The formation of a haemostatic thrombus is a useful defence mechanism for the closure of vascular lesions. However, undesirable thrombi are also formed in closed vessels, e.g. over atherosclerotic plaques or after rupture of such plaques. It has long been assumed that the primary function of the fibrinolytic system consists of dissolving such thrombi, a task to which it often does not measure up. Indeed, repeat venography in patients with deep venous thrombosis treated with heparin and oral anticoagulation alone often shows only minimal resorption of the venous thrombus (Duroux et al. 1991). The situation is somewhat more favourable for arterial thrombi. The classical work of Dewood et al. (1980) has demonstrated that coronary thrombi undergo thrombolysis in the absence of thrombolytic therapy. While thrombotic lesions were present in 87% of patients undergoing coronary angiography 1–4 h after the onset of symptoms, this figure was only 68% in patients examined 6–12 h after start of symptoms (p < 0.01). In the UPET study the spontaneous recanalisation of pulmonary emboli was quite remarkable. Seven days after the embolic event, pulmonary angiography no longer showed a difference between control patients and those who had been treated with urokinase (Urokinase Pulmonary Embolism Trial 1970).