OBJECTIVE To review the evidence on the effects of angiotensin converting enzyme (ACE) inhibitors in coronary artery disease. METHODS In studies of experimental atherosclerosis involving hypertensive and normotensive hyperlipidemic animals, ACE inhibitors have had potent anti-atherogenic effects, reducing the total aortic intimal surface involved and the aortic cholesterol content. In balloon-injured animals, ACE inhibitors have suppressed the myointimal proliferative response in rats and rabbits, but not in higher species such as pigs and baboons, indicating possible species-specific effects. In spontaneously hypertensive rats, ACE inhibitors have modulated alterations in endothelium-related vasodilation, although similar effects have not been observed in human hypertension. METHODS ACE inhibition has not been shown to prevent restenosis after percutaneous transluminal coronary angioplasty. However, cardiac ischemic events have been prevented by ACE inhibition in patients with coronary artery disease and left ventricular dysfunction in a number of studies, including the Studies of Left Ventricular Dysfunction (SOLVD), Survival and Ventricular Enlargement (SAVE) study, Acute Infarction and Ramipril Efficacy (AIRE) study and the Gruppo Italiano per lo Studio della Streptochinesi dell'Infarto Micardico 3 (GISSI-3) trial. Other ongoing studies such as the QUinapril Ischemic Event Trial (QUIET) are assessing ACE inhibitor effects in patients with coronary artery disease and a normal left ventricular function. CONCLUSIONS ACE inhibitors prevent the development of atherosclerosis in hyperlipidemic animal models. They also prevent the myointimal proliferative response to injury in some animal models, but not in higher animal species or in humans. They can reduce the number of cardiac ischemic events in patients with coronary artery disease and left ventricular dysfunction; their effects in those patients with a normal left ventricular function are now being assessed.