Duplex scan surveillance after carotid angioplasty and stenting: A rational definition of stent stenosis

Objective: A duplex ultrasound (DUS) surveillance algorithm used after carotid endarterectomy (CEA) was applied to patients after carotid stenting and angioplasty (CAS) to determine the incidence of high-grade stent stenosis, its relationship to clinical symptoms, and the outcome of reintervention. Methods. In III patients who underwent 114 CAS procedures for symptomatic (n = 62) or asymptomatic (n = 52) atherosclerotic or recurrent stenosis after CEA involving the internal carotid artery (ICA), DUS surveillance was performed <= 30 days and every 6 months thereafter. High-grade stenosis (peak systolic velocity [PSV] > 300 cm/s, diastolic velocity > 125 cm/s, internal carotid artery stent/proximal common carotid artery ratio > 4) involving the stented. arterial segment prompted diagnostic angiography and repair when > 75% diameter-reduction stenosis was confirmed. Criteria for > 50% CAS stenosis was a PSV > 150 cm/s with a PSV stent ratio > 2. Results: All 114 carotid stents were patent on initial DUS imaging, including 90 (79%) with PSV < 150 cm/s (94 +/- 24 cm/s), 23 (20%) with PSV > 150 cm/s (183 +/- 34 cm/s), and one with high-grade, residual stenosis (PSV = 355). During subsequent surveillance, 81 CAS sites (71%) exhibited no change in stenosis severity, nine sites demonstrated stenosis regression to < 50% diameter reduction, and five sites developed velocity spectra of a high-grade stenosis. Angiography confirmed > 75% diameter reduction in all six CASs with DUS-detected high-grade stenosis, all patients were asymptomatic, and treatment consisted of endovascular (n = 5) or surgical (n = 1) repair. During the mean 33-month follow-up period, three patients experienced ipsilateral, reversible neurologic events at 30, 45, and 120 days after CAS; none was associated with severe stent stenosis. No stent occlusions occurred, and no patient with > 50% CAS stenosis on initial or subsequent testing developed a permanent ipsilateral permanent neurologic deficit or stroke-related death. Conclusion: DUS surveillance after CAS identified a 5% procedural failure rate due to the development of high-grade in-stent stenosis. Both progression and regression of stent stenosis severity was observed on serial testing, but 70% of CAS sites demonstrated velocity spectra consistent with < 50% diameter reduction. The surveillance algorithm used, including reintervention for asymptomatic high-grade CAS stenosis, was associated with stent patency and the absence of disabling stroke.