Explanations for coagulation activation after air travel

Summary Background:It is unknown whether venous thrombosis after long haul air travel is exclusively attributable to immobilization. Objectives:We determined whether the following mechanisms were involved: hypoxia, stress, inflammation or viral infection. Patients/Methods: In a case crossover setting in 71 healthy volunteers who were exposed to an 8-h flight, 8-h movie marathon and 8 h of regular activities, we compared markers for several hypothetical pathways: plasminogen activator inhibitor-1 (PAI-1), stress, plasma factor (F)VIII coagulant activity (FVIIIc), soluble P-selectine (sP-selectine), interleukin-8 (IL-8) and neutrophil elastase. We reported earlier an activated clotting system, as evidenced by thrombin generation, in 17% of volunteers after the flight. Results:PAI-1 increased by 4.2 ng mL−1 (CI95:−49.5 to 6.5) in volunteers with an activated clotting system whereas it decreased in those without (−20.0 ng mL−1, CI95:−33.2 to −14.0). FVIIIc levels rose more in individuals with clotting activation (18.0%, CI95:−1.0 to 33.0) than in those without (2.0%, CI95:−2.0 to 5.0). The increases in FVIIIc were not associated with stress, which appeared unrelated to clotting activation. sP-selectin increased in those with clotting activation (3.5 μg L−1, CI95: −3.0 to 10.0), but decreased in those without (−0.5 μg L−1, CI95: −2.0 to 2.0). Changes in levels of neutrophil elastase or IL-8 were not different between the subjects with and without clotting activation. Conclusions:Our results do not support the hypotheses that stress, infection or air pollution are involved in the development of a prothrombotic state in air travellers. After long haul air travel, this state is more pronounced in patients with risk factors and may be caused by hypoxia, triggering systemic inflammation and platelet activation, leading to coagulation induction and degranulation of platelets.