The renin-angiotensin-aldosterone system (RAAS) is both a trophic factor and an apoptotic trigger in postinfarct ventricular remodeling. Its cardiac paracrine impact on endothelium, small vessel tone, and fluid-electrolyte balance hastens the heart failure syndrome. Although the current consensus, based largely on first year follow-up data, favors modulating the RAAS with a combination of angiotensin-converting enzyme (ACE) inhibitors and ß-blockers, studies to date may have overestimated the degree of longerterm benefit. Meta-analysis of postinfarct trials shows that survival curves in patients with and without ACE-inhibitor therapy become roughly parallel after the initial 1 to 2 years. Thus, the RAAS may eventually become refractory to ACE inhibitor blockade. Ongoing trials aim to determine whether angiotensin II receptor blockade will prove more effective, in isolation or in combination with ACEI...