ACE inhibitors result in a reduction in angiotensin II with an increase in bradykinin. These changes in the physiological balance between angio- tensin II and bradykinin could contribute to the reductions in LV and vascular hypertrophy, atherosclerosis progression, plaque rupture, and thrombosis; the favorable changes in cardiac hemodynamics; and the improved myocardial oxygen supply/demand that result from treatment with ACE inhibi- tors and ARBs.798 801 Clinical studies have demonstrated significant reductions in the incidence of AMI, UA, and the need for coronary revascularization in patients after MI with LV dysfunction, independent of etiology.559,561,801 The benefits of ACE inhibitors extend to patients with IHD in the absence of LV dysfunction. In patients with Fihn et al Stable Ischemic Heart Disease: Full Text e405 atherosclerotic vascular disease or diabetes mellitus and at least 1 other IHD risk factor, the HOPE (Heart Outcomes Prevention Evaluation) study301 showed that compared with placebo, ramipril significantly decreased the primary composite endpoint of cardiovascular death, AMI, and stroke by 22%.301 MICRO-HOPE (Microalbuminuria, Car- diovascular, and Renal Outcomes), a substudy of HOPE, additionally showed, in middle-aged patients with diabetes mellitus who were at high risk for cardiovascular events, significant reductions in MI by 22%, stroke by 33%, cardiovascular death by 37%, and the combined primary event outcome by 25%.802 Furthermore, the need for revascularization and incidence of worsening angina also were significantly reduced. 