The metabolic syndrome is characterized by a combination of obesity, chronic inflammation and insulin resistance. This syndrome also has features of a hypercoagulable state, consisting of increased levels of clotting factors (tissue factor, factor VII and fibrinogen) as well as inhibition of the fibrinolytic pathway (increased plasminogen activator inhibitor-1 and decreased tissue plasminogen activator activity). Simultaneously, the presence of endothelial dysfunction and dyslipidemia triggers platelet aggregability, thus further increasing the risk of thrombotic events both in the arterial and venous system. Although mechanisms of coagulation activation are well described for other diseases, the precise etiology is not well known in the metabolic syndrome. Thus far, only obesity has been shown to be a modest risk factor for venous thromboembolic events, whereas accurate data for metabolic syndrome patients are lacking. Hence, routine interventions for prevention of venous thromboembolism are not yet warranted. However, as dyslipidemia is associated with procoagulant changes, this could be a possible target for therapeutic intervention. In view of the rising incidence of metabolic syndrome even at a young age, both the incidence of venous thromboembolism and the effect of intervention on markers of hypercoagulability in metabolic syndrome call for further studies.