Activation of the renin-angiotensin system (RAS) has been implicated i
n the pathogenesis of acute myocardial infarction (AMI). Similarly, re
duced 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 interr
uption of the RAS exerts a positive effect on endogenous fibrinolytic
balance. This relationship appears to provide a partial explanation fo
r the newly recognized effect of angiotensin converting enzyme inhibit
ors in preventing AMI.