardiovascular morbidity and mortality.1 OSA is associated with an increased risk of atrial fibrillation,2 coronary artery disease,3 congestive heart failure,4 cerebrovascular disease,5 and increased risk of sudden cardiac death during sleep.6 In addition to left ventricular hypertrophy (LVH), both systolic and diastolic dysfunction have been observed in patients with OSA.79

Continuous positive airway pressure (CPAP) is used as the primary treatment modality for patients with OSA.10 There is a correlation between regular CPAP use and a reduction in cardiovascular morbidity in patients with preexisting heart failure.1 Improvements in cardiovascular function have been identified as a decrease in BP,1 an increase in LV ejection fraction (LVEF),11,12 and a decrease in LVH7 as assessed primarily by transthoracic echocardiography (TTE). Little is known, however, about the use of serial cardiac MRI (CMR) for the delineation of both LV and right ventricular (RV) remodeling in patients with OSA receiving regular CPAP therapy over the long term.13,14

In addition to noninvasive imaging, serum levels of C-reactive protein (CRP), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and troponin T (TnT) have been evaluated previously in the setting of OSA.1520 There are conflicting results on whether CPAP therapy has any impact on biomarker levels in patients with OSA.1522 Little is known, however, on the effects of CPAP therapy on these cardiac biomarkers over 1-year follow-up. The objective of the present study was to determine using cardiac biomarkers, echocardiography, and CMR the long-term benefits of CPAP use on both RV and LV systolic and diastolic function in patients with OSA.

A prospective study of 52 consecutive patients who fulfilled eligibility criteria was performed at two tertiary-care centers between 2007 and 2010. Study subjects were recruited and written informed consent obtained after a diagnosis of OSA was made based on an overnight polysomnographic examination (PSG). CPAP-naive patients who had received a new diagnosis of OSA (apnea-hypopnea index [AHI] > 15/h) and who were determined to experience excessive daytime sleepiness as indicated by a score > 10 on the Epworth Sleepiness Scale were included.23 Patients with LV systolic dysfunction (LVEF < 50%), who refused CPAP therapy or who had used CPAP in the past were excluded. Additionally, patients with hypertension (> 140/90 mm Hg), atrial fibrillation, moderate to severe valvular heart disease, coronary artery disease, previous cardiac surgery, or any contraindication to CMR were excluded from the study. Five patients with OSA had a baseline LVEF < 50% on echocardiography and were excluded from the study. The final patient cohort consisted of 47 patients with OSA. The study protocol was approved by the University of Manitoba research ethics board (B2007:091).

Overnight PSG was performed in the sleep laboratory using standard recording techniques. Briefly, all study participants underwent either 2 consecutive nights or a split-night PSG using the Sandman NT system (Nellcor Puritan Bennett Ltd). PSG consisted of the following variables: EEG; electrooculogram; submental electromyogram; ECG; oxygen saturation monitoring (N200; Nellcor Puritan Bennett Ltd); chest, abdominal wall, and sum channel movements using respiratory inductance plethysmography; bilateral tibial electromyograms; nasal/oral airflow using a thermistor device (Edentec Corporation); nasal pressure (Ultima Airflow Pressure Sensor Model 0580; Braebon Medical Corporation); end-tidal carbon dioxide monitoring (Model 1265; Novametrix Medical Systems); and transcutaneous carbon dioxide monitoring (Radiometer Medical ApS). Sleep stages were scored according to the standard criteria of the American Academy of Sleep Medicine.24 AHI was defined as the number of apnea and hypopnea events per hour of sleep.25 The CPAP machines were equipped with compliance monitors that measured CPAP use. Adequate compliance to the prescribed pressure of CPAP was defined as > 4.5 h of CPAP use per night on a routine basis.26

In total, the patient population was evaluated at four separate time points: (1) before the initiation of CPAP for a new diagnosis of OSA, (2) 3 months, (3) 6 months, and (4) 12 months after the initiation of CPAP. At each visit, blood was drawn to measure TnT, CRP, and NT-proBNP levels, and a standard TTE was performed. The patients underwent a CMR at baseline and 6 and 12 months after the initiation of CPAP treatment.

CRP, NT-proBNP, and TnT levels were evaluated at four separate time points. CRP levels were measured using the Image 800 (Beckman Coulter Inc) antigen-antibody precipitant rate reaction. NT-proBNP levels were measured with an electrochemiluminescence sandwich immunoassay (Elecsys ProBNP; Roche Diagnostics Inc) using the Roche 2010 system. Quantitative determination of TnT levels was performed using a third-generation Roche Elecsys assay.

Serial TTE with tissue velocity imaging was performed on a GE Vivid 7 platform (GE Healthcare Inc). Cardiac dimensions and systolic function were determined from 2-dimensional images according to established criteria.27,28 The peak early and late diastolic variables, early/late diastolic ratio, and deceleration time were manually traced using the transmitral LV filling signal. Tissue Doppler echocardiography-derived indices were recorded at the base of the lateral and septal mitral annuli to determine longitudinal endocardial velocities. Continuous-wave Doppler echocardiography was used to measure the peak velocity across the tricuspid valve, and the maximal RV systolic pressure (RVSP) was estimated using the simplified Bernoulli equation.

