From a pathological point of view, atherosclerotic plaques can be classified into two components. These include an atheromatous and a fibrous plaque, which are generally consistent with vulnerable and stable plaques, respectively [9]. Of course, ACS patients have more plaques with characteristics of vulnerability, leading to plaque disruption and thrombosis [3]. From an angioscopic findings, vulnerable plaques show plaque disruption which is defined as having high-yellow color intensity plaque and a mural thrombus formation. Plaque disruption is further classified into two types of plaque morphology such as plaque rupture and erosion [10, 11].

Angioscopically, plaque rupture is defined as the plaque showing dissection, fissuring, ulceration, or confirmed atheroma contents [11]. Plaque erosion is defined as eroded if it shows only reddening and erosion with no evidence of dissection, cleft, or depressed ulceration [11]. On the other hand, plaques in SAP patients usually have a smooth surface with white or light yellow color and no thrombi [12]. Representative image of plaque rupture, erosion, and stable plaque is shown in Fig. 10.1.

Plaque color differs in patients with ACS and SAP. According to the relationship between the color of the plaque and its histopathological features, deep-yellow and yellow-red lesions represent either atheroma (53 %) or degenerated plaque (42 %), whereas pate-yellow or gray-yellow lesions were predominantly with degenerated plaque (64 %) and, to a lesser extent, with fibrous plaque (14 %) or atheroma (14 %) [13]. In SAP patients, both types of lesions, smooth gray-white and yellow lesions, were found to be equally distributed [13]. On the other hand, in ACS patients, the yellow color and plaque rupture were frequently found [13]. A previous angioscopic study reported that the number of yellow plaques in a coronary artery is an independent future risk of cardiovascular events and that patients with multiple yellow plaques per vessel have 2.2-fold higher risk of suffering ACS than patients with no or a single yellow plaque per vessel [14].

Recently, yellow plaques were further classified according to yellow color intensity: grade 0, white; grade1, light yellow; grade2, yellow; and grade3, intensive yellow (Fig. 10.2) [15]. Several studies reported that yellow color intensity was associated with plaque vulnerability. Uchida et al. reported that ACS events occurred in 3.3 % of white plaque, 7.6 % of non-glistening yellow plaque, and 68.4 % of glistening yellow plaque [16]. Ueda et al. demonstrated that yellow plaques with higher color grade have a higher incidence of thrombus on the plaque (Fig. 10.3) [15]. Furthermore, Kubo et al. revealed that there was a significant negative correlation between yellow color intensity and fibrous cap thickness evaluated by angioscopy and OCT (Fig. 10.4) [17]. Therefore, it is considered that plaque color grade assessed by angioscopy showed a good correlation with plaque stability or instability. Based on these findings, the relationship between plaque color changes and effect of statin therapy was evaluated using angioscopy. The TWINS (evaluaTion With simultaneous angIoscopy and iNtravascular ultraSound) study and TOGETHAR trial demonstrated that reduction of yellow grade detected by angioscopy occurred independently of volumetric plaque change by statin therapy [18, 19].

The major limitation of angioscopic evaluation is that color grading is often different from each observer. Therefore, in order to avoid this problem, Okada and Ishibashi, et al. have attempted a quantitative assessment color analysis using colorimetry apparatus [20, 21].