Volume 11 Supplement 1

Abstracts of the 12th Annual SCMR Scientific Sessions – 2009

Open Access

Mt Everest trek causes impaired cardiac high energy phosphate metabolism and diastolic impairment

  • Cameorn J Holloway1,
  • Andrew Murray1,
  • Lowri E Cochlin1,
  • Yaso Emmanuel1,
  • Denny ZH Levett2,
  • Oliver J Rider1,
  • Damian J Tyler1,
  • Matthew Robson1,
  • Jane M Francis1,
  • Hugh Montgomery2,
  • Michael PW Grocott2,
  • Stefan Neubauer1 and
  • Kieran Clarke1
Journal of Cardiovascular Magnetic Resonance200911(Suppl 1):O6

https://doi.org/10.1186/1532-429X-11-S1-O6

Published: 28 January 2009

Background

Cardiac function in normal subjects is altered by exposure to hypobaric hypoxia, yet the cellular mechanisms leading to such changes are unknown. We have examined the impact of sustained exposure to environmental hypobaric hypoxia, on cardiac function and energetics.

Methods and results

Healthy normal volunteers (n = 7) were studied immediately before, and within four days of return from 17 days exposure to environmental hypobaric hypoxia whilst trekking to Mount Everest Base Camp (17388 feet, 5300 m) and back. 31P magnetic resonance (MR) spectroscopy was used to measure cardiac phosphocreatine (PCr)/ATP, and MR imaging and echocardiography were used to assess cardiac function. All measurements were repeated six months after return from Everest. Immediately after their return from Everest, subjects showed a 24% decrease in cardiac PCr/ATP, from 2.19 ± 0.09 to 1.67 ± 0.13 (p < 0.01) (see Figure 1). Peak left ventricular filling rates had declined from 832 ± 64 ml/sec to 691 ± 56 ml/sec (p < 0.05) and transmitral E/A was reduced from 1.56 ± 0.11 to 1.16 ± 0.08 (p < 0.05). Left and right ventricular stroke volumes had fallen by 13%. No change on cardiac mass was observed. Six months later, all measures had returned to baseline values.

Figure 1

Conclusion

Exposure to prolonged hypobaric hypoxia is associated with significant, but reversible, energetic and functional abnormalities in the human heart.

Authors’ Affiliations

(1)
University of Oxford
(2)
UCL, London

Copyright

© Holloway et al; licensee BioMed Central Ltd. 2009

This article is published under license to BioMed Central Ltd.

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