Serial CMR was performed using a 1.5-T scanner (Avanto; Siemens Healthcare) at baseline and 6 and 12 months of follow-up. Cine bright-blood images in the four-chamber long-axis and two-chamber long-axis planes were performed using a breath hold-balanced steady-state free-precession sequence. LV mass was calculated by the summation of slices method whereby the endocardial and epicardial contours were manually traced in each end-diastolic slice and then multiplied by slice thickness to yield the myocardial volume.29 Quantitative analysis was performed using dedicated computer software (CMR42 release 3.0.0; Circle Cardiovascular Imaging Inc).

The reproducibility of the cardiac volumes and mass at baseline by TTE and CMR was evaluated by calculating the intraobserver and interobserver variability of both techniques. Intraobserver variability of TTE and CMR measurements were assessed by the primary interpreter (D. J.) in 20 randomly selected patients. A second interpreter (J. W.) assessed interobserver variability in 20 other randomly selected patients. Both interpreters were blinded to the results of the other imaging techniques.

The data were summarized as mean ± SD or percentage. Power analysis was performed to calculate the sample size of 45 patients, with a significance level of .05. The null hypothesis was evaluated with a 1−β probability of 80% to detect a significant difference in CMR-derived LV mass index (LVMI) over time. Repeated measures were analyzed by a two-way analysis of variance (ANOVA), and pairwise comparisons were made only if the ANOVA was significant (SAS version 8.01; SAS Institute Inc). Intraobserver and interobserver variability of the cardiac volumes by each imaging modality, expressed as a percentage, was computed using the coefficient of variability, calculated as the mean of absolute differences between two measurements divided by the average of the two measurements times 100. A P < .05 was considered statistically significant. Statistical analyses were performed with SAS version 9.01 (SAS Institute Inc) and Statistica version 6.1 (StatSoft, Inc) software.

The study population included 47 patients (mean age, 51 ± 10 years; 32 men) (Table 1). At baseline, mean BMI was 38 ± 9 kg/m2, with 22 patients being overweight (BMI, 25-30 kg/m2) and the remaining 25 patients obese (BMI > 30 kg/m2). At 1-year follow-up, the mean BMI was 37 ± 10 kg/m2. All patients had severe OSA, with a mean AHI of 63 ± 30/h and time with an arterial oxygen saturation < 90% of 25.2 ± 10.5 min. At time of enrollment, the mean systolic and diastolic BP were 131 ± 6 mm Hg and 70 ± 9 mm Hg, respectively. At 1-year follow-up, the mean systolic and diastolic BP were 133 ± 7 mm Hg and 68 ± 12 mm Hg, respectively. The Epworth Sleepiness Scale score at baseline was 14 ± 3. All patients were compliant with their CPAP therapy throughout the study period.

Table Graphic Jump Location
Table 1 —Baseline Characteristics of Total Population (N = 47)

Data are presented as mean ± SD or No. (%). AHI = apnea-hypopnea index; ESS = Epworth Sleepiness Scale; O2 = oxygen.

At baseline, the cardiac biomarkers CRP, NT-proBNP, and TnT were within normal limits for the entire population (Table 2). At 3, 6, and 12 months of follow-up, there was no significant change in biomarker levels compared with baseline (Table 2).

Table Graphic Jump Location
Table 2 —Summary of Serial Cardiac Biomarkers of Total Population (N = 47)

Data are presented as mean ± SD, unless otherwise indicated. ANOVA = analysis of variance; CRP = C-reactive protein; NT-proBNP = N-terminal pro-B-type natriuretic peptide; TnT = troponin T.

a 

P < .05 was considered significant vs baseline using repeated-measures ANOVA and Dunnett test.

There were early benefits in cardiovascular remodeling on TTE as early as 3 months into CPAP therapy, which continued to improve up to 1 year (Table 3). The right atrial (RA) volume index decreased from 48 ± 5 mL/m2 to 35 ± 4 mL/m2 (P < .05), and the RV end-diastolic diameter decreased from 41 ± 3 mm to 36 ± 5 mm (P < .05) at 3-month follow-up (Figs 1A, 1B). A decrease also was noted in the peak RVSP over serial follow-up (P < .05). On serial TTE, left atrial volume index (LAVI) decreased from 45 ± 4 mL/m2 to 36 ± 4 mL/m2 at 3-month follow-up. The LAVI continued to improve with CPAP therapy over 1 year of follow-up to 31 ± 3 mL/m2 (Table 3). The mean early diastolic filling/early diastolic annular velocity (E/E′) ratio, a surrogate marker of LV filling pressure, decreased from 16 ± 3 to 8 ± 2 at 12 months (P < .05) (Table 4).

