The role of the platelets in the pathogenesis of venous thrombosis is still not fully defined. Evidence suggests that platelets contribute to venous clot formation, particularly under certain circumstances. Supporting evidence comes from laboratory studies as well as from clinical trials investigating the role of antiplatelet therapy.
In addition to their well-known function in thrombosis and hemostasis, platelets also mediate vascular integrity and regulate angiogenesis. The connection between hypercoagulation, thrombosis, and malignancy is by now well established. Thrombin exerts effects on tumor cells, vascular endothelium, and platelets, enhancing tumor cell growth, adhesion, angiogenesis, metastasis, and thrombosis. Thrombin thereby potentiates the malignant phenotype and initiates a “vicious cycle.”
PLATELETS IN VENOUS THROMBOSIS
The role of platelets in arterial thrombosis has been well defined, as noted elsewhere in this volume. Under conditions of high flow or shear stress, such as those found in arterioles, collagen exposed by injury to the endothelial surface activates von Willebrand factor, which subsequently recruits platelets to the site of injury or vessel narrowing. The platelets become activated and both recruit additional platelets as well as facilitate coagulation at the site of the nascent clot. The role of the platelet in venous thrombosis is less clear. However, several lines of evidence indicate that platelets are also involved in the pathogenesis of venous thromboembolism (VTE).