OCT Investigation of Very Late Scaffold Thrombosis
What are the mechanisms underlying very late scaffold thrombosis (VLScT), as assessed by optical coherence tomography (OCT)?
The INVEST (Independent OCT Registry on Very Late Bioresorbable Scaffold Thrombosis) authors identified 38 lesions in 36 patients who suffered VLScT and underwent OCT to identify mechanisms of VLScT.
Median time to VLScT was 20 months. Mechanisms identified included scaffold discontinuity (42%), malapposition (18%), neoatherosclerosis (18%), underexpansion/scaffold recoil (11%), uncovered struts (5%), and edge-related progression (3%). More than 80% of patients were on aspirin monotherapy at the time of presentation and 17% were on dual antiplatelet therapy (DAPT).
The most common mechanism for VLScT was noted to be scaffold discontinuity, suggesting issues with scaffold resorption as the main mediator of LScT.
This paper sheds light on possible mechanisms surrounding the hazardous signal of VLScT associated with the Absorb (bioresorbable vascular scaffold) BVS. OCT evaluation was performed by a dedicated team of OCT experts. Of note, among the patients studied, 31% underwent intracoronary imaging at the time of stent deployment, 68% underwent appropriate balloon pre-dilation, and 60% underwent appropriate post-dilation. ‘Appropriate’ BVS sizing was noted in less than half of the patients (44%). With this background, it is noted that on OCT, the most common mechanism for VLScT was scaffold discontinuity. This finding is thought to occur due to device degradation with rogue struts being exposed to the lumen and potentiating thrombogenesis. The second most common cause was neoatherosclerosis. Based on mechanisms described, failure of BVS may be related to scaffold design and the resorption process. The impact of ‘proper’ device deployment and prolonged DAPT on lowering VLScT remains to be determined.
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