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 finding in fatal cases of late and very late stent thrombosis [71, 78–80]. However, biological and mechanical factors (including levels of circulating endothelial progenitor cells or regional shear stress) can also have a role in neointimal healing and differences in percentage coverage cannot always entirely explain clinically overt stent thrombosis [80].
Tissue protrusion
In OCT, plaque protrusion is characterized by a smooth surface and no signal attenuation, and thrombus protrusion by irregular surface and significant signal attenuation. OCT can provide better images and clearer visualization of tissue protrusion compared with IVUS. Tissue protrusion is more frequently in the culprit lesions of acute coronary syndromes, as unstable lesions contain soft lipid tissue and thrombi. In a multicenter registry, including 780 patients, 50% ACS, irregular protrusion was more common in patients treated for MI and was an independent predictor of target lesion revascularization. In fact, tissue prolapse has a worse clinical impact in ACS as suggested in CLI‐OPCI substudies [54].
Vascular injury: dissections
OCT is a very sensitive tool in detecting micro‐dissections and subclinical dissections [81]. Dissections occur more frequently when the plaque at the edge of the stent is fibro‐calcific or lipid‐rich than when is fibrous [82]. Distal stent edge dissections (>200 μm) in CLI OPCI II Study revealed by OCT emerged as an independent predictor of MACE; minimal dissection, at the edge or instent, were not associated with adverse effects [54].
Guidance of complex lesion treatment: bifurcations, calcified, CTO, long and distal, ostial lesions
Bifurcations are coronary lesions with high rates of acute and late stent failure. Knowing the reference diameter of the vessel distal and proximal to the side branch is critical in the correct sizing of stents and post‐dilatation balloons. In both simple (one stent) and especially complex (two‐stents) strategies of bifurcation stenting, OCT showed that the rate of malapposed struts is significantly higher at the side branch ostium than in the vessel side opposite to the ostium [83]. In a series of 45 lesions, OCT showed that the persistence of malapposition was as high as 43%, despite consistent use
