Myocardial infarction is an anatomical and therefore functional amputation of some of the myocardial tissues. Moments after acute coronary occlusion, a cascade of metabolic, mechanical and electrical ischaemia related events is observed. Contraction stops and regional left ventricular akinesis (then dyskinesis) occurs in the zone at risk of irreversible myocardial damage. This is partially compensated by hyperkinetic motion of non-ischaemic myocardium. The degree of alteration of the global ejection fraction is the resultant of these akinetic and hyperkinetic wall motions. It is lower in cases of anterior myocardial infarction, of occlusion of the proximal segment of the left anterior descending artery and of multivessel disease. Its eventual outcome depends on coronary blood flow. If the artery responsible is recanalized early, the global ejection fraction stabilises or improves. When this does not happen, the global ejection fraction decreases. The end-diastolic volume, an indicator of left ventricular remodeling, increases in relation to the size of the infarct and to the persistence of coronary artery occlusion. The delay before the appearance of the first irreversible lesions, the rate of their propagation within the myocardial wall and the presence of reperfusion lesions are poorly understood factors in the clinical setting and influence the efficacy of methods of myocardial protection.