ABSTRACT
The purpose of this chapter is to summarize the current knowledge regarding the coronary plaque rupture in patients with ACS.
In vitro pathological studiesdemonstrated that most cases of ACS are thought to result from sudden luminal narrowing caused by
thrombosis based on plaque rupture, erosion, and superfi cial calcifi ed nodule (Naghavi et al. 2003, Virmani et al. 2005). Within these three different pathologies, plaque rupture has been reported to be the most frequent, plaque erosion to be the second and superfi cial calcifi ed nodule to be the least (Naghavi et al. 2003, Virmani et al. 2005).Plaque rupture is defi ned as a lesion consisting of a large necrotic core with ruptured thin fi brous cap with overlying thrombus, and thin-cap fi broatheroma (TCFAs) without rupture are thought to be precursor lesions of ACS in pathology(Virmani et al. 2005). Plaque erosion demonstrates intra-luminal thrombus without discontinuity of the thick fi brous cap even in cases with necrotic core, although it is mostly devoid of a necrotic core (Naghavi et al. 2003, Virmani et al. 2005). Superfi cial calcifi ed nodule, the least frequent cause of intracoronary thrombus, reveals the discontinuity of fi brous cap without endothelial cells by bony calcifi ed nodule with overlying thrombus. Based on these three different features of plaque morphology in the culprit lesion in ACS, vulnerable plaques, which are defi ned as plaques prone to disruption and to be culprit plaques with thrombus, are proposed by fi ve major and fi ve minor criteria as listed in Table 3.1 (Naghavi et al. 2003). Major criteria for detection of a vulnerable plaque is as follows. (1) Active infl ammation: Plaque with active infl ammation may be identifi ed by extensive macrophage accumulation. (2) Thin cap with large lipid core: These plaques have a cap thickness <100µm and a lipid core accounting for >40% of plaque’s total volume. (3) Endothelial denudation with superfi cial aggregation: These plaques are characterized by superfi cial erosion and platelet aggregation or fi brin deposition. (4) Fissured/injured plaque: Plaques with a fi ssured cap (most of them involving a recent rupture) that did not result in occlusive thrombi may be prone to subsequent thrombosis, entailing occlusive thrombi or thromboemboli. (5) Severe stenosis: On the surface of plaques with severe stenosis, shear stress imposes a signifi cant risk of thrombosis and sudden occlusion.
