Fig. 8.1
Optimal minimal stent area in the sirolimus-eluting stent (a), paclitaxel-eluting stent (b), zotarolimus-eluting stent (c), and everolimus-eluting stent (d) to predict angiographic restenosis (Reproduced from Song et al. 2014, Doi et al. 2009). MSA minimal stent area
Fig. 8.2
Major adverse cardiovascular events rate for patients with and without minimal lumen area (MLA) < 5.0 mm2 or distal reference segment lumen area in the RESET trial and the IVUS-XPL trial (Reproduced from Lee et al. 2016). MLA minimal lumen area
Stent underexpansion is associated with stent thrombosis as well as stent restenosis. Lui et al. reported that underexpansion associated with thrombosis is more severe, diffuse, and proximal in location compared with restenosis [6].
8.1.2 Stent Fracture
Stent fracture is defined as the presence of an angiographically visible interrupted connection of stent struts or fewer visible stent struts at the suspected site than normal looking stented area on intravascular ultrasound. The classification of stent fracture varies from study to study (Table 8.1) [7]. Intravascular ultrasound can identify complete stent fracture (complete strut absent) and partial stent fracture (stent struts absent in ≥1/3 of the vessel wall) (Fig. 8.3) [8]. Most stent fracture occurred in sirolimus-eluting stent, but several cases of stent fracture were also reported in other type of stents. Especially, stent fracture of 2nd generation drug-eluting stent can be associated with longitudinal stent deformation due to their weak compressive force (Fig. 8.4). Stent fracture can be incidental finding in asymptomatic patients, however, it also presents as recurrent angina, myocardial infarction, and even sudden death. The uses of intravascular ultrasound increase the rate of stent fracture detection, and provide associated information regarding neointima formation, vessel remodeling, stent expansion, and aneurysmal formation (Fig. 8.5).
Table 8.1
Classification of stent fracture
Type | Description |
---|---|
I | A single-strut fracture |
II | 2 or more strut fractures without deformation |
III | 2 or more strut fractures with deformation |
IV | Multiple strut fractures with acquired transection but without gap |
V | Multiple strut fractures with acquired transection with gap |
Fig. 8.3
Intravascular ultrasound definition of stent fracture
Fig. 8.4
A case of everolimus-eluting stent fracture . Partial fracture was followed by longitudinal deformation and overlap of fractured edges leading to excessive neointimal hyperplasia
Fig. 8.5
A case of sirolimus-eluting stent fracture associated with coronary aneurysm
8.1.3 Late Stent Malapposition
Stent malapposition was defined as a separation of at least 1 stent strut not in contact with the intimal surface of the arterial wall that was not overlapping a side branch, was not present immediately after stent implantation, and had evidence of blood speckling behind the strut. Late stent malapposition was defined as stent malapposition developing between 30 days and 1 year, but typically detected on 6-month follow-up intravascular ultrasound [9]. Very late stent malapposition was defined as a late stent malapposition lesion that developed after 1 year (Fig. 8.6). A meta-analysis showed that the risk of late stent malapposition was significantly greater after drug-eluting stent than bare-metal stent, whereas other studies showed that primary stenting in acute myocardial infarction was an independent predictor after both drug-eluting stent and bare-metal stent implantation [10, 11]. Late stent malapposition of drug-eluting stent is associated with positive vascular remodeling and vascular remodeling can be progression [9]. Therefore, stent malapposition could continuously progress and new areas of malapposion also could develope in later stage.
Fig. 8.6
Example of late stent malapposition 3-year after sirolimus-eluting stent implantation
The clinical impact of stent malapposition has been a matter of concern and debate. In the harmonizing outcomes with revascularization and stents in acute myocardial infarction (HORIZONS-AMI) trial, stent malapposition was not associated with stent thrombosis (Fig. 8.7) [12]. Hong et al. also reported that late stent malapposition after drug-eluting stent implantation was not a predictor of major adverse cardiac events or stent thrombosis at 3 years after the 6-month intravascular ultrasound [13]. However, Cook et al. reported that late stent malapposition associated with stent thrombosis had higher maximal malapposition area, length, and depth than without stent thrombosis (Fig. 8.8) [14]. The prognostic impact of late stent malapposition on long-term clinical outcomes requires further investigation.
Fig. 8.7
3-year follow-up of HORIZONS-AMI intravascular substudy (Reproduced from Yakushiji T, et al. ACC 2012)
Fig. 8.8
Quantification of late stent malapposition in patients with very late stent thrombosis. ST stent thrombosis, LSM late stent malapposition. (Modified from Cook S et al. 2007)
8.1.4 In-Stent Neoatherosclerosis
In-stent neoatherosclerosis has emerged as an important contributing factor to late vascular complications including very late stent thrombosis and late in-stent restenosis. Histologically, neoatherosclerosis is characterized by accumulation of lipid-laden foamy macrophages within the neointima with or without necrotic core formation and/or calcification. The development of neoatherosclerosis may occur in months to years following stent placement. Pathologic and clinical imaging studies have demonstrated that neoatherosclerosis occurs more frequently and at an earlier time point in drug-eluting stent when compared with bare-metal stent [15, 16]. In intravascular ultrasound, in-stent plaque rupture likely accounts for most thrombotic events associated with neoatherosclerosis (Fig. 8.9). However, because intravascular ultrasound has poor resolution (spatial resolution = 150–250 μm), intravascular optical coherence tomography is the best image tool for detection of neoatherosclerosis. The detailed discussion will be described in optical coherence tomography section.
Fig. 8.9
A case of very late stent thrombosis . Intravascular ultrasound after thrombus aspiration showed significant neointimal tissue growth and neointimal flap (arrow)