Optical coherence tomography(OCT), a light based imaging modality, has recently become available for intracoronary application. Until the development of OCT, there was no direct way to see if struts had been covered, except through pathology. Because of the shorter wavelength of infrared light compared to ultrasound, OCT has a ten-fold higher image resolution than conventional intravascular ultrasound (IVUS), 150 micron for IVUS as compared to 15 micron for OCT.
Unlike conventional stents, which develop circumferential coverage with an average thickness of 500 micron or more, well visualized with IVUS and angiography, drug-eluting stents delay and prevent the hyperplastic response so that the average late lumen loss for drug-eluting stents can be lower than 100 micron which means this thin layer of intimal thickening can be below the resolution of IVUS. OCT can reliably detect early and very thin layers of tissue coverage on stent struts and provide the quantification of tissue coverage with high reliability. And also, OCT permits the characterization of neointimal tissue in a qualitative way. By using of OCT, neointimal tissue can show a variety of morphologies ranging from homogeneous, bright, uniform tiussue to optically heterogeneous tissue or eccentric tissue of various thickness. OCT findings, such as dark, signal-poor halos around stent struts may reflect fibrin deposition and incomplete healing, as described in pathologic and animal experimental series. Peter et,all. Reported 2 cases of late drug-eluting stent (DES) thrombosis examined by OCT. The one was late stent thrombosis three months after DES implantation in the LCX. There was focal in-stent restenosis with severe lumen narrowing. The neointimal showed a layered appearance with a luminal bright, highly reflective layer, an intermediate layer and a dark, signal poor layer surrounding the struts. The other case was very late stent thrombosis four years after DES implantation in the LAD. OCT revealed incomplete stent strut apposition at the proximal stent edge with incomplete tissue coverage in 21% of struts. So, Stent strut malapposition is another concern about stent thrombosis. This can cause non-laminar and turbulent blood flow characteristics, which in turn can trigger platelet activation and thrombosis. Therefore, serial OCT observations immediately and at longer term follow-up after stenting may improve our understanding of these complex mechanisms and shed light on the likely clinical significance of stent malapposition.
In concousions, OCT can reliably visualize very thin stent strut tissue coverage after implantation, and permits for its qualitative and precise quantitative assessment. This may better guide the optimal duration of dual anti-platelet therapy that currently remains unclear.