Reduced risk of myocardial infarction (MI) mortality with angiotensin-converting enzyme (ACE) inhibition suggests a link between the renin-angiotensin-system (RAS) and fibrinolytic function. Excessive endothelial production of plasminogen activator inhibitor type 1 (PAI-1) and deficient endothelial secretion of tissue-type plasminogen activator (t-PA) are associated with thrombosis and ischemic events, such as stroke, atherosclerosis, and MI. Angiotensin II (A-II) regulates PAI-1 production. Suppression of A-II formation by ACE inhibitors likely has a positive effect on Fibrinolytic balance by reducing the production of PAI-1. ACE inhibition also enhances bradykinin levels, which, in turn, increases t-PA secretion and further reduces thrombotic tendency.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Myocardial Ischemia|
|Issue number||SUPPL. 1|
|State||Published - Jan 1 1995|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine