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Drug eluting stents (DES) have undoubtedly been efficacious in attenuating restenosis. There is comparatively little in vivo data however, on the influence of DES and the powerful cytostatic agents they employ on arterial healing in patients. Even in the early DES trials, intravascular ultrasound (IVUS) demonstrated adverse (expansive) arterial remodelling with late acquired malapposition of stent struts, though the clinical relevance of this was overlooked until associations with late stent thrombosis (LST) were demonstrated.1
Autopsy studies of patients dying of late DES thrombosis show a pattern of delayed arterial healing characterised by incomplete re-endothelialisation and persistence of fibrin. A high ratio (>30%) of stent struts uncovered by any tissue in any one examined section was the morphometric feature most predictive of both incomplete re-endothelialisation and the occurrence of LST.2 Prior technology has not allowed us to study this relationship in vivo as up to 67% of neointima can have a thickness below the maximum axial resolution of IVUS (100 μm).3 4 Angioscopy does allow direct visualisation of neointima but is limited by the inability to provide quantitative information. In contrast, optical coherence tomography (OCT) is able to provide detailed quantitative information at a resolution 10× higher than IVUS, and can document strut tissue coverage in close agreement to histopathology.5 This technology allows us, for the first time, to document healing of DES in living patients.
Clear differences in OCT delineated …
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