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Effect of simulated obstructive hypopnea and apnea on thoracic aortic wall transmural pressures

机译:模拟阻塞性呼吸不足和呼吸暂停对胸主动脉壁透壁压的影响

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摘要

Preliminary evidence supports an association between obstructive sleep apnea (OSA) and thoracic aortic dilatation, although potential causative mechanisms are incompletely understood; these may include an increase in aortic wall transmural pressures, induced by obstructive apneas and hypopneas. In patients undergoing cardiac catheterization, mean blood pressure (MBP) in the thoracic aorta and esophageal pressure was simultaneously recorded by an indwelling aortic pigtail catheter and a balloon-tipped esophageal catheter in randomized order during: normal breathing, simulated obstructive hypopnea (inspiration through a threshold load), simulated obstructive apnea (Mueller maneuver), and end-expiratory central apnea. Aortic transmural pressure (aortic MBP minus esophageal pressure) was calculated. Ten patients with a median age (range) of 64 (46–75) yr were studied. Inspiration through a threshold load, Mueller maneuver, and end-expiratory central apnea was successfully performed and recorded in 10, 7, and 9 patients, respectively. The difference between aortic MBP and esophageal pressure (and thus the extra aortic dilatory force) was median (quartiles) +9.3 (5.4, 18.6) mmHg, P = 0.02 during inspiration through a threshold load, +16.3 (12.8, 19.4) mmHg, P = 0.02 during the Mueller maneuver, and +0.4 (−4.5, 4.8) mmHg, P = 0.80 during end-expiratory central apnea. Simulated obstructive apnea and hypopnea increase aortic wall dilatory transmural pressures because intra-aortic pressures fall less than esophageal pressures. Thus OSA may mechanically promote thoracic aortic dilatation and should be further investigated as a risk factor for the development or accelerated progression of thoracic aortic aneurysms.
机译:初步证据支持阻塞性睡眠呼吸暂停(OSA)与胸主动脉扩张之间的关联,尽管尚未完全了解潜在的致病机制。这些可能包括阻塞性呼吸暂停和呼吸不足引起的主动脉壁透壁压升高。在接受心脏导管插入术的患者中,留置主动脉尾纤导管和带气囊的食管导管同时以随机顺序记录胸主动脉的平均血压(MBP)和食管压力,在正常呼吸,模拟阻塞性呼吸不足(通过阈负荷),模拟阻塞性呼吸暂停(Mueller动作)和呼气末中央呼吸暂停。计算主动脉透壁压力(主动脉MBP减去食管压力)。研究了十名中位年龄(范围)为64(46-75)岁的患者。通过阈值负荷,Mueller动作和呼气末中央呼吸暂停的吸气被成功执行,并分别记录在10、7和9位患者中。主动脉MBP和食管压力之间的差异(以及主动脉外扩张力)之间的差值为中位(四分位数)+9.3(5.4,18.6)mmHg,通过阈值负荷吸气时P = 0.02,+ 16.3(12.8,19.4)mmHg,在Mueller操纵期间,P = 0.02,在呼气末中央呼吸暂停期间,P = +0.4(-4.5,4.8)mmHg,P = 0.80。模拟的阻塞性呼吸暂停和呼吸不足会增加主动脉壁的扩张透壁压力,因为主动脉内压力的下降幅度小于食管压力。因此,OSA可能会机械地促进胸主动脉扩张,应进一步研究其作为胸主动脉瘤发展或加速进展的危险因素。

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