Very late stent thrombosis due to probable plaque erosion and not plaque rupture

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A 72-year-old man presented to the ER with an inferior ST-segment-elevation myocardial infarction (STEMI) 14 months after the initial emergent zotarolimus-eluting stent (Resolute Intergrity 3.5/30 mm; Medtronic, Santa Rosa, California, USA) implantation for a totally occluded lesion in his right coronary artery. The stent had been examined by optical coherence tomography (OCT) 10 months after the initial procedure as scheduled according to the clinical research protocol to determine the optimal duration of the dual antiplatelet therapy after drug-eluting stent implantation, which showed a heterogeneous pattern of neointima (Fig. 1, Supplementary Movie 1, Supplemental digital content 1, with angiographically mild stenosis. The emergent angiogram, after 4 months from the 10-month follow-up angiogram, revealed a tight stenosis within the stent in the absence of angiographic thrombus (Fig. 2, Supplementary Movie 2, Supplemental digital content 2, However, OCT images revealed an intraluminal white thrombus superposed on a layered pattern neointima with a gradual signal attenuation (Fig. 2b and c) that was transformed from the heterogenous neointima shown in the previous OCT examination (Fig. 1b and c). Moreover, a lipid-laden neointima at the proximal portion of the lesion had progressed (Figs 1d and 2d). There was no obvious intimal disruption detected inside the stent neointima. Thereafter, the culprit lesion was dilated by paclitaxel drug-coated balloon (Sequent Please 3.5/20 mm; B.Braun Melsungen AG, Berlin, Germany) followed by a compliant balloon dilatation, which achieved an excellent immediate result.
ST still remains a major concern of contemporary percutaneous coronary intervention. Mechanism of stent thrombosis has been intensively investigated in in-vivo and ex-vivo studies. In a prospective multicenter registry study by OCT 1, the leading cause of very late stent thrombosis (VLST) was attributed to malapposed struts and rupture of neoatherosclerotic neointima. In the present case of VLST at 14 months after initial zotarolimus-eluting stent implantation, OCT detected a neoatherosclerotic change without rupture behind the thrombus and all the struts were covered by neointima, which suggested another cause of thrombosis, possibly endothelial erosion similar to that in native coronary arteries. Histopathological study reported a neointimal erosion as a relatively rare cause of VLST, but the contribution of neoatherosclerosis to the development of neointimal erosion remains unknown 2. The present serial OCT examinations demonstrated a neoatherosclerotic change of heterogenic neointima in its volume and property that contributed to a thrombosis, which may explain the worse clinical outcomes of heterogenic neointima reported in a previous study 3 and potentially be related to the erosion representing an immaturity of endothelialization. To the best of our knowledge, this is the first case report of serial OCT assessment of stent thrombosis potentially caused by neointimal erosion. This report could be highly suggestive to warrant investigation of a potential role of erosion in VLST.

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