Ya-Shu Chang1, Brendon J Yee2, Camilla M Hoyos3, Keith K Wong2, David R Sullivan4, Ronald R Grunstein2, Craig L Phillips5. 1. CIRUS, Centre for Sleep and Chronology, Woolcock Institute of Medical Research, Sydney, New South Wales, Australia; Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia. 2. CIRUS, Centre for Sleep and Chronology, Woolcock Institute of Medical Research, Sydney, New South Wales, Australia; Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia; Discipline of Sleep Medicine, Sydney Medical School, University of Sydney, New South Wales, Australia. 3. CIRUS, Centre for Sleep and Chronology, Woolcock Institute of Medical Research, Sydney, New South Wales, Australia; School of Psychology, Faculty of Science, University of Sydney, New South Wales, Australia. 4. Biochemistry Department, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia. 5. CIRUS, Centre for Sleep and Chronology, Woolcock Institute of Medical Research, Sydney, New South Wales, Australia; Discipline of Sleep Medicine, Sydney Medical School, University of Sydney, New South Wales, Australia; Department of Respiratory and Sleep Medicine, Royal North Shore Hospital, St. Leonards, Sydney, New South Wales, Australia. Electronic address: craig.phillips@sydney.edu.au.
Abstract
INTRODUCTION:Untreated obstructive sleep apnoea (OSA) is associated with increased risk of coronary artery disease (CAD) and heart failure. High-sensitivity cardiac troponin (hs Trop-T) and B-type natriuretic peptide (NT-pro-BNP) are sensitive biomarkers for myocardial injury and heart failure respectively. No randomised controlled trials have examined the treatment effect of continuous positive airway pressure (CPAP) in patients with OSA on these biomarkers. METHOD: Patients >21 years old with apnoea-hypopnoea index (AHI) ≥25/h by overnight polysomnography were recruited. Main exclusion criteria were previous CPAP use and any significant comorbidities including CAD and heart failure. Eligible subjects were randomised to receive CPAP or sham CPAP for eight weeks each in a crossover design with a wash out period of one month between the treatments. Blood samples were collected at 8pm, 3am, and 8am during sleep studies conducted at the end of each eight-week treatment period. RESULTS: Of the 37 patients who were randomised, 28 patients had stored frozen samples available for analysis. In comparison to sham treatment, CPAP significantly lowered the NT-pro-BNP level by 0.91 pmol/L (p = 0.0002). The reduction of 0.235 ng/L in hs Trop-T on CPAP therapy was not statistically significant (p = 0.052). There were no overnight changes, across the three time points, in either biomarker with either treatment. CONCLUSION: Our study confirms CPAP therapy in patients with moderate-severe OSA reduces NT-pro-BNP, but we did not confirm a significant effect on hs Trop-T. Future larger studies of longer duration incorporating biomarkers and cardiac functional measures are needed to better establish the benefit of OSA treatment. Crown
RCT Entities:
INTRODUCTION: Untreated obstructive sleep apnoea (OSA) is associated with increased risk of coronary artery disease (CAD) and heart failure. High-sensitivity cardiac troponin (hs Trop-T) and B-type natriuretic peptide (NT-pro-BNP) are sensitive biomarkers for myocardial injury and heart failure respectively. No randomised controlled trials have examined the treatment effect of continuous positive airway pressure (CPAP) in patients with OSA on these biomarkers. METHOD:Patients >21 years old with apnoea-hypopnoea index (AHI) ≥25/h by overnight polysomnography were recruited. Main exclusion criteria were previous CPAP use and any significant comorbidities including CAD and heart failure. Eligible subjects were randomised to receive CPAP or sham CPAP for eight weeks each in a crossover design with a wash out period of one month between the treatments. Blood samples were collected at 8pm, 3am, and 8am during sleep studies conducted at the end of each eight-week treatment period. RESULTS: Of the 37 patients who were randomised, 28 patients had stored frozen samples available for analysis. In comparison to sham treatment, CPAP significantly lowered the NT-pro-BNP level by 0.91 pmol/L (p = 0.0002). The reduction of 0.235 ng/L in hs Trop-T on CPAP therapy was not statistically significant (p = 0.052). There were no overnight changes, across the three time points, in either biomarker with either treatment. CONCLUSION: Our study confirms CPAP therapy in patients with moderate-severe OSA reduces NT-pro-BNP, but we did not confirm a significant effect on hs Trop-T. Future larger studies of longer duration incorporating biomarkers and cardiac functional measures are needed to better establish the benefit of OSA treatment. Crown
Authors: Sheila Sivam; David Wang; Keith K H Wong; Amanda J Piper; Yi Zhong Zheng; Gislaine Gauthier; Christine Hockings; Olivia McGuinness; Collette Menadue; Kerri Melehan; Sara Cooper; Hugi Hilmisson; Craig L Phillips; Robert J Thomas; Brendon J Yee; Ronald R Grunstein Journal: J Clin Sleep Med Date: 2022-04-01 Impact factor: 4.062