The Basic Principles of Pathophysiology of Venous Thrombosis

The past few decades have brought tremendous insight into the molecular and pathophysiological mechanisms responsible for thrombus generation. For the clinician it is usually sufficient to explain the incident deep vein thrombosis (DVT) with provoking factors such as trauma with vascular injury, immobilization, hormonal factors, or inherited or acquired coagulation defects. About half of the DVTs are, however, lacking such triggers and are called unprovoked. Venous stasis and hypoxia at the valve sinus level may start a chain of reactions. In order to better understand the mechanisms behind DVT and reach beyond the above-mentioned simplifications animal models and clinical epidemiological studies have informed of the complex interplay between leukocytes, platelets, endothelium, cytokines, complements and coagulation factors and inhibitors. These pathways and the interplay will be reviewed here.