The main problem after originally successful thrombolytic reperfusion is early thrombotic reocclusion which occurs in up to 20% despite adequate anticoagulant therapy. Early rethrombosis can be attributed to a permanent procoagulatory state caused by residual stenosis, residual thrombosis, by a "paradoxical" procoagulatory effect of the thrombolytic agents used, and by the existence of systemic thrombogenic risk factors. Thereby, most important mechanisms of rethrombosis are generation, exposition and activation of thrombin and a thrombin-induced increase in platelet aggregability. Up to now, therapeutic measures have not proved useful (early balloon angioplasty, prolonged t-PA infusion), have not been effective enough (platelet inhibition with aspirin, anticoagulation with heparin), or are not entirely investigated (combination therapy of fibrin-specific with non-specific thrombolytic agents, use of t-PA mutants with prolonged biological efficacy). As far as thrombin plays the key role in the process of rethrombosis, it is believed that the use of specific and highly active thrombin inhibitors, e.g. hirudin, might mostly be appropriate in solving the problem of "reocclusion".