Читать книгу Interventional Cardiology - Группа авторов - Страница 241

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].