Table Graphic Jump Location
Table 3 —Conventional Echocardiographic Data in Patient Population (N = 47)

Data are presented as mean ± SD. IVS = interventricular septum; LA = left atrial; LAVI = left atrial volume index; LV = left ventricular; LVEDD = left ventricular end-diastolic diameter; LVEDV = left ventricular end-diastolic volume; LVEF = left ventricular ejection fraction; LVESD = left ventricular end-systolic diameter; LVESV = left ventricular end-systolic volume; PWT = posterior wall thickness; RA = right atrial; RAVI = right atrial volume index; RV = right ventricular; RVEDD = right ventricular end-diastolic diameter in parasternal long-axis view; RVSP = right ventricular systolic pressure. See Table 2 legend for expansion of other abbreviation.

a 

P < .05 was considered significant vs baseline using repeated-measures ANOVA and Dunnett test.

Figure Jump LinkFigure 1. A-D, Serial improvement in RAVI (A), RVEDD (B), RVEDVI (C), and LVMI (D) by either transthoracic echocardiography (A, B) or cardiac MRI (C, D) with corresponding number of months of CPAP therapy in the obstructive sleep apnea population. CPAP = continuous positive airway pressure; LVMI = left ventricular mass index; RAVI = right atrial volume index; RVEDD = right ventricular end-diastolic diameter; RVEDVI = right ventricular end-diastolic volume index.Grahic Jump Location
Table Graphic Jump Location
Table 4 —Diastolic Echocardiographic Data in Patient Population (N = 47)

Data are presented as mean ± SD. A = late diastolic filling; A′ = late diastolic annular velocity; DT = deceleration time; E = early diastolic filling; E′ = early diastolic annular velocity; IVRT = isovolumetric relaxation time; S′ = systolic annular velocity; TDI = tissue Doppler echocardiographic imaging. See Table 2 legend for expansion of other abbreviation.

a 

P < .05 was considered significant vs baseline using repeated-measures ANOVA and Dunnett test.

Similar to the TTE data, RA volume index, LAVI, and RV end-diastolic volume index significantly improved over the 1-year follow-up as assessed by CMR (Fig 1C, Table 5). The LV mass decreased from 159 ± 9 g/m2 to 141 ± 8 g/m2 as early as 6 months into CPAP therapy and continued to improve until completion of the study at 1-year follow-up (Fig 1D, Table 5).

Table Graphic Jump Location
Table 5 —CMR Data in Patient Population (N = 47)

Data are presented as mean ± SD. CMR = cardiac MRI; LVEDVI = left ventricular end-diastolic volume index; LVMI = left ventricular mass index; RVEDVI = right ventricular end-diastolic volume index; RVEF = right ventricular ejection fraction; RVMI = right ventricular mass index. See Table 2 and 3 legends for expansion of other abbreviations.

a 

P < .05 was considered significant vs baseline using repeated-measures ANOVA and Dunnett test.

Table 6 shows the results of the intraobserver and interobserver variability of RA, LA, and RV dimensions derived from both techniques of TTE and CMR. CMR allowed for higher reproducibility of cardiac dimensions than did TTE.

Table Graphic Jump Location
Table 6 —Intraobserver and Interobserver Variability of Cardiac Dimensions in the Patient Population (N = 47)

CV = coefficient of variability; TTE = transthoracic echocardiography. See Table 3 and 5 legends for expansion of other abbreviations.

OSA is associated with adverse structural and functional cardiac abnormalities that may lead to increased patient morbidity and mortality.12 In the current study, we confirmed positive cardiac remodeling over the long term using both TTE and CMR in patients with OSA receiving CPAP therapy. Our study demonstrates a reduction in RA and RV chamber diameters and volumes as early as 3 months into CPAP therapy, which continued to improve over 1 year of follow-up. Additionally, there was favorable improvement in LA diastolic function, manifested by a decrease in LA volume, amelioration in the LV filling pressures (reflected by the E/E′ ratio), and regression of LV mass as assessed by CMR.

Previous studies have demonstrated an improvement in RV volume and systolic function in patients with OSA with consistent CPAP use.12,3033 Although these studies demonstrated TTE evidence of improved RV remodeling, quantitative assessment of the RV is difficult because of its complex geometry and limited acoustic windows in obese patients with OSA.28 Unlike TTE, CMR is not affected by body habitus and serves as the gold standard for noninvasive assessment of cardiac dimensions, volumes, and EF because of its higher spatial resolution and lower intraobserver and interobserver variabilities.34 A recent study using CMR in 13 patients with severe OSA demonstrated favorable improvement in RV volumes after 3 months of CPAP therapy.14 In our larger study population, we confirmed these findings using both TTE and CMR, demonstrating an improvement in cardiac remodeling of both the RA and the RV over 1-year follow-up.

