PATHOPHYSIOLOGICAL MECHANISMS OF DEEP VEIN THROMBOSIS

Abstract

Deep venous thrombosis is a frequent multifactorial disease and most of the time is triggered by the interaction between acquired risk factors, particularly immobility, and hereditary risk factors such as thrombophilias. The mechanisms underlying deep venous thrombosis are not fully elucidated; however, in recent years the role of venous flow, endothelium, platelets, leukocytes, and the interaction between inflammation and hemostasis has been determined. Alteration of venous blood flow produces endothelial activation, favoring the adhesion of platelets and leukocytes, which, through tissue factor expression and neutrophil extracellular traps formation, contribute to the activation of coagulation, trapping more cells, such as red blood cells, monocytes, eosinophils, lymphocytes. The coagulation factor XI-driven propagation phase of blood coagulation plays a major role in venous thrombus growth, but a minor role in hemostasis. In this work, the main mechanisms involved in the pathophysiology of deep vein thrombosis are described.