Minimal stent area (MSA ) of bare metal stent (BMS) for long-term patency was considered as 6.4–6.5 mm² [11, 12], and adequate post-interventional MSA of DES was 5.0–5.7 mm² (Fig. 7.2) [13–15]. In left main lesions, optimal MSA was reported as 8.7 mm² in the MAIN-COMPARE (revascularization for unprotected left main coronary artery stenosis: comparison of percutaneous coronary angioplasty versus surgical revascularization) study [2]. Considering 4 segments of left main bifurcation, the best minimal stent area criteria to predict angiographic restenosis were 5.0 mm² (ostial left circumflex artery), 6.3 mm² (ostial left anterior descending artery), 7.2 mm² (polygon of confluence [POC]), and 8.2 mm² (proximal left main artery above the POC) (Fig. 7.3) [16].

In the BMS era, MUSIC study (multicenter ultrasound stenting in coronaries study) defined adequate expansion as >90% of the average reference cross-sectional area (CSA), or >100% of a smaller reference CSA with complete apposition and symmetric expansion [4]. CRUISE (Can Routine Ultrasound Influence Stent Expansion) study showed better stent expansion of IVUS-guided PCI than angiography-guided PCI, especially in terms of target vessel revascularization (TVR), but not in mortality or myocardial infarction [17]. In contrast to the BMS era, early studies of IVUS-guided PCI with DES had no significant benefit in terms of TVR or clinical events. AVIO (Angiography Versus IVUS Optimization) study which defined optimal stent expansion as final minimum stent CSA of at least 70% of the hypothetical CSA of the fully inflated balloon used for post-dilatation did not show any difference in clinical outcome [18]. However, attention should be paid to avoid stent underexpansion. Several evidences indicate that stent underexpansion is one of the major causes of stent failure such as stent restenosis or stent thrombosis (Table 7.1) [14, 19–21]. ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents) study showed reduction in stent thrombosis, myocardial infarction, and major adverse cardiac events by IVUS-guided optimization of stent expansion and apposition [22]. Representative IVUS images of underexpansion and well expansion are shown in Fig. 7.4.

Stent edge dissection is a tear in the plaque parallel to the vessel wall with visualization of blood flow in the false lumen <5 mm to a stent edge. The incidence of edge dissections by IVUS is approximately 10–20% and 40% of the IVUS-identified dissections was not detected by angiography [23–25]. Significant (major) edge dissections, defined by IVUS as lumen area < 4 mm² or dissection angle ≥60°, have been associated with early stent thrombosis [26]. However, minor non-flow-limiting dissection at the edge of stent may not be associated with an increased incidence of clinical events although no consensus exists on an optimal strategy. Figure 7.5 is an example of stent edge dissection.

Incomplete stent apposition (ISA) , synonymous with stent malapposition, was defined as the absence of contact between at least one strut and the lumen wall that did not overlap a side branch with evidence of blood speckle behind the strut and can occur acutely after stent implantation (acute ISA) or develop over time (late-acquired ISA). Acute ISA is almost due to suboptimal stent deployment. The frequency of acute ISA has been reported to be nearly 10% and it appears not to be associated with increased cardiac events [27, 28].

Tissue protrusion (TP ) was defined as a visible tissue extrusion through the stent struts by IVUS (Fig. 7.6) [29, 30]. Although thrombus was characterized by heterogeneous echodensity tissue with a sparkling pattern by IVUS [31], the accurate discrimination of atherosclerotic plaque and thrombus within stent is very difficult because of limited resolution of IVUS. Thus, TP includes plaque and/or thrombus extrusion within stent [32]. The incidence of TP has been reported in various ranges between 20% and 73%, depended on characteristics of enrolled patients (Table 7.2) [29, 30, 32–36]. In fact, TP is likely to develop in patients with acute coronary syndrome, especially ST-segment elevation myocardial infarction owing to a higher chance of thrombus or friable plaque compared to stable patients [32, 35] and receiving longer stent probably caused by unequal distribution of inflation pressure during stent deployment [30, 34]. Other predictors of TP are larger reference lumen area, greater plaque burden, more plaque rupture, attenuated plaque, positive vascular remodeling, and virtual histology thin-cap fibroatheroma by IVUS [30, 32]. The clinical impact of TP remains a controversy. Previous studies suggested that TP after stent implantation may increase the risk of stent thrombosis [26, 37]. Other studies, however, have been failed to show this relationship [29, 32, 38].

Although some investigators demonstrated greater cardiac enzyme elevation after stent implantation in patients with TP, it did not translate into the increased risk of stent thrombosis or periprocedural myocardial infarction [30, 32]. An IVUS substudy from ADAPT-DES reported the 2-year clinical outcomes of TP after stenting. At 2-year clinical follow-up, there was no difference in the rate of major adverse cardiac events between patients with or without TP. Interestingly, patients with TP showed a less frequency of clinically driven target lesion revascularization at 2 years (1.9% vs. 4.0%, p = 0.008), probably due to larger minimal stent area at the end of procedure [32]. Taken together, TP may influence the early clinical phase rather than late clinical stage after stent implantation even though its clinical significance is still uncertain.