Effect of CPAP Withdrawal on myocardial perfusion in OSA: A randomized controlled trial.
Obstructive sleep apnoea (OSA) is highly prevalent and associated with an increased incidence of cardiovascular events. Endothelial dysfunction is the proposed causative mechanism. Continuous positive airway pressure (CPAP) is presumed to improve cardiovascular outcome in OSA. CPAP withdrawal was recently shown to lead to peripheral endothelial dysfunction. However, it is not known whether short-term CPAP withdrawal reduces myocardial perfusion in OSA.



In this double-blind randomized controlled study, 45 patients with moderate to severe OSA previously adherent to CPAP were assigned to either subtherapeutic or continuing therapeutic CPAP for 2 weeks. The primary outcome was adenosine-induced myocardial blood flow (MBF) as a measure of endothelial function, assessed by (13) N-ammonia positron emission tomography. Secondary outcomes were measures of dermal and renal microvascular function, morning blood pressure (BP) and heart rate.



Despite return of OSA associated with significant increases in BP (+9.1 mm Hg, 95% CI +4.9 to +13.4 mm Hg, P < 0.001) and heart rate (+9.6 bpm, 95% confidence interval (CI) +4.6 to +14.6 bpm, P < 0.001), CPAP withdrawal had no significant effect on maximal myocardial perfusion capacity (hyperaemic MBF -0.01 ml/min/g, 95% CI -0.33 to +0.24 ml/min/g, P = 0.91), nor renal and dermal microvascular function.



In patients with OSA, a short-term CPAP withdrawal does not lead to detectable impairment of coronary endothelial function, as has been demonstrated in the brachial artery, despite a clinically relevant increase in BP of nearly 10 mm Hg. There was also no evidence of an impairment of renal or dermal microvascular function.
Sleep Disorders Center and Pulmonary Division, University Hospital of Zurich, Zurich, Switzerland.
Esther I
EI
Schwarz
Sleep Disorders Center and Pulmonary Division, University Hospital of Zurich, Zurich, Switzerland.
Christian
C
Schlatzer
Cardiac Imaging, Department of Nuclear Medicine, University Hospital of Zurich, Zurich, Switzerland.
Julia
J
Stehli
Cardiac Imaging, Department of Nuclear Medicine, University Hospital of Zurich, Zurich, Switzerland.|Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland.
Philipp A
PA
Kaufmann
Sleep Disorders Center and Pulmonary Division, University Hospital of Zurich, Zurich, Switzerland.|Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland.
Konrad E
KE
Bloch
National Institute for Health Research (NIHR), Oxford Biomedical Research Centre, Oxford University Hospitals NHS Foundation Trust and University of Oxford, Oxford, UK.
John R
JR
Stradling
Sleep Disorders Center and Pulmonary Division, University Hospital of Zurich, Zurich, Switzerland.|Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland.
Malcolm
M
Kohler
D000368:Aged; D045422:Continuous Positive Airway Pressure / Q000379:methods*; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D055414:Myocardial Perfusion Imaging / Q000379:methods; D017063:Outcome Assessment, Health Care; D020181:Sleep Apnea, Obstructive / Q000503:physiopathology / Q000628:therapy; D013997:Time Factors; D028761:Withholding Treatment / Q000706:statistics & numerical data
cardiovascular consequences; continuous positive airway pressure; microvascular endothelial function; myocardial perfusion; obstructive sleep apnoea