Mild pulmonary hypertension leading to RV enlargement often is a feature of OSA, occurring in up to 20% of patients without any underlying lung or heart disease.35,36 RVSP, as determined by echocardiography, is only a surrogate measure of peak pulmonary arterial systolic pressure, which is better defined by invasive right-sided heart catheterization. A previous randomized, controlled, crossover study demonstrated a favorable reduction in RVSP after 12 weeks of consistent CPAP use.37 The current study confirms a similar decrease in RVSP as early as 3 months into CPAP therapy that continued to improve over the long term with 1-year follow-up. Given the limitations of echocardiography, however, this notable finding would be best validated by assessing an improvement in mean pulmonary arterial pressures using serial pulmonary arterial catheterization in this patient population.

In addition to pulmonary hypertension and RV remodeling, the role of diastolic dysfunction in the OSA population has gained attention in recent years.9,38,39 In a recent study, Bayram et al10 demonstrated an improvement in conventional diastolic and tissue Doppler echocardiographic imaging parameters in patients with moderate to severe OSA after 6 months of CPAP therapy. Similarly, in 15 patients treated with CPAP, the E/E′ ratio decreased from 10.3 ± 1.9 at baseline to 7.9 ± 1.3 at 6 months.40 The current study demonstrates similar improvements in diastolic function in a larger patient population with severe OSA, with increased endocardial velocities and a reduction in the E/E′ ratio after just 3 months of CPAP therapy that extended up to 1-year of follow-up.

Diastolic dysfunction of the LV can lead to LA myocardial stretch and enlargement.40 To our knowledge, the current study is the first to demonstrate a reduction in LAVI on both TTE and CMR in the OSA patient population over a 1-year course of CPAP use. These results suggest that LA enlargement may be reversed with regular CPAP use, thus potentially lowering the risk of future cardiovascular complications, including atrial rhythm disturbances,2 in the OSA population.

In addition to LA abnormalities, diastolic dysfunction often is accompanied by LVH in patients with OSA. Recent studies using TTE have demonstrated that LVH was present in up to 50% of patients with severe OSA, which regressed after 6 months of nasal CPAP therapy.7 Dursunoglu et al31 also demonstrated an improvement in LVMI in 25 patients with OSA receiving CPAP therapy, as assessed by TTE. Because obesity is a common finding in patients with OSA, the reliability of LVH assessment by TTE in this population becomes questionable. A more-reliable measurement of LVH is LVMI measured in the short-axis plane on CMR. The current study is the first to our knowledge to demonstrate a favorable regression in LVMI using CMR in patients with OSA receiving CPAP therapy over 1 year.

There were notable limitations in the current study. We did not include a group of patients with untreated OSA, which is a major limitation. A larger multicenter study evaluating cardiac remodeling using CMR in patients with OSA randomized to no therapy vs CPAP would be required to further substantiate our findings. Additionally, because we only evaluated patients with OSA and without preexisting cardiac disease, future CMR studies are required to evaluate the effects of compliant CPAP therapy on cardiac remodeling in patients with OSA and heart failure.

Both systolic and diastolic abnormalities in patients with OSA can be reversed as early as 3 months into CPAP therapy, with progressive improvement in cardiovascular remodeling over 1 year as assessed by both TTE and CMR. Because we only evaluated patients with OSA without preexisting cardiac disease, future CMR studies are required to evaluate the effects of regular CPAP therapy on cardiac remodeling in patients with OSA and heart failure.

Author contributions: Ms Colish and Dr Jassal had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Ms Colish: contributed to data collection and interpretation, the writing of the manuscript, and review and approval of the final version.

Mr Walker: contributed to data collection and interpretation, the writing of the manuscript, and review and approval of the final version.

Dr Elmayergi: contributed to data collection and interpretation, the writing of the manuscript, and review and approval of the final version.

Dr Almutairi: contributed to data collection and interpretation, the writing of the manuscript, and review and approval of the final version.

Dr Alharbi: contributed to data collection and interpretation, the writing of the manuscript, and review and approval of the final version.

My Lytwyn: contributed to the writing of data collection and interpretation, the manuscript, and review and approval of the final version.

My Francis: contributed to data collection and interpretation, the writing of the manuscript, and review and approval of the final version.

Ms Bohonis: contributed to data collection and interpretation, the writing of the manuscript, and review and approval of the final version.

Mr Zeglinski: contributed to data collection and interpretation, the writing of the manuscript, and review and approval of the final version.

Dr Kirkpatrick: contributed to the writing of the manuscript and review and approval of the final version.

Dr Sharma: contributed to the writing of the manuscript and review and approval of the final version.

Dr Jassal: contributed to the study design, data collection, data interpretation, the writing of the manuscript, and review and approval of the final version.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Role of sponsors: The sponsors had no role in the design of the study, the collection and analysis of the data, or in the preparation of the manuscript.

