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J Vasc Surg. 2020 Feb 18. pii: S0741-5214(19)32310-9. doi: 10.1016/j.jvs.2019.07.100. [Epub ahead of print]

Predictors of midterm high-grade restenosis after carotid revascularization in a multicenter national database.

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Division of Vascular and Endovascular Surgery, University of California San Diego, La Jolla, Calif.
Section of Vascular Surgery and The Dartmouth Institute, Dartmouth-Hitchcock Medical Center, Lebanon, NH.
Division of Vascular and Endovascular Surgery, Beth Israel Deaconess Medical Center, Boston, Mass.
Division of Vascular and Endovascular Surgery, University of California San Diego, La Jolla, Calif. Electronic address:



Restenosis after carotid revascularization is clinically challenging. Several studies have looked into the management of recurrent restenosis; however, studies looking into factors associated with restenosis are limited. This study evaluated the predictors of restenosis after carotid artery stenting (CAS) and carotid endarterectomy (CEA) using a large national database.


Patients undergoing CEA or CAS in the Vascular Quality Initiative data set (2003-2016) were analyzed. Patients with no follow-up (33%) and those who had prior ipsilateral CEA or CAS were excluded. Significant restenosis was defined as ≥70% diameter-reducing stenosis, target artery occlusion or peak systolic velocity ≥300 cm/s, or repeated revascularization. Kaplan-Meier survival analysis and bootstrapped Cox regression models with stepwise forward and backward selection were used.


A total of 35,720 procedures were included (CEA, 31,329; CAS, 4391). No significant difference in restenosis rates was seen between CEA and CAS at 2 years (7.7% vs 9.4% [P = .09]; hazard ratio [HR], 0.99; 95% confidence interval [CI], 0.79-1.25; P = .97). However, after adjustment for age, sex, and symptomatic status at the time of the index operation, CAS patients who had postoperative restenosis were more likely to have a symptomatic presentation (odds ratio, 2.2; 95% CI, 1.2-4.0; P = .01) and to undergo repeated revascularization at 2 years (HR, 1.75; 95% CI, 1.3-2.4; P < .001) compared with patients who had restenosis after CEA. Predictors of restenosis after CAS included a common carotid artery lesion (HR, 1.65; 95% CI,1.06-2.57; P = .03), whereas age (HR, 0.91; 95% CI, 0.84-0.99; P = .03) and dilation after stent placement (HR, 0.53; 95% CI, 0.39-0.72; P < .001) were associated with decreased restenosis at 2 years. Predictors of restenosis after CEA included female sex (HR, 1.55; 95% CI, 1.38-1.74; P < .001), prior neck irradiation (HR, 2.35; 95% CI, 1.66-3.30; P < .001), and prior bypass surgery (HR, 1.29; 95% CI, 1.01-1.65; P = .04). On the other hand, factors associated with decreased restenosis after CEA included age (HR, 0.95; 95% CI, 0.92-0.98; P < .001), black race (HR, 0.57; 95% CI, 0.37-0.89; P = .01), patching (HR, 0.61; 95% CI, 0.47-0.79; P < .001), and completion imaging (HR, 0.70; 95% CI, 0.52-0.95; P = .02).


Our results show no significant difference in restenosis rates at 2 years between CEA and CAS. Restenosis after CAS is more likely to be manifested with symptoms and to undergo repeated revascularization compared with that after CEA. Poststent ballooning after CAS and completion imaging and patching after CEA are associated with decreased hazard of restenosis; however, further research is needed to assess longer term outcomes and to balance the risks vs benefits of certain practices, such as poststent ballooning.


Carotid artery stenting; Carotid endarterectomy; Predictors; Restenosis


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