Angiotensin converting enzyme (ACE) inhibitors (ACE-I) reduce the incidence of re-infarction in patients with myocardial infarction (MI), and the DD genotype for the ACE gene is an independent risk factor of MI. These findings suggest involvement of ACE in the natural history of coronary plaques and in the pathogenesis of acute coronary syndrome (ACS). ACE-I potentially prevent coronary plaque rupture by suppressing angiotensin II-induced vasoconstriction and sympathetic nerve activity. Actions of ACE-I on risk factors, including insulin resistance, may retard the progression of atheromatous changes in the coronary artery. Furthermore, ACE-I attenuate contractile dysfunction due to myocardial stunning and hibernation, while it augments anti-infarct tolerance of the myocytes afforded by preconditioning. These actions on the myocardium may also be beneficial in ACS. Although favorable effects of ACE-I on the mortality rate of MI patients has been established, the benefit of chronic therapy with ACE-I for patients who have coronary artery disease without MI remains to be clarified.