The total ischemic myocardial burden starts from the production of atherosclerotic plaque initiated by events affecting endothelial integrity. The development of fissure rupture, thrombus formation and the role of vasospastic mechanisms lead to a significant epicardial arterial occlusion. Microvascular occlusion by leucocyte pllead to a no-reflow phenomenon. Even at AMI, spontaneous reperfusion, frustrated phagocyte bursts and vasoactive events produce free radicals to overcome tissue oxygen radical scavengers. Repurfusion injuries causing lethal or non-lethal intracellular damage and/or fatal and non-fatal arrhythmia have been documented in experimental and human studies. Thus, the additive role of anti-oxidants seems to give a promising future in maximizing myocardial salvage at the acute myocardial infarction phase of the total ischemic myocardial burden.