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Effect of Hypobaric Hypoxia, Simulating Conditions During Long-Haul Air Travel, on Coagulation, Fibrinolysis, Platelet Function, and Endothelial Activation
William D. Toff, MD;
Chris I. Jones, MSc;
Isobel Ford, PhD;
Robert J. Pearse, RGN;
Henry G. Watson, MD;
Stephen J. Watt, MB,BS;
John A. S. Ross, MB, ChB, PhD;
David P. Gradwell, MB, PhD, DAvMed;
Anthony J. Batchelor, MB,BS, DAvMed;
Keith R. Abrams, PhD;
Joost C. M. Meijers, PhD;
Alison H. Goodall, PhD;
Michael Greaves, MD
JAMA. 2006;295:2251-2261.
Context The link between long-haul air travel and venous thromboembolism is the subject of continuing debate. It remains unclear whether the reduced cabin pressure and oxygen tension in the airplane cabin create an increased risk compared with seated immobility at ground level.
Objective To determine whether hypobaric hypoxia, which may be encountered during air travel, activates hemostasis.
Design, Setting, and Participants A single-blind, crossover study, performed in a hypobaric chamber, to assess the effect of an 8-hour seated exposure to hypobaric hypoxia on hemostasis in 73 healthy volunteers, which was conducted in the United Kingdom from September 2003 to November 2005. Participants were screened for factor V Leiden G1691A and prothrombin G20210A mutation and were excluded if they tested positive. Blood was drawn before and after exposure to assess activation of hemostasis.
Interventions Individuals were exposed alternately ( 1 week apart) to hypobaric hypoxia, similar to the conditions of reduced cabin pressure during commercial air travel (equivalent to atmospheric pressure at an altitude of 2438 m), and normobaric normoxia (control condition; equivalent to atmospheric conditions at ground level, circa 70 m above sea level).
Main Outcome Measures Comparative changes in markers of coagulation activation, fibrinolysis, platelet activation, and endothelial cell activation.
Results Changes were observed in some hemostatic markers during the normobaric exposure, attributed to prolonged sitting and circadian variation. However, there were no significant differences between the changes in the hypobaric and the normobaric exposures. For example, the median difference in change between the hypobaric and normobaric exposure was 0 ng/mL for thrombin-antithrombin complex (95% CI, –0.30 to 0.30 ng/mL); –0.02 nmol/L for prothrombin fragment 1 + 2 (95% CI, –0.03 to 0.01 nmol/L); 1.38 ng/mL for D-dimer (95% CI, –3.63 to 9.72 ng/mL); and –2.00% for endogenous thrombin potential (95% CI, –4.00% to 1.00%).
Conclusion Our findings do not support the hypothesis that hypobaric hypoxia, of the degree that might be encountered during long-haul air travel, is associated with prothrombotic alterations in the hemostatic system in healthy individuals at low risk of venous thromboembolism.
Author Affiliations: Departments of Cardiovascular Sciences (Drs Toff and Goodall and Messrs Jones and Pearse) and Health Sciences (Dr Abrams), University of Leicester, Leicester, England; Departments of Medicine and Therapeutics (Drs Ford, Watson, and Greaves) and Environmental and Occupational Medicine (Drs Watt and Ross), University of Aberdeen, Aberdeen, Scotland; Royal Air Force Centre of Aviation Medicine, Henlow, Bedfordshire, England (Drs Gradwell and Batchelor); and Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands (Dr Meijers).
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