AHI

apnea-hypopnea index

ANOVA

anaylsis of variance

CMR

cardiac MRI

CPAP

continuous positive airway pressure

CRP

C-reactive protein

E/E′

early diastolic filling/early diastolic annular velocity

EF

ejection fraction

LAVI

left atrial volume index

LV

left ventricular

LVH

left ventricular hypertrophy

LVMI

left ventricular mass index

NT-proBNP

N-terminal pro-B-type natriuretic peptide

OSA

obstructive sleep apnea

PSG

polysomnographic examination

RA

right atrial

RV

right ventricular

RVSP

right ventricular systolic pressure

TTE

transthoracic echocardiography

TnT

troponin T

Kaneko Y, Floras JS, Usui K, et al. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med. 2003;34813:1233-1241. [PubMed] [CrossRef]
 
Gami AS, Pressman G, Caples SM, et al. Association of atrial fibrillation and obstructive sleep apnea. Circulation. 2004;1104:364-367. [PubMed]
 
Shahar E, Whitney CW, Redline S, et al. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med. 2001;1631:19-25. [PubMed]
 
Javaheri S, Parker TJ, Liming JD, et al. Sleep apnea in 81 ambulatory male patients with stable heart failure. Types and their prevalences, consequences, and presentations. Circulation. 1998;9721:2154-2159. [PubMed]
 
Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med. 2005;35319:2034-2041. [PubMed]
 
Partinen M, Guilleminault C. Daytime sleepiness and vascular morbidity at seven-year follow-up in obstructive sleep apnea patients. Chest. 1990;971:27-32. [PubMed]
 
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;1242:594-601. [PubMed]
 
Laaban JP, Pascal-Sebaoun S, Bloch E, Orvoën-Frija E, Oppert JM, Huchon G. Left ventricular systolic dysfunction in patients with obstructive sleep apnea syndrome. Chest. 2002;1224:1133-1138. [PubMed]
 
Fung JW, Li TS, Choy DK, et al. Severe obstructive sleep apnea is associated with left ventricular diastolic dysfunction. Chest. 2002;1212:422-429. [PubMed]
 
Bayram NA, Ciftci B, Durmaz T, et al. Effects of continuous positive airway pressure therapy on left ventricular function assessed by tissue Doppler imaging in patients with obstructive sleep apnoea syndrome. Eur J Echocardiogr. 2009;103:376-382. [PubMed]
 
Malone S, Liu PP, Holloway R, Rutherford R, Xie A, Bradley TD. Obstructive sleep apnoea in patients with dilated cardiomyopathy: effects of continuous positive airway pressure. Lancet. 1991;3388781:1480-1484. [PubMed]
 
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 pressure. J Am Coll Cardiol. 2006;477:1433-1439. [PubMed]
 
Mintorovitch J, Duerinckx AJ, Goldman MD, Meissner HH. Breathhold cine MRI of left ventricular function in patients with obstructive sleep apnea: work-in-progress. Magn Reson Imaging. 2000;181:81-87. [PubMed]
 
Magalang UJ, Richards K, McCarthy B, et al. 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;52:110-114. [PubMed]
 
Shamsuzzaman AS, Winnicki M, Lanfranchi P, et al. Elevated C-reactive protein in patients with obstructive sleep apnea. Circulation. 2002;10521:2462-2464. [PubMed]
 
Yokoe T, Minoguchi K, Matsuo H, et al. Elevated levels of C-reactive protein and interleukin-6 in patients with obstructive sleep apnea syndrome are decreased by nasal continuous positive airway pressure. Circulation. 2003;1078:1129-1134. [PubMed]
 
Steiropoulos P, Tsara V, Nena E, et al. Effect of continuous positive airway pressure treatment on serum cardiovascular risk factors in patients with obstructive sleep apnea-hypopnea syndrome. Chest. 2007;1323:843-851. [PubMed]
 
Gami AS, Svatikova A, Wolk R, et al. Cardiac troponin T in obstructive sleep apnea. Chest. 2004;1256:2097-2100. [PubMed]
 
Møller DS, Lind P, Strunge B, Pedersen EB. Abnormal vasoactive hormones and 24-hour blood pressure in obstructive sleep apnea. Am J Hypertens. 2003;164:274-280. [PubMed]
 
Svatikova A, Shamsuzzaman AS, Wolk R, Phillips BG, Olson LJ, Somers VK. Plasma brain natriuretic peptide in obstructive sleep apnea. Am J Cardiol. 2004;944:529-532. [PubMed]
 
Barceló A, Barbé F, Llompart E, et al. Effects of obesity on C-reactive protein level and metabolic disturbances in male patients with obstructive sleep apnea. Am J Med. 2004;1172:118-121. [PubMed]
 
Akashiba T, Akahoshi T, Kawahara S, Majima T, Horie T. Effects of long-term nasal continuous positive airway pressure on C-reactive protein in patients with obstructive sleep apnea syndrome. Intern Med. 2005;448:899-900. [PubMed]
 
Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep. 1991;146:540-545. [PubMed]
 
Iber C, Ancoli-Israel S, Chesson A, Quan S. American Academy of Sleep Medicine American Academy of Sleep Medicine The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specification. 2007;1st ed Westchester, IL American Academy of Sleep Medicine
 
Nieto FJ, Young TB, Lind BK, et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA. 2000;28314:1829-1836. [PubMed]
 
