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Updated: Jun 24, 2026

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
Published on: May 24, 2020
Pathophysiology of venous thrombosis
1Puget Sound Blood Center and University of Washington, Seattle, USA. josel@psbcresearch.org
Using Virchow's triad as framework, it is clear that alterations in any of its components (blood composition, the vessel wall, and blood flow) can influence the propensity for the development of venous thromboembolism. Each can also influence the others in ways that enhance or reduce thrombotic propensity. While past work has concentrated on blood components that influence thrombogenicity, their influences generally are manifest only after the thrombotic process has begun, and it is initiation of thrombosis on the vessel wall that is the least well understood. This brief review attempts to link risk factors such as stasis and cancer to the mechanisms that initiate thrombosis.
Using Virchow's triad as framework, it is clear that alterations in any of its components (blood composition, the vessel wall, and blood flow) can influence the propensity for the development of venous thromboembolism. Each can also influence the others in ways that enhance or reduce thrombotic propensity. While past work has concentrated on blood components that influence thrombogenicity, their influences generally are manifest only after the thrombotic process has begun, and it is initiation of thrombosis on the vessel wall that is the least well understood. This brief review attempts to link risk factors such as stasis and cancer to the mechanisms that initiate thrombosis.
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