Coronary plaque formation has been

Coronary plaque formation has been well underway prior to NSTE-ACS presentation8. The plaque prone to cause ACS has a thin fibrous cap, large lipid pool and is susceptible to disruption via inflammation, metalloproteinases and collagenases (Fig. 1). Intra-plaque hemorrhage, plaque neovascularization and outward (positive) vessel wall remodeling further identify the vulnerable plaque. After a triggering event, a superimposed thrombus forms upon contact between luminal blood and the plaque’s highly thrombogenic lipid core; in 20–40% of ACS, coronary thrombosis occurs with only superficial plaque erosion (Fig. 2, Movies 1–4) rather than plaque rupture. Myocyte necrosis ensues via either subtotal occlusion or transient episodes of flow reduction (Fig. 1). In UA, subtotal occlusion and transient ischemia stop short of myocardial necrosis. Embolization of plaque and thrombotic materials may occlude the downstream microvasculature9. External compression by edematous tissue, in situ thrombosis, vasospasm, leukostasis and reperfusion injury exacerbate microvascular obstruction and myocyte necrosis, particularly after mechanical reperfusion.