Allemann Yves, Hutter Damian, Lipp Ernst, Sartori Claudio, Duplain Hervé, Egli Marc, Cook Stéphane, Scherrer Urs, Seiler Christian
Department of Cardiology, Swiss Cardiovascular Center Bern, University Hospital, Inselspital, Bern, Switzerland.
JAMA. 2006 Dec 27;296(24):2954-8. doi: 10.1001/jama.296.24.2954.
Individuals susceptible to high-altitude pulmonary edema (HAPE) are characterized by exaggerated pulmonary hypertension and arterial hypoxemia at high altitude, but the underlying mechanism is incompletely understood. Anecdotal evidence suggests that shunting across a patent foramen ovale (PFO) may exacerbate hypoxemia in HAPE.
We hypothesized that PFO is more frequent in HAPE-susceptible individuals and may contribute to more severe arterial hypoxemia at high altitude.
DESIGN, SETTING, AND PARTICIPANTS: Case-control study of 16 HAPE-susceptible participants and 19 mountaineers resistant to this condition (repeated climbing to peaks above 4000 m and no symptoms of HAPE).
Presence of PFO determined by transesophageal echocardiography, estimated pulmonary artery pressure by Doppler echocardiography, and arterial oxygen saturation measured by pulse oximetry in HAPE-susceptible and HAPE-resistant participants at low (550 m) and high altitude (4559 m).
The frequency of PFO was more than 4 times higher in HAPE-susceptible than in HAPE-resistant participants, both at low altitude (56% vs 11%, P = .004; odds ratio [OR], 10.9 [95% confidence interval {CI}, 1.9-64.0]) and high altitude (69% vs 16%, P = .001; OR, 11.7 [95% CI, 2.3-59.5]). At high altitude, mean (SD) arterial oxygen saturation prior to the onset of pulmonary edema was significantly lower in HAPE-susceptible participants than in the control group (73% [10%] vs 83% [7%], P = .001). Moreover, in the HAPE-susceptible group, participants with a large PFO had more severe arterial hypoxemia (65% [6%] vs 77% [8%], P = .02) than those with smaller or no PFO.
Patent foramen ovale was roughly 4 times more frequent in HAPE-susceptible mountaineers than in participants resistant to this condition. At high altitude, HAPE-susceptible participants with a large PFO had more severe hypoxemia. We speculate that at high altitude, a large PFO may contribute to exaggerated arterial hypoxemia and facilitate HAPE.
易患高原肺水肿（HAPE）的个体在高原时具有肺动脉高压和动脉血氧不足加剧的特征，但其潜在机制尚未完全明确。有轶事证据表明，经未闭卵圆孔（PFO）的分流可能会加重HAPE患者的低氧血症。
我们假设PFO在易患HAPE的个体中更为常见，并且可能导致高原时更严重的动脉血氧不足。
设计、地点和参与者：对16名易患HAPE的参与者和19名对该病有抵抗力的登山者（多次攀登至海拔4000米以上且无HAPE症状）进行病例对照研究。
通过经食管超声心动图确定PFO的存在，通过多普勒超声心动图估计肺动脉压力，以及通过脉搏血氧饱和度测定法测量易患HAPE和有HAPE抵抗力的参与者在低海拔（550米）和高海拔（4559米）时的动脉血氧饱和度。
在低海拔（56%对11%，P = 0.004；优势比[OR]，10.9[95%置信区间{CI}，1.9 - 64.0]）和高海拔（69%对16%，P = 0.001；OR，11.7[95%CI，2.3 - 59.5]）时，易患HAPE的参与者中PFO的发生率比有HAPE抵抗力的参与者高出4倍多。在高海拔时，肺水肿发作前，易患HAPE的参与者的平均（标准差）动脉血氧饱和度显著低于对照组（73%[10%]对83%[7%]，P = 0.001）。此外，在易患HAPE的组中，有大PFO的参与者比有较小PFO或无PFO的参与者有更严重的动脉血氧不足（65%[6%]对77%[8%]，P = 0.02）。
易患HAPE的登山者中未闭卵圆孔的发生率大约是有抵抗力参与者的4倍。在高海拔时，有大PFO的易患HAPE的参与者有更严重的低氧血症。我们推测，在高海拔时，大PFO可能会导致动脉血氧不足加剧并促进HAPE的发生。
