Thrombosis is the main cause of acute coronary syndrome and myocardial infarction (Naghavi et al., 2003). The mechanism underlying thrombus formation is presently under debate, but several pathological conditions have been identified fromhuman postmortem studies that correspondwith the presence of thrombus. Of these conditions plaque rupture is the most common, but erosion of the endothelial layer and existence of calcified nodules without the existence of plaque rupture have also been identified. Plaques that have been ruptured have certain features in common (Falk, 1999; Virmani et al., 2002): (i) size of the lipid core (40% of the entire plaque), (ii) thickness of the fibrous cap (less than 65 μm), (iii) presence of inflammatory cells, (iv) amount of remodeling and extent of plaque-free vessel wall. Several terms have been identified focusing either on the pathological aspects (“thin-cap fibroatheroma”) or on the possibility to rupture (“rupture-prone plaques”) or on the possibility to induce thrombosis (“vulnerable plaque”). As vulnerable plaque is the term encompassing all other terms, therefore this term will be used throughout the chapter.