ABSTRACT
The incidence of chronic venous insufficiency was approximately 29% after 8 years in treated patients, with the development of ipsilateral recurrent venous thrombosis being strongly associated with an increased risk of this syndrome. The acute phase or thrombogenesis is led by neutrophils and the chronic phase or thrombus resolution is led by monocytes, progressively increasing fibrin deposition. Pro-inflammatory and anti-inflammatory mediators are involved in the ultimate vein wall and thrombus response. Tissue factor expression on monocyte surfaces promotes monocyte interactions with activated platelets and endothelial cells, leading to fibrin formation and deposition into the developing thrombus. The effect of plasminogen activator inhibitor-1 inhibition has been studied by S. Baxi in a rat stenosis model, demonstrating that its inhibition significantly reduced thrombus weight compared to controls. Although polymorphonuclear neutrophils may cause vein wall injury, they are essential for early thrombus resolution by promoting both fibrinolysis and collagenolysis.
