Carotid artery stenting (CAS) was introduced 3 decades ago − in the absence (then) of dedicated stents and cerebral protection − as a treatment modality “to prevent strokes in thousands of patients, offering a number of potential advantages over surgical revascularisation”1.
Carotid-related strokes are mechanistically linked to the thrombotic rupture or erosion of atherosclerotic plaque, resulting in cerebral embolism and/or carotid occlusion2. As pharmacotherapy, despite its progress, fails to universally guard against carotid-related stroke1, surgical removal of plaque or mechanical plaque pacification − the objective of CAS − remain fundamental stroke prevention tools2. Multiple longitudinal studies in symptomatic and asymptomatic patients have convincingly demonstrated that CAS and carotid endarterectomy (CEA) are similarly effective in stroke prevention2.
Despite the primary (powered) endpoint of the CREST Trial demonstrating the equivalence of CAS and CEA2, CAS, employing a translesionally delivered filter and a single-layer metallic stent2, had a relative “excess” of 30-day minor strokes – the vascular surgery community’s key argument for the relative “inferiority” of CAS3. The 30-day “excess” strokes with 1st-generation CAS (≈40-80% of those...
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