It was shown in ischemia/reperfusion models that after reopening of the occluded epicardial coronary artery, following initial hyperemic flow, myocardial blood flow in the area at risk rapidly and progressively declines and get stabilised approximately within 30 minutes.This finding implies that, in spite of the initial ischemic insult, coronary auto-regulation in the reperfused myocardial territory recovers. Nevertheless, this recovery requires some time after reperfusion was achieved. During total occlusion of an epicardial coronary artery, pre-arteriolar sphincters can be expected to be paralysed in widely open position in response to severely increased distal myocardial demand. Ischemic myocyte damage also contributes to malfunctioned pre-arteriolar sphincters. Therefore, full restoration of perfusion pressure distal to the infarct related artery by immediate stenting (direct or after angioplasty) may then fail to induce an immediate adaptive autoregulatory response (compensatory vasoconstriction) in the related microvascular territory, resulting in an inappropriately increased pressure in the damaged microcirculation. During total epicardial occlusion, ischemia/hypoxia induced damage and increased permeability at the capillary level lead to loss of structural integrity in the related microvascular territory. After immediate stenting, this severely damaged microcirculation is exposed to a suddenly increased uncontrolled intracoronary pressure which may consequently substantially contribute to intramyocardial haemorrhage and oedema.