Reeves-Hoche MK, Meck R, Zwillich CW. Nasal CPAP: an objective evaluation of patient compliance. Am J Respir Crit Care Med. 1994;1491:149-154. [PubMed]
 
Lang RM, Bierig M, Devereux RB, et al; Chamber Quantification Writing Group;American Society of Echocardiography’s Guidelines and Standards Committee;European Association of Echocardiography Chamber Quantification Writing Group;American Society of Echocardiography’s Guidelines and Standards Committee;European Association of Echocardiography Recommendations for chamber quantification: a report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005;1812:1440-1463. [PubMed]
 
Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;237:685-713. [PubMed]
 
Papavassiliu T, Kühl HP, van Dockum W, et al. Accuracy of one- and two-dimensional algorithms with optimal image plane position for the estimation of left ventricular mass: a comparative study using magnetic resonance imaging. J Cardiovasc Magn Reson. 2004;64:845-854. [PubMed]
 
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;1662:159-165. [PubMed]
 
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 apnoea. Sleep Med. 2007;81:51-59. [PubMed]
 
Romero-Corral A, Somers VK, Pellikka PA, et al. Decreased right and left ventricular myocardial performance in obstructive sleep apnea. Chest. 2007;1326:1863-1870. [PubMed]
 
Nahmias J, Lao R, Karetzky M. Right ventricular dysfunction in obstructive sleep apnoea: reversal with nasal continuous positive airway pressure. Eur Respir J. 1996;95:945-951. [PubMed]
 
Grothues F, Moon JC, Bellenger NG, Smith GS, Klein HU, Pennell DJ. Interstudy reproducibility of right ventricular volumes, function, and mass with cardiovascular magnetic resonance. Am Heart J. 2004;1472:218-223. [PubMed]
 
Alchanatis M, Tourkohoriti G, Kakouros S, Kosmas E, Podaras S, Jordanoglou JB. Daytime pulmonary hypertension in patients with obstructive sleep apnea: the effect of continuous positive airway pressure on pulmonary hemodynamics. Respiration. 2001;686:566-572. [PubMed]
 
Atwood CW Jr, McCrory D, Garcia JG, Abman SH, Ahearn GS. American College of Chest Physicians American College of Chest Physicians Pulmonary artery hypertension and sleep-disordered breathing: ACCP evidence-based clinical practice guidelines. Chest. 2004;1261 suppl:72S-77S. [PubMed]
 
Arias MA, García-Río F, Alonso-Fernández A, Martínez I, Villamor J. Pulmonary hypertension in obstructive sleep apnoea: effects of continuous positive airway pressure: a randomized, controlled cross-over study. Eur Heart J. 2006;279:1106-1113. [PubMed]
 
Niroumand M, Kuperstein R, Sasson Z, Hanly PJ. Impact of obstructive sleep apnea on left ventricular mass and diastolic function. Am J Respir Crit Care Med. 2001;1637:1632-1636. [PubMed]
 
Tkacova R, Rankin F, Fitzgerald FS, Floras JS, Bradley TD. Effects of continuous positive airway pressure on obstructive sleep apnea and left ventricular afterload in patients with heart failure. Circulation. 1998;9821:2269-2275. [PubMed]
 
Oliveira W, Campos O, Cintra F, et al. Impact of continuous positive airway pressure treatment on left atrial volume and function in patients with obstructive sleep apnoea assessed by real-time three-dimensional echocardiography. Heart. 2009;9522:1872-1878. [PubMed]
 

Figures

Figure Jump LinkFigure 1. A-D, Serial improvement in RAVI (A), RVEDD (B), RVEDVI (C), and LVMI (D) by either transthoracic echocardiography (A, B) or cardiac MRI (C, D) with corresponding number of months of CPAP therapy in the obstructive sleep apnea population. CPAP = continuous positive airway pressure; LVMI = left ventricular mass index; RAVI = right atrial volume index; RVEDD = right ventricular end-diastolic diameter; RVEDVI = right ventricular end-diastolic volume index.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1 —Baseline Characteristics of Total Population (N = 47)

Data are presented as mean ± SD or No. (%). AHI = apnea-hypopnea index; ESS = Epworth Sleepiness Scale; O2 = oxygen.

Table Graphic Jump Location
Table 2 —Summary of Serial Cardiac Biomarkers of Total Population (N = 47)

Data are presented as mean ± SD, unless otherwise indicated. ANOVA = analysis of variance; CRP = C-reactive protein; NT-proBNP = N-terminal pro-B-type natriuretic peptide; TnT = troponin T.

a 

P < .05 was considered significant vs baseline using repeated-measures ANOVA and Dunnett test.

Table Graphic Jump Location
Table 3 —Conventional Echocardiographic Data in Patient Population (N = 47)

Data are presented as mean ± SD. IVS = interventricular septum; LA = left atrial; LAVI = left atrial volume index; LV = left ventricular; LVEDD = left ventricular end-diastolic diameter; LVEDV = left ventricular end-diastolic volume; LVEF = left ventricular ejection fraction; LVESD = left ventricular end-systolic diameter; LVESV = left ventricular end-systolic volume; PWT = posterior wall thickness; RA = right atrial; RAVI = right atrial volume index; RV = right ventricular; RVEDD = right ventricular end-diastolic diameter in parasternal long-axis view; RVSP = right ventricular systolic pressure. See Table 2 legend for expansion of other abbreviation.

a 

P < .05 was considered significant vs baseline using repeated-measures ANOVA and Dunnett test.

Table Graphic Jump Location
Table 4 —Diastolic Echocardiographic Data in Patient Population (N = 47)

Data are presented as mean ± SD. A = late diastolic filling; A′ = late diastolic annular velocity; DT = deceleration time; E = early diastolic filling; E′ = early diastolic annular velocity; IVRT = isovolumetric relaxation time; S′ = systolic annular velocity; TDI = tissue Doppler echocardiographic imaging. See Table 2 legend for expansion of other abbreviation.

a 

P < .05 was considered significant vs baseline using repeated-measures ANOVA and Dunnett test.

Table Graphic Jump Location
Table 5 —CMR Data in Patient Population (N = 47)

Data are presented as mean ± SD. CMR = cardiac MRI; LVEDVI = left ventricular end-diastolic volume index; LVMI = left ventricular mass index; RVEDVI = right ventricular end-diastolic volume index; RVEF = right ventricular ejection fraction; RVMI = right ventricular mass index. See Table 2 and 3 legends for expansion of other abbreviations.

a 

P < .05 was considered significant vs baseline using repeated-measures ANOVA and Dunnett test.

Table Graphic Jump Location
Table 6 —Intraobserver and Interobserver Variability of Cardiac Dimensions in the Patient Population (N = 47)

CV = coefficient of variability; TTE = transthoracic echocardiography. See Table 3 and 5 legends for expansion of other abbreviations.

References

Kaneko Y, Floras JS, Usui K, et al. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med. 2003;34813:1233-1241. [PubMed] [CrossRef]
 
Gami AS, Pressman G, Caples SM, et al. Association of atrial fibrillation and obstructive sleep apnea. Circulation. 2004;1104:364-367. [PubMed]
 
Shahar E, Whitney CW, Redline S, et al. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med. 2001;1631:19-25. [PubMed]
 
Javaheri S, Parker TJ, Liming JD, et al. Sleep apnea in 81 ambulatory male patients with stable heart failure. Types and their prevalences, consequences, and presentations. Circulation. 1998;9721:2154-2159. [PubMed]
 
Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med. 2005;35319:2034-2041. [PubMed]
 
Partinen M, Guilleminault C. Daytime sleepiness and vascular morbidity at seven-year follow-up in obstructive sleep apnea patients. Chest. 1990;971:27-32. [PubMed]
 
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;1242:594-601. [PubMed]
 
Laaban JP, Pascal-Sebaoun S, Bloch E, Orvoën-Frija E, Oppert JM, Huchon G. Left ventricular systolic dysfunction in patients with obstructive sleep apnea syndrome. Chest. 2002;1224:1133-1138. [PubMed]
 
Fung JW, Li TS, Choy DK, et al. Severe obstructive sleep apnea is associated with left ventricular diastolic dysfunction. Chest. 2002;1212:422-429. [PubMed]
 
Bayram NA, Ciftci B, Durmaz T, et al. Effects of continuous positive airway pressure therapy on left ventricular function assessed by tissue Doppler imaging in patients with obstructive sleep apnoea syndrome. Eur J Echocardiogr. 2009;103:376-382. [PubMed]
 
Malone S, Liu PP, Holloway R, Rutherford R, Xie A, Bradley TD. Obstructive sleep apnoea in patients with dilated cardiomyopathy: effects of continuous positive airway pressure. Lancet. 1991;3388781:1480-1484. [PubMed]
 
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 pressure. J Am Coll Cardiol. 2006;477:1433-1439. [PubMed]
 
Mintorovitch J, Duerinckx AJ, Goldman MD, Meissner HH. Breathhold cine MRI of left ventricular function in patients with obstructive sleep apnea: work-in-progress. Magn Reson Imaging. 2000;181:81-87. [PubMed]
 
Magalang UJ, Richards K, McCarthy B, et al. 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;52:110-114. [PubMed]
 
Shamsuzzaman AS, Winnicki M, Lanfranchi P, et al. Elevated C-reactive protein in patients with obstructive sleep apnea. Circulation. 2002;10521:2462-2464. [PubMed]
 
Yokoe T, Minoguchi K, Matsuo H, et al. Elevated levels of C-reactive protein and interleukin-6 in patients with obstructive sleep apnea syndrome are decreased by nasal continuous positive airway pressure. Circulation. 2003;1078:1129-1134. [PubMed]
 
Steiropoulos P, Tsara V, Nena E, et al. Effect of continuous positive airway pressure treatment on serum cardiovascular risk factors in patients with obstructive sleep apnea-hypopnea syndrome. Chest. 2007;1323:843-851. [PubMed]
 
