Key result
High-altitude exposure linked to a ~32 mm Hg sPAP increase in HAPH subjects versus controls.
Why the study?
Data on changes in cardiac morphology and function at high altitude compared to individuals who do not develop high-altitude pulmonary hypertension were scarce.
Does high-altitude exposure cause different acute changes in cardiac dimensions and function in healthy individuals who develop high-altitude pulmonary hypertension compared to those who do not?
Observational (n=53)
Does high-altitude exposure cause different acute changes in cardiac dimensions and function in healthy individuals who develop high-altitude pulmonary hypertension compared to those who do not?
Absolute Event Rate: 32% vs 10.2%
p-value: p=<.001
High-altitude exposure induces more pronounced right ventricular and right atrial dimensional increases and left ventricular eccentricity in individuals who develop high-altitude pulmonary hypertension compared to those who do not.
Greater SPAP rises and LV distortion in HAPH may signal vulnerability at altitude; leaves open targeted prevention strategies.
Background High‐altitude pulmonary hypertension (HAPH) has a prevalence of approximately 10%. Changes in cardiac morphology and function at high altitude, compared to a population that does not develop HAPH are scarce. Methods Four hundred twenty‐one subjects were screened in a hypoxic chamber inspiring a FiO 2 = 12% for 2 h. In 33 subjects an exaggerated increase in systolic pulmonary artery pressure (sPAP) could be confirmed in two independent measurements. Twenty nine of these, and further 24 matched subjects without sPAP increase were examined at 4559 m by Doppler echocardiography including global longitudinal strain (GLS). Results SPAP increase was higher in HAPH subjects (∆ = 10.2 vs. ∆ = 32.0 mm Hg, p < .001). LV eccentricity index (∆ = .15 vs. ∆ = .31, p = .009) increased more in HAPH. D‐shaped LV (0 [0%] vs. 30 [93.8%], p = .00001) could be observed only in the HAPH group, and only in those with a sPAP ≥50 mm Hg. LV‐EF (∆ = 4.5 vs. ∆ = 6.7%, p = .24) increased in both groups. LV‐GLS (∆ = 1.2 vs. ∆ = 1.1 –%, p = .60) increased slightly. RV end‐diastolic (∆ = 2.20 vs. ∆ = 2.7 cm 2 , p = .36) and end‐systolic area (∆ = 2.1 vs. ∆ = 2.7 cm 2 , p = .39), as well as RA end‐systolic area index (∆ = −.9 vs. ∆ = .3 cm 2 /m 2 , p = .01) increased, RV‐FAC (∆ = −2.9 vs. ∆ = −4.7%, p = .43) decreased, this was more pronounced in HAPH, RV‐GLS (∆ = 1.6 vs. ∆ = −.7 –%, p = .17) showed marginal changes. Conclusions LV and LA dimensions decrease and left ventricular function increases at high‐altitude in subjects with and without HAPH. RV and RA dimensions increase, and RV longitudinal strain increases or remains unchanged in subjects with HAPH. Changes are negligible in those without HAPH.
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Mereles et al. (2024) conducted an observational in High-altitude pulmonary hypertension (n=53). High-altitude exposure vs. Matched subjects without high-altitude pulmonary hypertension was evaluated on Increase in systolic pulmonary artery pressure (sPAP) (p=<.001). High-altitude exposure at 4559 m induced greater increases in systolic pulmonary artery pressure (∆ 32.0 vs 10.2 mm Hg, p<.001) and LV eccentricity index in HAPH subjects compared to matched controls.
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