Apart from their established use in the treatment of
hypertension and
heart failure,
ACE inhibitors have been suggested to exert anti-ischemic effects. This article reviews the mechanisms of systemic and intracardiac
angiotensin formation, as well as its interaction with the
bradykinin, the
prostaglandin, and the sympathetic nervous system. While high doses of
angiotensin can precipitate
myocardial ischemia. experimental data on a potential beneficial effect of
ACE inhibitors on ischemic myocardial blood flow and function are inconsistent and controversial. Pooling the few available clinical data, several
ACE inhibitors may attenuate
myocardial ischemia at rest and during exercise. However, a significant fraction of patients does not benefit or even deteriorates. Recent experimental studies suggest a beneficial role of
ACE inhibitors in attenuating reperfusion arrhythmias and postinfarction
left ventricular remodeling. Unless the mechanisms and determinants of potential anti-ischemic actions of
ACE inhibitors can be better defined, their use for treatment of
myocardial ischemia cannot be recommended at present.