Gami AS, Svatikova A, Wolk R, et al. Cardiac troponin T in obstructive sleep apnea. Chest. 2004;1256:2097-2100. [PubMed]
 
Møller DS, Lind P, Strunge B, Pedersen EB. Abnormal vasoactive hormones and 24-hour blood pressure in obstructive sleep apnea. Am J Hypertens. 2003;164:274-280. [PubMed]
 
Svatikova A, Shamsuzzaman AS, Wolk R, Phillips BG, Olson LJ, Somers VK. Plasma brain natriuretic peptide in obstructive sleep apnea. Am J Cardiol. 2004;944:529-532. [PubMed]
 
Barceló A, Barbé F, Llompart E, et al. Effects of obesity on C-reactive protein level and metabolic disturbances in male patients with obstructive sleep apnea. Am J Med. 2004;1172:118-121. [PubMed]
 
Akashiba T, Akahoshi T, Kawahara S, Majima T, Horie T. Effects of long-term nasal continuous positive airway pressure on C-reactive protein in patients with obstructive sleep apnea syndrome. Intern Med. 2005;448:899-900. [PubMed]
 
Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep. 1991;146:540-545. [PubMed]
 
Iber C, Ancoli-Israel S, Chesson A, Quan S. American Academy of Sleep Medicine American Academy of Sleep Medicine The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specification. 2007;1st ed Westchester, IL American Academy of Sleep Medicine
 
Nieto FJ, Young TB, Lind BK, et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA. 2000;28314:1829-1836. [PubMed]
 
Reeves-Hoche MK, Meck R, Zwillich CW. Nasal CPAP: an objective evaluation of patient compliance. Am J Respir Crit Care Med. 1994;1491:149-154. [PubMed]
 
Lang RM, Bierig M, Devereux RB, et al; Chamber Quantification Writing Group;American Society of Echocardiography’s Guidelines and Standards Committee;European Association of Echocardiography Chamber Quantification Writing Group;American Society of Echocardiography’s Guidelines and Standards Committee;European Association of Echocardiography Recommendations for chamber quantification: a report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005;1812:1440-1463. [PubMed]
 
Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;237:685-713. [PubMed]
 
Papavassiliu T, Kühl HP, van Dockum W, et al. Accuracy of one- and two-dimensional algorithms with optimal image plane position for the estimation of left ventricular mass: a comparative study using magnetic resonance imaging. J Cardiovasc Magn Reson. 2004;64:845-854. [PubMed]
 
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;1662:159-165. [PubMed]
 
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 apnoea. Sleep Med. 2007;81:51-59. [PubMed]
 
Romero-Corral A, Somers VK, Pellikka PA, et al. Decreased right and left ventricular myocardial performance in obstructive sleep apnea. Chest. 2007;1326:1863-1870. [PubMed]
 
Nahmias J, Lao R, Karetzky M. Right ventricular dysfunction in obstructive sleep apnoea: reversal with nasal continuous positive airway pressure. Eur Respir J. 1996;95:945-951. [PubMed]
 
Grothues F, Moon JC, Bellenger NG, Smith GS, Klein HU, Pennell DJ. Interstudy reproducibility of right ventricular volumes, function, and mass with cardiovascular magnetic resonance. Am Heart J. 2004;1472:218-223. [PubMed]
 
Alchanatis M, Tourkohoriti G, Kakouros S, Kosmas E, Podaras S, Jordanoglou JB. Daytime pulmonary hypertension in patients with obstructive sleep apnea: the effect of continuous positive airway pressure on pulmonary hemodynamics. Respiration. 2001;686:566-572. [PubMed]
 
Atwood CW Jr, McCrory D, Garcia JG, Abman SH, Ahearn GS. American College of Chest Physicians American College of Chest Physicians Pulmonary artery hypertension and sleep-disordered breathing: ACCP evidence-based clinical practice guidelines. Chest. 2004;1261 suppl:72S-77S. [PubMed]
 
Arias MA, García-Río F, Alonso-Fernández A, Martínez I, Villamor J. Pulmonary hypertension in obstructive sleep apnoea: effects of continuous positive airway pressure: a randomized, controlled cross-over study. Eur Heart J. 2006;279:1106-1113. [PubMed]
 
Niroumand M, Kuperstein R, Sasson Z, Hanly PJ. Impact of obstructive sleep apnea on left ventricular mass and diastolic function. Am J Respir Crit Care Med. 2001;1637:1632-1636. [PubMed]
 
Tkacova R, Rankin F, Fitzgerald FS, Floras JS, Bradley TD. Effects of continuous positive airway pressure on obstructive sleep apnea and left ventricular afterload in patients with heart failure. Circulation. 1998;9821:2269-2275. [PubMed]
 
Oliveira W, Campos O, Cintra F, et al. Impact of continuous positive airway pressure treatment on left atrial volume and function in patients with obstructive sleep apnoea assessed by real-time three-dimensional echocardiography. Heart. 2009;9522:1872-1878. [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Find Similar Articles
CHEST Journal Articles
PubMed Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543