Rapid Fire Abstracts
Nithin R. Iyer, MD
Doctor
Woodlands Health, Singapore
Nithin R. Iyer, MD
Doctor
Woodlands Health, Singapore
Yi-hui Ou, BSc
Ph.D candidate
National university of Singapore, Singapore
Jennifer Ann A. Bryant, PhD
Principal Radiographer
National Heart Centre Singapore, Singapore
Thu Thao Le, PhD
Senior Research Fellow
National Heart Centre Singapore, Singapore
Juliana Colpani, MD, MSc
Lecturer
National University of Singapore, Singapore
Crystal Cheong, MD
Consultant, Department of Otolaryngology
National University Hospital, Singapore
Weiqiang Loke, MD, MSc
Visiting Consultant
National University Center for Oral Health, Singapore, Singapore
Peter Cistulli, MD, PhD
Professor of Sleep Medicine
The University of Sydney, Australia
.jpg "Martin Ugander, MD, PhD photo")
Martin Ugander, MD, PhD
Professor of Cardiac Imaging
Kolling Institute, Royal North Shore Hospital and University of Sydney/ Karolinska University Hospital and Karolinska Institutet, Australia
Chi-hang Lee, MD
Professor of Medicine
National University of Singapore, Singapore
Calvin Chin, MD, PhD
Associate Professor
National Heart Centre Singapore, Singapore
Obstructive sleep apnea (OSA) is a highly prevalent condition that is characterised by recurrent hypoxemia, sympathetic activation, and intrathoracic pressure swing during sleep. Adverse cardiac remodelling is often observed in OSA, including left ventricular hypertrophy, left ventricular dysfunction and diffuse myocardial fibrosis. The effect of treatment of OSA on cardiac remodelling is not well characterised. This exploratory cardiovascular magnetic resonance (CMR) substudy of the CRESCENT randomised trial (Cardiosleep Research Program on Obstructive Sleep Apnea, Blood Pressure Control and Maladaptive Myocardial Remodeling—Non-inferiority Trial) aimed to determine the effects of continuous positive airways pressure (CPAP) and mandibular advancement device (MAD) on myocardial structure and function in patients with OSA.
Methods:
In this CMR substudy, 86 patients with hypertension and increased cardiovascular risk, with newly diagnosed moderate to severe OSA (AHI ≥ 15 events/hour), underwent CMR with contrast (Siemens 1.5T) at baseline and following 12 months of treatment with CPAP (n=49) or MAD (n=37). Left ventricular (LV) mass, volumes, function and markers of diffuse myocardial fibrosis, including the extracellular volume fraction (ECV) and interstitial volume (Myocardial volume*ECV/100) were measured. Myocyte volume was calculated as: Myocardial volume*(1-ECV/100).
Results:
Amongst the CMR markers in the entire cohort, there was a reduction in the ECV (25.0±2.0 vs 24.4±2.2%; p=0.014) (Figure 1A). This was associated with a reduction in the interstitial volume (24.0[21.1-27.3] vs 23.3[20.4-27.4]mL; p=0.046) (Figure 1C). These findings did not differ between treatment arms (p >0.05 for all analyses). All other parameters, including LV mass and LV myocyte volume did not differ (Figure 1B and 1D; Table 1). Exploratory analysis suggested that obese patients (baseline BMI ≥30kg/m2) were more likely to experience a reduction in ECV (change: -0.3[-1.6 to 0.8] vs -1.1[-2.0 to -0.3]%; p=0.02).
Conclusion:
Treatment of OSA in the setting of hypertension is associated with a reduction in myocardial ECV, a surrogate marker of diffuse myocardial fibrosis, at 12 months, with accompanying reduction in the myocardial interstitial volume. Both CPAP and MAD were similarly effective. Further confirmation of these findings in larger cohorts are merited.
