The severity of myocardial damage following acute myocardial infarction (AMI) is essentially influenced by the duration of coronary flow interruption during the acute episode. Furthermore the duration and severity of "culprit" lesion before AMI, as well as the presence of adequate collaterals to the culprit vessel represent important factors able to influence the severity of myocardial dysfunction after AMI. Left ventricular damage might evolve progressively depending on the infarct size, the presence of diffuse and severe coronary artery disease and concomitant systemic disease, such as diabetes and systemic hypertension. From a therapeutic point of view, in the presence of irreversible myocardial damage (scar tissue) following AMI medical therapy must be addressed to reduce myocardial consumption and to prevent ventricular dilatation. However myocardial dysfunction following AMI might be reversible (hibernated myocardium). It is of remarkable value the recognition of the hibernated but viable tissue because restoration of normal blood flow, which is the gold standard therapy in these patients, improves myocardial function and clinical outcome in AMI patients. In the presence of hibernated tissue following AMI, pharmacological therapy might temporarily protect the hibernated areas; however, when restoration of normal blood flow (myocardial revascularization) is not performed early, myocardial dysfunction might worsen and progressively evolve becoming irreversible event with restoration of normal coronary flow.