The Role of Hypoxia and Platelets in Air Travel-Related Venous Thromboembolism

Abstract

Although somewhat controversial, there is good evidence that long-distance travel in general is a risk factor for venous thromboembolism, even in the absence of other risk factors. This is probably due to effects consequent to prolonged sitting but air travel in particular may be associated with risk factors other than this. One likely factor is hypoxia caused by the low ambient pressure of aircraft cabins. There is an association between venous thromboembolism and the hypoxia of altitude, chronic respiratory disease, neonatal hypoxia, sleep apnoea and experimentally-induced hypoxia. Platelet number and/or function are altered in all of these circumstances. Platelet aggregation is pivotal to venous thromboembolism and hypoxia alters platelet number and function. The early-onset thrombocytosis caused by hypoxia may be due to increased release of platelets from megakaryocytes and the late-onset thrombocytopaenia may be due to decreased platelet production and/or stem cell competition between erythrocytes and megakaryocytes. Hypoxia-induced platelet activation and aggregation may be due to increased circulating catecholamine levels but it is not known whether hypoxia can affect platelets directly. There is a need for further studies on the possible involvement of hypoxia-induced changes in platelet number and function in air travel-related venous thromboembolism.

Extracellular Chromatin Is an Important Mediator of Ischemic Stroke in Mice

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Early Adaption to the Antarctic Environment at Dome C: Consequences on Stress-Sensitive Innate Immune Functions

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Blood Platelets and Systemic Sclerosis

“…SSc-associated microangiopathy results in a disturbed blood flow in the capillaries with consequent hypoxia, which is likely to be aggravated by tissue fibrosis [169][170][171][172]. Hypoxia alters vascular endothelium but also directly activates platelets [173,174] (our unpublished results). Altogether, conditions that turn EC phenotype to proinfammatory/prothrombotic are translated into platelet adhesion and activation, with the consequent release of inflammatory, mitogenic, angiogenic and fibrogenic platelet-derived mediators described above.…”