Symptomatic atherosclerotic plaque progression in a first-generation carotid stent: management and 5-year clinical and imaging outcome-a case report

Background Restenosis in first-generation (single-layer) carotid stents (FGS) is believed to represent an exaggerated healing response of (neo)intimal hyperplasia (NIH) formation. Rather than NIH, we describe symptomatic in-FGS unstable plaque (neo)atherosclerosis mandating re-revascularization. To halt continued plaque evolution, we propose a novel treatment strategy involving a microNet-covered stent (MCS, second-generation carotid stent) to sequestrate the plaque from the vessel lumen. A durable long-term result is documented using multi-modal imaging. Case summary With a seemingly optimal result of FGS (Precise) symptomatic carotid lesion revascularization followed by optimal medical therapy, a late (>= 3 years) progressive in-stent restenosis (ISR) arose. At Year 11, crescendo ipsilateral transient ischaemic attacks occurred. Angiography showed an ulcerated tight lesion throughout stent length. Intravascular ultrasound (IVUS) virtual histology imaging revealed thin-cap fibroatheroma. Reintervention was performed under distal protection. Undersized balloon predilatation to insert a stent caused symptomatic no-flow, and aspiration catheter was used to reduce the filter load. A MCS (CGuard) was implanted and post-dilated to ensure full lumen gain; IVUS confirmed complete plaque sequestration. The optimal anatomic result remained unchanged throughout 5 years (ultrasound and computed tomography verification); this was accompanied by clinical cure. Discussion This is the first demonstration of in-FGS (neo)atherosclerosis resolution using an MCS to sequestrate and insulate the atherosclerotic plaque. We show that ISR may be underlined by atherosclerotic plaque progression via the FGS single-layer stent struts that may show vulnerable plaque phenotype and may be associated with cerebral ischaemia. The anatomically and clinically effective exclusion of the atherosclerotic plaque by an MCS enabled lasting, optimal endovascular reconstruction and clinical cure.