ACE Inhibitor and ARB Therapy ACE inhibitors exert their effects by suppressing the effects of angiotensin II, a potent vasoconstrictor that reduces renal perfusion, stimulates LV hypertrophy and cardiac remodel- ing, and enhances the release of arginine, vasopressin, proin- flammatory cytokines, and aldosterone.237 Inhibition of ACE results in decreased levels of angiotensin II and inhibits the breakdown of bradykinin, a peptide with favorable properties, including antihypertensive, antiremodeling, and natriuretic effects. ARBs directly inhibit the action of angiotensin II by blocking the type 1 receptor, but their effects on bradykinin Oral ACE inhibitors have been shown to reduce symptom- atic heart failure and mortality among patients with previous MI and reduced EF.241 243 Among patients with reduced EF and active or prior heart failure symptoms, ACE inhibitors reduce mortality and heart failure hospitalization, improve New York Heart Association (NYHA) classification, reduce heart size, and prevent the need for escalating medical therapy.244 246 The routine initiation of an ACE inhibitor early after CABG is not recommended for patients with an EF >40%.233 However, it is unlikely that surgical revascularization mitigates the benefits of an ACE inhibitor in the post-CABG patient with a persis- tently reduced EF. 