Pathogenesis of venous thrombosis: a new insight.

Overview

Venous thrombosis and thrombophlebitis have long been observed to result in painful inflammation around the affected veins. The full extent of the synergistic interaction between thrombosis and the inflammatory response and how this leads to the later sequelae of chronic venous insufficiency is only now beginning to be understood. Venous thrombosis is known directly to elicit an inflammatory response in the thrombus and vein wall. Leukocytes including neutrophils and monocytes roll, adhere, activate and extravasate into the vein wall based on a vein wall cytokine/chemokine gradient producing an inflammatory response. Such a response leads to amplification of thrombus formation through mechanisms such as the elaboration of tissue factor on the surface of monocytes and the release of cathespin G from activated neutrophils (distrupting the endothelial cell barrier), exposing the thrombogenic subendothelial vein wall collagen. Selectins such as P-selectin and the proinflammatory cytokine tumor necrosis factor appear important in this vein wall response. Inhibition of inflammation before the initiation of the thrombotic event may decrease the detrimental vein wall changes that contribute to vein wall and vein valve damage and thrombus formation.