Coronary angiogram is still gold standard for diagnosis of ischemic heart disease. However, this method is just luminology and powerless to estimate the quality of the vessel wall. To date several sorts of intracoronary imaging devices (e.g., conventional gray-scale IVUS, virtual histology IVUS, integrated backscatter IVUS, optical coherence tomography [OCT], near-infrared spectroscopy [NIRS]) have been developed, and they are available for evaluation of plaque composition [10–13]. Coronary angioscopy is a unique imaging system that provides direct visualization of vessel lumen. Information about forward-looking angioscopic image, such as color, three-dimensional, and detailed configuration of lumen surface, is capable of diagnosing macro-morphology of atherosclerotic plaque, thrombus, and proliferating neointima in coronary bare-metal and drug-eluting stents [14–21].

Atherosclerotic plaque is broadly divided into white plaque and yellow one according to its surface color. Similarly, intracoronary thrombus is classified into white, red, mixed (white and red), and pinkish thrombus [22, 23]. On the basis of superficial form of the plaque, that is also categorized into simple plaque with smooth surface and complex one of irregularity. Findings of complex plaque include intimal flap, dissection, fissuring, ulceration, and disruption.

It is noticeable that coronary angioscopy can sensitively detect a tiny thrombus in comparison with other imaging [24]. Although thrombus transformed digital signals on the other imaging may be missed, visual color on the angioscopy simplifies diagnosis of the thrombus. By contrast, there is some weakness in angioscopic evaluation; quantification of distance or volume is impossible and its diagnosis is limited only to the lumen surface. They are compensated by cross-sectional IVUS or OCT images.

Disrupted plaque in the culprit lesion of ACS is no longer vulnerable in the narrowest sense. Nevertheless, observation of the culprit plaque surely makes us understand plaque vulnerability before the conclusive event. At angioscopic examination in the case of ACS, massive thrombus covering disrupted plaque is commonly found as pathological reports have proved [25]. The plaque usually has yellow surface, and so yellow plaque is considered to be vulnerable. The degree of yellow color is really various, and its grading or scoring system is often used for semiquantitative analysis as the following: grade 1 = light yellow, grade 2 = medium yellow, grade 3 = intense or dark yellow, and grade 0 = no yellow (white) [26, 27] (Fig. 19.1).

In pathological validation, angioscopically yellow plaque corresponds with fibro-lipidic atheroma [28]. Integrated backscatter IVUS, virtual histology IVUS, and OCT demonstrate that the majority of yellow plaques are composed of lipid-laden elements including necrotic core [11, 29–32]. Also, yellow plaque is relevant to positive vessel remodeling on IVUS images [33]. The yellow plaque with positive remodeling has large plaque burden, and that probably contributes to local vulnerability. Thickness of fibrous tissue covering lipidic content is determinant of the plaque color, and yellow grade is conversely correlated with the fibrous cap thickness (Fig. 19.2) [31, 32]. These data suggest that intense yellow plaque is identical with TCFA of pathological definition. In contrast, white plaque is a lipidic plaque with thick fibrous cap (thick-cap fibroatheroma) or a complete fibrous plaque without lipid. With regard to thrombogenicity, the frequency of thrombus adhesion gradually increases according to the yellow grade [34]. Some intense yellow-plaque, angioscopy-derived TCFA is located in the segment of a large lumen area measured by OCT [32]. The phenomenon implies that vulnerable plaque may hide in the lesion of nonsignificant stenosis. Few small-scale prospective researches exhibit that the incidence of ACS is higher in patients having glistening yellow plaque or plural yellow plaques than in patients without those [35, 36]. Hence, it is generally believed that white plaque achieves clinically stable condition and intense yellow plaque may have potential for its disruption and thrombus formation in the future.

Complex plaque features, intimal injury recognized by the naked eye through angioscopy, reflect microscopic endothelial denudation, and they are often accompanied with attachment of mural thrombus [37, 38]. Therefore, complexity is regarded as a factor of plaque vulnerability as well as color of the high-intense yellow.