Heart failure is a worldwide health problem. It appears most often in patients with ischemic cardiomyopathy. Angiotensin-converting enzyme (ACE) inhibitors have been shown to improve survival and quality of life in patients with chronic heart failure, whether asymptomatic and without renin-angiotensin-aldosterone system (RAAS) activation or symptomatic and with RAAS activation, as well as in patients with acute myocardial infarction (MI) accompanied by left ventricular systolic dysfunction. Factors responsible for these salutory responses are under investigation. MI involves a segmental loss of cardiac myocytes followed by tissue repair, ie, scar tissue formation (“the good”). Fibrosis also appears remote to the MI (“the bad”) and is considered the major component of adverse structural remodeling. De novo generation of angiotensin (Ang) II at sites of repair by myofibroblasts regulates the fibrogenic cytokine TGF-ß1, thus modulating the expression of extracellular matrix proteins. Chronic activation of the circulating RAAS and elevations in its effector hormones—Ang II and aldosterone—promote further fibrosis (“the ugly”) at these sites. This overview addresses: (i) post–MI rebuilding and remodeling; (ii) the molecular and cellular events and regulatory signals involved in tissue repair; (iii) pharmacologic and molecularbased approaches as cardioprotective strategies; and (iv) the potential use of noninvasive monitoring modalities and genetic predisposition to remodeling...