Activation of the renin-angiotensin system (RAS) has been implicated in the pathogenesis of acute myocardial infarction (AMI). Similarly, reduced fibrinolytic activity has been associated with an increased risk of AMI. Evidence is now accumulating that the RAS plays an important role in the regulation of fibrinolysis and that pharmacological interruption of the RAS exerts a positive effect on endogenous fibrinolytic balance. This relationship appears to provide a partial explanation for the newly recognized effect of angiotensin converting enzyme inhibitors in preventing AMI.