Involvement of inflammatory markers in pathogenesis of venous thromboembolism

Inflammation of the venous wall is involved in thrombogenesis, thrombus resolution, wall remodeling and the post-thrombotic syndrome. Different mechanisms are involved in both arterial and venous thrombosis and patients with atherothrombosis hold a higher risk of venous thrombosis. Although inflammation may represent the connection between arterial and venous thrombosis, it is not yet sure if it is the cause or consequence of venous thrombosis. Consequently, the relationships between inflammation markers as indicators of the inflammatory process and clinical venous thromboembolism need to be investigatd. For example, inflammation mediators such as the pro-inflammatory cytokines interleukin 8 (IL-8), IL-6, monocyte chemotactic protein 1 (MCP-1), C Reactive Protein (CRP), vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), matrix metalloproteinases and tumor necrosis factor alpha (TNF alpha) are all involved in thrombogenesis. Studies of venous thromboembolism on animal models proved that there are specific phases of the inflammatory process in venous thromboembolism and thrombus resolution. Knowing the molecular and immunologic mechanisms, identifying and understanding the inflammation markers which are relevant for venous thrombosis, can help to target specific pathways and to develop future therapies of this disease