the fibrinolytic degradation product D-dimer in plasma (110-250 ng/ ml).Therapy with tPA alone was believed to the biological pathway.However, this idea represented a fundamental misunderstanding of the biological system, which remains to be addressed [1].Ever since the FDA approved tPA for the treatment of AMI I 1987, it has been the activator choice.However, the body has two plasminogen activators, the second one being urokinase Plasminogen Activator (uPA), the native form of which is a proenzyme (prouPA) [2].Since both are required for an effective and safe fibrinolytic effect, the full potential of fibrinolytic therapy has never been evaluated.