Venous and arterial thromboembolic disorders are usually considered as two separate pathophysiological entities. At first glance, this belief appears to be indisputable. Arterial thrombi consist mainly of platelets and are induced by arterial plaque ruptures that tend to occur at sites where shear rates are high. Conversely, venous thrombi consist mainly of red blood cells and fibrin and tend to occur at sites where the vein wall is often normal, but blood flow and shear rates are low [1]. Furthermore, major known risk factors for arterial thrombosis (e.g. tobacco smoking, arterial hypertension, diabetes, and dyslipidemia) appear to differ somewhat from risk factors that are known to provoke venous thrombosis (e.g. trauma, surgery, and cancer).