Schwarz Esther I, Schlatzer Christian, Stehli Julia, Kaufmann Philipp A, Bloch Konrad E, Stradling John R, Kohler Malcolm
Sleep Disorders Center and Pulmonary Division, University Hospital of Zurich, Zurich, Switzerland.
Cardiac Imaging, Department of Nuclear Medicine, University Hospital of Zurich, Zurich, Switzerland.
Respirology. 2016 Aug;21(6):1126-33. doi: 10.1111/resp.12798. Epub 2016 Apr 20.
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.
阻塞性睡眠呼吸暂停（OSA）非常普遍，且与心血管事件发生率增加相关。内皮功能障碍被认为是其致病机制。持续气道正压通气（CPAP）被推测可改善OSA患者的心血管结局。最近有研究表明，停用CPAP会导致外周内皮功能障碍。然而，短期停用CPAP是否会降低OSA患者的心肌灌注尚不清楚。
在这项双盲随机对照研究中，45例既往坚持使用CPAP的中重度OSA患者被随机分为接受低于治疗剂量CPAP或继续接受治疗剂量CPAP治疗2周。主要结局指标为通过（13）N-氨正电子发射断层扫描评估的腺苷诱导的心肌血流量（MBF），作为内皮功能的指标。次要结局指标为皮肤和肾脏微血管功能指标、晨起血压（BP）和心率。
尽管停用CPAP后OSA复发，导致血压显著升高（+9.1 mmHg，95%可信区间[CI]为+4.9至+13.4 mmHg，P<0.001）和心率显著加快（+9.6次/分，95%可信区间为+4.6至+14.6次/分，P<0.001），但停用CPAP对最大心肌灌注能力（充血时MBF -0.01 ml/min/g，95%CI为-0.33至+0.24 ml/min/g，P=0.91）以及肾脏和皮肤微血管功能均无显著影响。
在OSA患者中，尽管血压临床相关升高近10 mmHg，但短期停用CPAP并未导致如肱动脉所显示的可检测到的冠状动脉内皮功能损害。也没有证据表明肾脏或皮肤微血管功能受损。
