Interventional Cardiology. Группа авторов

the right coronary system shown on the left with a red arrow at the site of maximal stenosis in the mid‐RCA. The other two panels show the baseline OCT interface with the co‐registered angiogram in the upper left corner, OCT cross‐section upper right corner, and longitudinal profile and “L‐mode” at the lower portion of the image. Panel A highlights the measurements at the distal reference, with an EEL diameter of 3.23mm. Panel B demonstrates the measurements at the proximal reference with an EEL diameter of 3.65mm. These measurements are obtained manually. The distance between distal and proximal reference is automatically calculated and determines the stent length. In this example, the length is 18mm and circled in red. The minimum lumen area (MLA) is automatically localized and measured, and in this case is 1.13mm².

Figure 9.5b OCT following stent implantation with stent rendering on the longitudinal profile. The color‐coded apposition bar confirms complete stent apposition. Stent expansion is automatically detected and demonstrates 73% in the distal portion of the stent and 90% for the proximal portion of the stent. The minimum stent area (MSA) is automatically localized and measured.

Figure 9.5c Final angiogram of the RCA following PCI is shown in the left image. Following stent optimization, OCT demonstrates 100% expansion in the distal portion of the stent with 107% expansion in the proximal portion of the stent. The OCT cross‐section confirms no edge dissection.

Several registries have investigated the role of OCT guidance in PCI. After full lesion predilatation, OCT pullback imaging suggested proceeding directly with stenting in 48% while in 52% advised further treatment. Out of the 207 pullback imagings after stenting, 14% suggested new stent implantation because of dissection or residual edge stenosis and 31% suggested further optimization with high pressure or larger sized balloon. A multicenter trial compared the outcomes of an angiographic‐guided strategy with an OCT‐guided strategy in 670 patients [54]. OCT disclosed adverse features requiring further interventions in 35% of cases. OCT guidance was associated with a significantly lower risk of cardiac death or myocardial infarction at one year, even after adjustment for potential confounders.

      A more recent trial by Burzotta et al. was aimed to compare OCT guidance and fractional flow reserve guidance in patients with angiographically intermediate coronary lesions in a single‐center, prospective, 1:1 randomized trial; a total of 350 patients were enrolled (176 randomized to FFR and 174 to OCT imaging). The primary endpoint of major adverse cardiac events or significant angina at 13 months occurred in 14.8% of patients in the FFR arm and in 8.0% in the OCT imaging arm (p= 0.048). As stated by the authors, OCT guidance was associated with lower occurrence of the composite of major adverse cardiac events or significant angina [55].

Traditional stent sizing with IVUS is based on measuring lumen, external elastic membrane (EEM) areas or a combination of the two. EEM‐based algorithms result in the selection of larger diameter balloons and stents. With OCT the EEM is more difficult to visualize if a large plaque area is present. Two randomized trials investigated OCT‐guided PCI versus IVUS‐guided PCI: ILUMIEN III examined 450 patients and showed that OCT‐guided PCI was non‐inferior to IVUS‐guided PCI. In this trial in 85% of cases the EEM‐area could be delineated in the distal reference leading to an aggressive strategy partially based on EEM‐area. In this trial OCT‐detected major stent edge dissections (dissection flap >60 degrees or >3 mm in length) were less common in the OCT‐guided arm versus the IVUS‐guided arm, and, when present, they were observed less frequently by IVUS than by OCT [59–67]. OCT guidance resulted in more frequent postdilatation, larger maximum balloon size, and higher balloon pressure than did angiography guidance alone. Intraprocedural MACEs were uncommon occurring similarly in the three groups, OCT, IVUS, and angiography alone. The Japanese OPINION trial included 829 patients and tested whether OCT‐guided PCI using a lumen‐based approach was non‐inferior to IVUS‐guided PCI with the primary endpoint of target vessel failure within 12 months, defined as a composite of cardiac death, target‐vessel related myocardial infarction and ischaemia‐driven target lesion revascularization). Primary endpoint did not differ, and also in‐stent minimum lumen diameter and binary restenosis, assessed with repeated angiography, were similar. A recent metanalysis by Buccheri et al. of 17 882 patients demonstrated an important MACE reduction and cardiovascular mortality using OCT‐ and/or IVUS‐guided versus angiography‐guided PCI alone [56, 57, 58]. The impact of OCT‐guided vs angiography‐guided PCI is being investigated with the same difference in endpoint selection by two larger OCT guided stenting protocols: ILUMIEN‐IV (NCT0350777) and OCTOBER trials (NCT03171311), both ongoing, see clinicaltrials.com.

      IVUS post‐PCI MSA is the strongest predictor of both restenosis and thrombosis. OCT‐MSA was also found to be an independent predictor of device‐oriented clinical endpoints and target lesion revascularisation, with an MSA cutoff value of 5.0 mm² for DES and 5.6 mm² for bare metal stents. OCT MSA <5.0 mm² was found in about one‐third of patients in ILUMIEN III trial, confirming that a small stent area is common in clinical practice.

      Apposition and malapposition

      Strut apposition is one of the optimal stent deployment criteria and is defined as the contact of the stent struts with the arterial wall. OCT detection of malapposition requires recognition that only the leading edge of the metallic stent strut is visible with OCT, therefore stent strut and polymer thickness for each type of drug‐eluting stent (DES) should be considered in assessing malapposition. Incomplete strut apposition is defined as a strut‐wall distance greater than the strut thickness (metal plus polymer) with the addition of a correction factor, (usually ranging between 10 and 30 μm taking into account the axial resolution of the current OCT systems) [68]. Automatic algorithm can display with a red colour encoding the malapposed struts, often using a less stringent criterion of >300 μm distance between leading strut edge and wall. Unlike metallic stents, BVS are transparent to light, therefore the abluminal border of the struts can be easily identified and incomplete strut apposition can simply be established as the presence of struts separated from the underlying vessel wall [69].

      The clinical implications of stent malapposition remain controversial. Ultrasound studies found conflicting results in the correlation between stent malapposition and adverse clinical e‐M bvents [70–72]. According to a recent OCT analysis of 356 coronary lesions that received a DES, acute stent malapposition was observed in 62% of lesions, approximately half of them being located at the stent edges [73]. Severe diameter stenosis, calcified lesions, and long stents were independent predictors of acute stent malapposition. Number of unopposed struts per cross‐section and length of the unopposed segment was suggested to cause more frequent late events. Acute stent malapposition with a volume >2.56 mm³ differentiated malapposition that persisted at follow‐up from stent malapposition that resolved. Moreover, in this study, long‐term clinical outcomes of late stent malapposition detected by OCT were favorable [73]. However, segments with acute incomplete strut apposition have higher risk of delayed coverage than well‐apposed segments. Acute incomplete strut apposition size (estimated as volume or maximum distance per strut) was an independent predictor of persistence of incomplete strut apposition and of delayed healing at follow‐up in 66 stents of different designs [74]. Strut malapposition can cause turbulent blood flow, which in turn can trigger platelet activation and thrombosis. Different recent registries performed OCT in patients with definite stent thrombosis, both BMS and DES. In the PESTO and PRESTIGE studies, malapposition was a frequent possible explanation of acute stent thrombosis, subacute one (from 1 to 30 days after stent implantation) and late stent thrombosis (to one year post‐PCI) [75–77].

      In fact, incomplete strut apposition in addition to delayed neointimal healing of the stent and incomplete endothelialization of the struts is a common morphologic