Acute changes in cardiac dimensions, function, and longitudinal mechanics in healthy individuals with and without high‐altitude induced pulmonary hypertension at 4559 m

• Published in: Echocardiography (Mount Kisco, N.Y.) Vol. 41; no. 2; pp. e15786 - n/a
• Main Authors: Mereles, Derliz, Rudolph, Jens, Greiner, Sebastian, Aurich, Matthias, Frey, Norbert, Katus, Hugo A., Bärtsch, Peter, Dehnert, Christoph
• Format: Journal Article
• Language: English
• Published: United States 01.02.2024
• Subjects: Doppler echocardiography; high‐altitude; hypoxia‐chamber echocardiography; longitudinal strain; pulmonary hypertension; high-altitude; Doppler echocardiography; hypoxia-chamber echocardiography; longitudinal strain; pulmonary hypertension
• ISSN: 0742-2822; 1540-8175; 1540-8175
• DOI: 10.1111/echo.15786

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 FiO2 = 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 cm2, p = .36) and end‐systolic area (∆ = 2.1 vs. ∆ = 2.7 cm2, p = .39), as well as RA end‐systolic area index (∆ = −.9 vs. ∆ = .3 cm2/m2, 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. (A) Timeline and altitude reached during the course of the study. First assessment 6 hours after arrival (M1), assessments at day 3 (M2) and 4 (M3) before descent. (B) Systolic pulmonary artery pressures assessed in normobaric normoxia in Heidelberg (H) and during each of 3 days under hypobaric hypoxia at 4559 m altitude (M). M‐HAPE: subjects who developed high‐altitude pulmonary edema in one of 3 days at M, H‐PH: subjects who developed pulmonary hypertension in the hypoxic chamber in H, H‐N: subjects who did not develop PH in H. (C) Sankey diagram showing shifts in groups from H to M according to the development (red) or not (green) of high‐altitude pulmonary hypertension. HAPE probands are shown in color blue. (D) sPAP in normobaric normoxia in Heidelberg (NN) and in hypobaric hypoxia at 4559 m (HH) (E) Arterial oxygen saturation (SaO2), dotted line shows a SaO2 cutoff level of 80 %