INTRODUCTION: Selection of the appropriate diameter of stent is difficult in patients with the size mismatch between the internal carotid artery (ICA) and the common carotid artery (CCA). Although stent overexpansion (SOE) in the ICA after carotid artery stenting (CAS) is suspected of producing restenosis, SOE has not been well established. We discuss its incidence, predictors, and outcomes. METHODS: We retrospectively reviewed follow-up angiographs of 206 CAS-treated arteries in 201 patients who had undergone CAS. SOE was defined as angiographic evidence of an intimal gap between the non-stented normal and the dilated stented ICA at the distal stent edge. We also collected data on the patients' clinical status, comorbidities, and radiological and procedural data. Patients with SOE were further followed up closely by duplex ultrasound scans. RESULTS: SOE was detected in nine of 206 CAS-treated ICAs (4.4%). Univariate analysis revealed a significant association between SOE and open-cell stents, the stent diameter (p < 0.01), pre-procedural stenosis, the ICA diameter, ICA/CCA ratio, and the ICA/stent ratio (p < 0.05). Entering these variables into a logistic regression model, open-cell stents were the only variable that significantly increased the risk for SOE (OR 2.36; 95% CI 0.99-4.60; p < 0.05). During a mean clinical follow-up of 31.1 months (range 24-39 months), none of the patients with SOE developed new neurologic ischemic symptoms, stent-edge stenosis, or in-stent restenosis. CONCLUSION: SOE after CAS was not associated with clinical adverse effects. This study suggests that the diameter of stent should be determined by reference to the CCA diameter without respect to the ICA diameter.
INTRODUCTION: Selection of the appropriate diameter of stent is difficult in patients with the size mismatch between the internal carotid artery (ICA) and the common carotid artery (CCA). Although stent overexpansion (SOE) in the ICA after carotid artery stenting (CAS) is suspected of producing restenosis, SOE has not been well established. We discuss its incidence, predictors, and outcomes. METHODS: We retrospectively reviewed follow-up angiographs of 206 CAS-treated arteries in 201 patients who had undergone CAS. SOE was defined as angiographic evidence of an intimal gap between the non-stented normal and the dilated stented ICA at the distal stent edge. We also collected data on the patients' clinical status, comorbidities, and radiological and procedural data. Patients with SOE were further followed up closely by duplex ultrasound scans. RESULTS: SOE was detected in nine of 206 CAS-treated ICAs (4.4%). Univariate analysis revealed a significant association between SOE and open-cell stents, the stent diameter (p < 0.01), pre-procedural stenosis, the ICA diameter, ICA/CCA ratio, and the ICA/stent ratio (p < 0.05). Entering these variables into a logistic regression model, open-cell stents were the only variable that significantly increased the risk for SOE (OR 2.36; 95% CI 0.99-4.60; p < 0.05). During a mean clinical follow-up of 31.1 months (range 24-39 months), none of the patients with SOE developed new neurologic ischemic symptoms, stent-edge stenosis, or in-stent restenosis. CONCLUSION: SOE after CAS was not associated with clinical adverse effects. This study suggests that the diameter of stent should be determined by reference to the CCA diameter without respect to the ICA diameter.
Authors: Joel L Berry; Emil Manoach; Choukri Mekkaoui; Pierre H Rolland; J E Moore; Alexander Rachev Journal: J Vasc Interv Radiol Date: 2002-01 Impact factor: 3.464
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