Obstructive Sleep Apnea

Effects of Continuous Positive Airway Pressure on Cardiac Remodeling as Assessed by Cardiac Biomarkers, Echocardiography, and Cardiac MRI

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


CHEST. 2012;141(3):674-681. 

In This Article

Abstract and Introduction


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.


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.[7–9]

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 LVH[7] 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 longterm.[13,14]

In addition to noninvasive imaging, serum levels of C-reactive protein (CRP), N-terminal pro-B-typenatriuretic peptide (NT-proBNP), and troponin T(TnT) have been evaluated previously in the setting of OSA.[15–20] There are conflicting results on whether CPAP therapy has any impact on biomarker levels inpatients with OSA.[15–22] 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.


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