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

Abstract

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 111 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 <or=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.