Higher altitude was associated with more severe nocturnal hypoxemia and higher adjusted mean pulmonary artery pressure at 12 months (28 mmHg at high altitude vs 23 mmHg at sea level).
Cohort (n=92)
Yes
Does residence at higher altitudes worsen nocturnal oxygenation and increase pulmonary artery pressure in children with cystic fibrosis?
In children with cystic fibrosis, higher altitude residence is associated with worse nocturnal hypoxemia and higher mean pulmonary artery pressure, highlighting the need to monitor pulmonary hemodynamics in this population across altitudes.
Effect estimate: β = -2.30
Absolute Event Rate: 28% vs 23%
p-value: p=0.094
Abstract Introduction Chronic hypobaric hypoxia at high altitude may alter nocturnal oxygenation and pulmonary hemodynamics in children with cystic fibrosis (CF), yet longitudinal evidence across different altitudes remains limited. Understanding how altitude shapes sleep physiology may help clarify adaptive or maladaptive cardiovascular responses in CF. Methods A multicenter prospective study included 92 children with confirmed CF residing at high (∼2600 m, n = 33), intermediate (∼1500 m, n = 33), and low altitude (sea level, n = 26). All participants underwent baseline polysomnography, and echocardiography was performed at baseline and after 12 months. Nocturnal oxygenation parameters—percentage of total sleep time with peripheral oxygen saturation (SpO2) 90% (T90), oxygen desaturation index (ODI), and apnea-hypopnea index (AHI)—and mean pulmonary artery pressure (mPAP) were analyzed. An ANCOVA model assessed predictors of mPAP at 12 months, adjusted for baseline mPAP, altitude, and mean sleep (SpO2). Complete follow-up echocardiographic data were available for 77 of 92 participants (83.7%), who were included in adjusted analyses. Marginal means were estimated with 95% confidence intervals. Results T90 and ODI increased progressively with altitude (p 0.01), indicating more severe sustained and intermittent nocturnal hypoxemia at higher elevations. In contrast, AHI did not preserve a monotonic trend with altitude. In the adjusted model, mean sleep SpO2 was inversely and significantly associated with mean pulmonary artery pressure (mPAP) at 12 months (β = −0.55; p = 0.011). Altitude showed a consistent near-significant trend toward higher mPAP (β = −2.30; p = 0.094), while baseline mPAP accounted for most of the explained variability (β = 0.52; p 0.001). Adjusted mean mPAP values were highest at high altitude (28 mmHg), intermediate at mid-altitude (25 mmHg), and lowest at sea level (23 mmHg), demonstrating a descending hemodynamic gradient with decreasing altitude. Conclusion Indices of nocturnal oxygenation (T90 and ODI) showed a clear altitudinal gradient, with more pronounced sustained and intermittent hypoxemia at higher elevations. In contrast, AHI did not follow a monotonic pattern, possibly reflecting lower sensitivity to barometric pressure-related changes. Nocturnal oxygenation, particularly mean sleep SpO2, was significantly associated with mean pulmonary artery pressure (mPAP), highlighting the interdependence between altitude, oxygenation, and pulmonary arterial pressure. These findings suggest partial hemodynamic adaptation to chronic hypobaric hypoxia and underscore the need to monitor nocturnal oxygenation and pulmonary pressure in pediatric CF populations across altitudes. This abstract is funded by: None
Hoz et al. (Fri,) conducted a cohort in Cystic fibrosis (n=92). High altitude (~2600 m) and intermediate altitude (~1500 m) vs. Low altitude (sea level) was evaluated on Mean pulmonary artery pressure (mPAP) at 12 months (β = -2.30, p=0.094). Higher altitude was associated with more severe nocturnal hypoxemia and higher adjusted mean pulmonary artery pressure at 12 months (28 mmHg at high altitude vs 23 mmHg at sea level).