**1.3 Limitations and problems of contemporary treatment**

The main goal of primary PCI is to open the occluded epicardial coronary artery, and thus to re-establish blood flow to the jeopardized myocardium. In order to nourish the myocardium, blood must flow through the epicardial coronary artery segments, resistance vessels, arterioles and capillaries before reaching venules and veins. The epicardial coronary arteries are larger than 400 um, serve as conduit vessels and their diameter is regulated by shear stress and do not contribute significantly to pressure drop. Coronary resistance vessels with diameter between 100 and 400 um are affected myogenically mainly by shear stress and luminal pressure. Resistance coronary vessels with diameter less than 100um are sensitive to local tissue metabolism and directly control perfusion to the low pressure capillary bed nourishing the myocardium. Myocardial capillary density is 3500/mm2 with inter-capillary distance of 17 um , greater in the subendocardium than in the subepicardium (Canty, 2008).

Microvascular injury is the leading cause for the decreased myocardial perfusion observed in about 80% of patients after successful PCI (Gibson et al, 2000; Stone et al, 1997; Zijlstra et al, 1997; Kondo et al, 1998). Various factors contribute to the limited myocardial perfusion, including micro-emboli, platelets, white blood cells, ischemic necrosis, and reperfusion injury(Chesebro et al, 1987; van't Hof, 1998; Gibson et al, 2000; Stone et al, 2002).
