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Published on: February 14, 2017
Explanations for coagulation activation after air travel
A J M Schreijer1, M F Hoylaerts, J C M Meijers
1Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, the Netherlands.
Journal of Thrombosis and Haemostasis : JTH
|February 24, 2010
Summary
Long haul air travel may induce a prothrombotic state, not solely due to immobilization. Hypoxia, inflammation, and platelet activation appear to be key factors, particularly in individuals with risk factors.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Aerospace Medicine
Background:
- Venous thromboembolism (VTE) risk after long haul flights is a concern.
- The role of immobilization as the sole cause of VTE is debated.
Purpose of the Study:
- To investigate potential mechanisms beyond immobilization contributing to VTE risk.
- To assess the involvement of hypoxia, stress, inflammation, and viral infection.
Main Methods:
- Case-crossover study with 71 healthy volunteers exposed to an 8-hour flight.
- Measured markers: plasminogen activator inhibitor-1 (PAI-1), stress, factor VIII coagulant activity (FVIIIc), soluble P-selectin (sP-selectin), interleukin-8 (IL-8), and neutrophil elastase.
- Assessed activated clotting system via thrombin generation post-flight.
Main Results:
- Clotting activation observed in 17% of volunteers post-flight.
- Increased PAI-1, FVIIIc, and sP-selectin in those with clotting activation.
- Stress, IL-8, and neutrophil elastase levels did not correlate with clotting activation.
Conclusions:
- Findings do not support stress, infection, or air pollution as primary drivers of prothrombotic state.
- Hypoxia, systemic inflammation, and platelet activation are implicated in VTE development.
- Prothrombotic state is exacerbated in air travelers with pre-existing risk factors.
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