Attenuated plaque by IVUS is characterized as attenuation of the ultrasound signal in the absence of overlying calcification (Fig. 10.2) [7–9]. When visualized with IVUS, attenuated plaque may in some cases represent lipid-rich plaque, as histologic analyses have demonstrated attenuated plaques by IVUS to contain greater amounts of lipid, cholesterol clefts, and necrotic core compared to non-attenuated plaques [8, 10]. Although attenuated plaque is frequently present at culprit lesions in acute coronary syndromes [11], the concept that attenuated plaque is a marker of plaque vulnerability has been challenged by data demonstrating the stability of such lesions over time [12].

Perhaps the most important reason to recognize attenuated plaque by IVUS is that the presence of attenuated plaque at the target site prior to percutaneous coronary intervention (PCI) is an independent predictor of both angiographic no-reflow and peri-procedural myocardial infarction [8, 9]. Importantly, the association between attenuated plaque and these acute PCI-related complications has been demonstrated in both ACS patients and those with stable angina [8, 9]. Finally, the circumferential extent of attenuation may also be important in determining the risk of PCI-related complications [7, 13].

Defined as the plaque plus media cross-sectional area divided by the external elastic membrane cross-sectional area [1], plaque burden has been demonstrated to be an independent predictor of adverse cardiovascular events [14, 15]. More specifically, the presence of a plaque burden ≥70 % was associated with a 9.6 % lesion-specific event over 3 years and was the strongest independent predictor of future events in the PROSPECT trial [14]. More recently, large plaque burden has been demonstrated to be an independent predictor of lesion progression in the PREDICTION study [16]. A description of how to measure plaque burden is provided in Fig. 10.3.

VH-IVUS, which uses radiofrequency analysis of backscattered IVUS signals to identify plaque composition, classifies intracoronary plaque as fibrotic, fibrofatty, densely calcified, or necrotic core (Fig. 10.4). These various VH-IVUS plaque components are each represented on the image display by a different color, wherein green represents fibrotic plaque, light green represents fibrofatty plaque, white represents densely calcified plaque, and red represents necrotic core plaque [17] (Fig. 10.4). A VH-fibroatheroma is defined as a lesion having >10 % necrotic core. If a VH-fibroatheroma has >30° of the necrotic core abutting the lumen in three consecutive frames (approximately 1.5 mm in length) it is considered a VH-thin cap fibroatheroma (VH-TCFA) [14, 15]. Alternatively, if the necrotic core is not adjacent to the lumen, the lesion is considered a VH-thick capped fibroatheroma [14, 15] (Fig. 10.5). VH-IVUS can be used to define several additional lesion types, including pathologic intimal thickening, fibrotic plaque, and fibrocalcific plaque, the definitions of which are summarized in Table 10.1.

Prior to performing PCI, plaque characterization using VH-IVUS may be useful to assess the risk of peri-procedural complications during PCI. The presence of VH-IVUS necrotic core at the PCI target site has been associated with the occurrence of angiographic no-reflow, peri-procedural myocardial infarction, and distal embolization [18–22]. The concept that necrotic core plaque by VH-IVUS is associated with acute PCI-related complications has been further demonstrated in a recent meta-analysis [23].

Apart from its use to assess the risk of peri-procedural complications, VH-IVUS has also been studied to identify lesions at risk of causing future coronary events. In the PROSPECT trial, nearly 700 patients with acute coronary syndromes underwent multi-vessel VH-IVUS imaging to identify lesion characteristics predictive of future coronary events [14]. Approximately half of all patients in PROSPECT were found to have at least one non-culprit VH-TCFA at baseline. Over approximately 3 years of follow-up, the presence of a VH-TCFA at baseline was an independent predictor of subsequent major adverse cardiovascular events, most of which were rehospitalizations for unstable or progressive angina. Despite this finding, the identification of a VH-TCFA was associated with a limited positive predictive value for future events, as only 26 of the 595 VH-TCFAs identified at baseline triggered a recurrent cardiovascular event during the 3 years of follow-up. A similarly low lesion-specific event rate for VH-TCFA was demonstrated in the VIVA study [15]. This low event associated with a VH-TCFA can be partially overcome in the presence of additional plaque characteristics, as lesions characterized as VH-TCFA that also had a minimal luminal area of 4.0 mm² or less and a plaque burden of at least 70 % had a lesion specific event rate was 18 % during follow-up [14].