Many studies in recent years have dealt with the use of angiotensin converting enzyme (ACE) inhibitors for the treatment of ischemic heart disease. The renin-angiotensin system is widely distributed in plasma and peripheral tissues and is activated following certain conditions including myocardial ischemia. The effects of ACE inhibitors on the ischemic heart are apparently many and achieved through a blockade of plasma and tissue ACE as well as through their property of scavenging free radicals. Captopril seem to exert a beneficial effect in preventing heart failure after myocardial infarction probably by restoring the contractile function of infarcted myocardium. An antianginal effect of ACE inhibitors has been demonstrated in patients with coronary artery disease along with a potentiation of isosorbide dinitrate coronary vasodilator capacity. The antiarrhythmic efficacy, clearly evident in animal models, deserves further investigations in humans. The above listed effects of ACE inhibitors and the suppressive action demonstrated for captopril on platelet aggregation could represent a very useful tool for the future treatment of patients with coronary artery disease.