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Updated: Sep 12, 2026

Stenosis of the Inferior Vena Cava: A Murine Model of Deep Vein Thrombosis
Published on: December 22, 2017
Pathophysiology of venous thromboembolism
1Cardiology Department, Skejby Hospital, University of Aarhus, Denmark.
Abstract:
Venous thromboembolism is complex with a multifactorial etiology. The Virchow triad (changes in blood flow, changes in vessel wall, and changes in the properties of blood) gives the main factors involved in venous thromboembolism. Venous stasis during immobilization in general anesthesia, stroke with hemiparesis, and heart failure plays a central role. The thromboembolic process can be initiated by a disturbance in the normal "hemostatic balance," with an increased thrombogenic potential, due to release of thromboplastin and collagen exposure during vessel wall injury by stasis and hypoxia, decreased fibrinolysis during surgery, malignancy, among others. Many substances modify these processes, including heparan sulfate, AT III, protein C, t-PA inhibitor, and alpha 2-antiplasmin.
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