Sleep Disorders Center and Pulmonary Division, University Hospital of Zurich, Zurich, Switzerland.
Division of Cardiology, University Hospital of Zurich, Zurich, Switzerland.
Chest. 2011 Sep;140(3):675-680. doi: 10.1378/chest.10-2799. Epub 2011 Mar 10.
Preliminary evidence supports an association between obstructive sleep apnea (OSA) and thoracic aortic dilatation. The mechanisms through which OSA may promote thoracic aortic dilatation are incompletely understood. Therefore, we studied the acute effects of simulated apnea and hypopnea on aortic diameter and BP in humans.
The diameter of the aortic root was measured in 20 healthy volunteers by echocardiography, and peripheral BP was continuously recorded prior, during, and immediately after simulated obstructive hypopnea (inspiration through threshold load), simulated obstructive apnea (Müller maneuver), end-expiratory central apnea, and normal breathing in randomized order.
Proximal aortic diameter increased significantly during inspiration through a threshold load (+6.48%; SE, 3.03; P = .007), but not during Müller maneuver (+3.86%; SE, 2.71; P = .336) or end-expiratory central apnea (+0.62%; SE, 2.94; P = .445). Maneuver-induced changes in mean BP were observed during inspiration through a threshold load (-10.5 mm Hg; SE, 2.2; P < .001), the Müller maneuver (-8.8 mm Hg; SE, 2.4; P < .001), and end-expiratory central apnea (-4.2 mm Hg; SE, 1.4; P = .052). There was a significant increase in mean BP on release of threshold load inspiration (+8.1 mm Hg; SE, 2.9 mm Hg; P = .002), Müller maneuver (+10.7 mm Hg; SE, 2.9; P < .001), and end-expiratory central apnea (+10.6 mm Hg; SE, 2.5; P < .001).
Simulated obstructive hypopnea/apnea and central apnea induced considerable changes in BP, and obstructive hypopnea was associated with an increase in proximal aortic diameter. Further studies are needed to investigate effects of apnea and hypopnea on transmural aortic pressure and aortic diameter to define the role of OSA in the pathogenesis of aortic dilatation.
初步证据表明阻塞性睡眠呼吸暂停(OSA)与胸主动脉扩张之间存在关联。OSA 促进胸主动脉扩张的机制尚不完全清楚。因此,我们研究了模拟呼吸暂停和低通气对人体主动脉直径和血压的急性影响。
通过超声心动图测量 20 名健康志愿者的主动脉根部直径,并在随机顺序下连续记录模拟阻塞性低通气(通过阈负荷吸气)、模拟阻塞性呼吸暂停(Müller 手法)、呼气末中枢性呼吸暂停和正常呼吸期间及之后的外周血压。
通过阈负荷吸气时,近端主动脉直径显著增加(+6.48%;SE,3.03;P =.007),但在 Müller 手法(+3.86%;SE,2.71;P =.336)或呼气末中枢性呼吸暂停(+0.62%;SE,2.94;P =.445)时则没有。在阈负荷吸气期间观察到与操作相关的平均血压变化(-10.5mmHg;SE,2.2;P <.001)、Müller 手法(-8.8mmHg;SE,2.4;P <.001)和呼气末中枢性呼吸暂停(-4.2mmHg;SE,1.4;P =.052)。在释放阈负荷吸气时,平均血压显著升高(+8.1mmHg;SE,2.9mmHg;P =.002)、Müller 手法(+10.7mmHg;SE,2.9;P <.001)和呼气末中枢性呼吸暂停(+10.6mmHg;SE,2.5;P <.001)。
模拟阻塞性低通气/呼吸暂停和中枢性呼吸暂停引起血压显著变化,阻塞性低通气与近端主动脉直径增加有关。需要进一步研究以探讨呼吸暂停和低通气对主动脉壁内压力和主动脉直径的影响,以确定 OSA 在主动脉扩张发病机制中的作用。