Claire Maufrais1,2, Thomas Rupp1,2,3, Pierre Bouzat4,5, Gregory Doucende6, Samuel Verges1,2, Stéphane Nottin7, Guillaume Walther7. 1. U1042, INSERM, Domaine de la Merci, F-38700, La Tronche - Grenoble, France. 2. Laboratoire HP2, Grenoble Alpes Université, Avenue Kimberley, F-38434, Echirolles - Grenoble, France. 3. Laboratoire Interuniversitaire de Biologie de la Motricité, Université Savoie Mont Blanc, 27 rue Marcoz F-73000, Chambéry, France. 4. Grenoble Institute of Neurosciences, INSERM U1216, Chemin Fortuné Ferrini, F-38700 La Tronche - Grenoble, France. 5. Pôle Anesthésie Réanimation, CHU de Grenoble, Avenue Maquis du Grésivaudan, F-38700 La Tronche - Grenoble, France. 6. Laboratoire Performance et Santé en Altitude, Université de Perpignan, 7 Avenue Pierre de Coubertin, F-66120, Font-Romeu, France. 7. Avignon University, LAPEC EA4278, 74 Rue Louis Pasteur, F-84000, Avignon, France.
Abstract
AIMS: The aim of this study was to analyse the underlying mechanisms of left and right ventricular (LV and RV) functional alterations during several days in high-altitude hypoxia. METHODS AND RESULTS: Resting evaluations of LV and RV function and mechanics were assessed by Speckle Tracking Echocardiography on 11 subjects at sea level (SLPRE), 3 ± 2 h after helicopter transport to high altitude (D0), at day 2 (D2), day 4 (D4) and day 6 (D6) at 4350 m and 5 ± 2 h after return to sea level (SLPOST). Subjects experienced acute mountain sickness (AMS) during the first days at 4350 m. LV systolic function, RV systolic and diastolic function, LV and RV strains and LV synchrony were unchanged at high altitude. Peak twist was increased at D0, continued to increase until D6 (SLPRE: 9.0 ± 5.1deg; D6: 13.0 ± 4.0deg, P < 0.05), but was normalized at SLPOST. Early filling decreased at high altitude with a nadir at D2 (SLPRE: 78 ± 13 cm s-1; D2: 66 ± 11 cm s-1, P < 0.05). LV filling pressures index was decreased at high altitude with the minimum value obtained at D2 and remained reduced at SLPOST. Untwisting, an important factor of LV filling, was not decreased but was delayed at 4350 m. CONCLUSIONS: High-altitude exposure impaired LV diastolic function with the greatest effect observed at D2, concomitantly with the occurrence of AMS. The LV early filling impairments resulted from an increased RV afterload, a decrease in LV filling pressure and a delayed LV untwist. However, the increased LV twist probably acted as a compensatory mechanism to maintain cardiac performance during high-altitude hypoxia. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: The aim of this study was to analyse the underlying mechanisms of left and right ventricular (LV and RV) functional alterations during several days in high-altitude hypoxia. METHODS AND RESULTS: Resting evaluations of LV and RV function and mechanics were assessed by Speckle Tracking Echocardiography on 11 subjects at sea level (SLPRE), 3 ± 2 h after helicopter transport to high altitude (D0), at day 2 (D2), day 4 (D4) and day 6 (D6) at 4350 m and 5 ± 2 h after return to sea level (SLPOST). Subjects experienced acute mountain sickness (AMS) during the first days at 4350 m. LV systolic function, RV systolic and diastolic function, LV and RV strains and LV synchrony were unchanged at high altitude. Peak twist was increased at D0, continued to increase until D6 (SLPRE: 9.0 ± 5.1deg; D6: 13.0 ± 4.0deg, P < 0.05), but was normalized at SLPOST. Early filling decreased at high altitude with a nadir at D2 (SLPRE: 78 ± 13 cm s-1; D2: 66 ± 11 cm s-1, P < 0.05). LV filling pressures index was decreased at high altitude with the minimum value obtained at D2 and remained reduced at SLPOST. Untwisting, an important factor of LV filling, was not decreased but was delayed at 4350 m. CONCLUSIONS: High-altitude exposure impaired LV diastolic function with the greatest effect observed at D2, concomitantly with the occurrence of AMS. The LV early filling impairments resulted from an increased RV afterload, a decrease in LV filling pressure and a delayed LV untwist. However, the increased LV twist probably acted as a compensatory mechanism to maintain cardiac performance during high-altitude hypoxia. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: David A Holdsworth; Matthew C Frise; Josh Bakker-Dyos; Christopher Boos; Keith L Dorrington; David Woods; Adrian Mellor; Peter A Robbins Journal: Eur Respir J Date: 2020-09-17 Impact factor: 16.671