Clinical Research External Carotid Artery Stenosis after Internal and Common Carotid Stenting Jeffrey J. Siracuse, Irene Epelboym, Boyangzi Li, Rahima Hoque, Diana Catz, and Nicholas J. Morrissey, New York, New York
Background: The external carotid artery (ECA) can be an important collateral for cerebral perfusion in the presence of severe internal carotid artery (ICA) disease. ICA stenting that covers the ECA origin may put the ECA at increased risk of stenosis. Our objective was to determine the rate of ECA stenosis secondary to ICA stenting, determine predictive factors, and describe any subsequent associated symptoms. Methods: We retrospectively reviewed clinical data on all ICA stents crossing the origin of the ECA placed by vascular surgeons at our institution. We analyzed patient demographics, comorbidities, stent type and sizes, as well as medication profile to determine predictors of ECA stenosis. Results: Between 2005 and 2013, there were 72 (out of 119 total ICA stenting) patients (mean age 71, 68% male) who underwent placement of ICA stents that also crossed the origin of the ECA. Six patients (8.3%) had a significantly increased ECA stenosis postprocedure. There were no occlusions. All patients with ECA stenosis maintained patency of their ICA stent and were asymptomatic. Age, gender, comorbidities, stent type and size, and medication profile were not associated with ECA stenosis after stenting. Conclusions: ECA stenosis after ICA stenting covering the ECA origin is uncommon and not clinically significant in patients with patent ICA stents. The clinical significance of concurrent ECA and ICA stenosis after stenting is unclear as it is not captured here. The potential for ECA stenosis should not deter stenting across the ECA origin if necessary. Patient and stent factors are not predictive of ECA stenosis.
INTRODUCTION Although the external carotid artery (ECA) normally does not contribute significantly to cerebral blood flow, in cases where there is a stenosis or occlusion of the internal carotid artery (ICA), the ECA can be an important source of collateral perfusion.1e3 This is particularly important for flow in the middle cerebral artery distribution.4
Section of Vascular Surgery and Endovascular Interventions, New York-Presbyterian Hospital, Columbia University, College of Physicians and Surgeons, New York, NY. Correspondence to: Jeffrey J. Siracuse, MD, Department of Surgery, Boston University, Boston Medical Center, 732 Harrison Avenue, Boston, MA 02218, USA; E-mail: [email protected] Ann Vasc Surg 2015; -: 1–4 http://dx.doi.org/10.1016/j.avsg.2014.08.030 Ó 2015 Elsevier Inc. All rights reserved. Manuscript received: July 15, 2014; manuscript accepted: August 30, 2014; published online: ---.
After interventions for common carotid artery (CCA) and ICA disease that involves the origin of the ECA, the ECA can become stenotic or even occluded. ECA stenosis can occur in 5e11% of cases after carotid endarterectomy.5,6 In contrast, higher rates of stenosis and progression of preexisting stenosis have been seen in the ECA after ICA stenting; however, the rates of occlusion remain low.6e8 In other studies, patients who underwent carotid stenting were observed to have a significantly greater mean increase in peak systolic velocities (PSVs) of the ECA and higher rate of occlusion when compared with patients who underwent open carotid procedures.7,9,10 Interestingly, however, this group of patients did not have evidence of progression to full occlusion at 2-year follow-up.10 These patients in general remain asymptomatic with regard to their cerebral circulation, although jaw claudication has been associated with ECA stenosis after stenting.11 1
2 Siracuse et al.
There are no data predicting stenosis of the ECA after stenting based on either the type of or size of stent, patient characteristics and comorbidities, or periprocedural medications. Analysis of ICA instent restenosis shows female gender, advanced age, diabetes, stent width, stent length, smoking, and low high-density lipoprotein levels as predictive factors of postprocedure occlusion; however, it is unknown whether these factors affect the ECA patency poststenting as well.12 Our objective was therefore to describe the natural history of ECA patency after ICA stenting that crosses the ECA origin, as well as to identify any factors predictive of long-term ECA stenosis, using internal data from our institution. Our second goal was to determine the clinical significance of ECA stenosis in this setting.
METHODS All patients who underwent carotid stenting by vascular surgeons at New York-Presbyterian Hospital/Columbia University Medical Center between 2005 and 2013 were reviewed in detail. Patients in whom the ECA origin was not covered with the stent were excluded from the analysis. Patient demographics, comorbidities, symptoms, stent type and size, and medications were recorded. Our cutoff for stenosis of the ECA was a PSV of 300 cm/sec or greater.13 We chose to treat the ECA more as an independent peripheral vessel and 300 cm/sec has also been used as a cutoff for ECA stenosis.13 Some studies have used ECA/CCA ratio as a measure of ECA stenosis; however, this has not been validated as it has for the ICA.6 We did however include it as a comparison to our criteria. We also used a 2fold increase in PSV as the cutoff for a significant change in the velocity pre- and poststenting. This is to take into account prestenting PSV values that approach or are above 300 cm/sec to more accurately see if there was a change between the 2 samplings rather than detecting a new stenosis with a small increase in velocity. All patients were started on aspirin and clopidogrel at completion of the stenting procedure if they were not already on antiplatelet therapy. Follow-up was initially performed for all patients at 1 month and then at every 6 months thereafter with assessment of symptoms, physical examination, and duplex ultrasonography. Preoperative variables were analyzed using Student’s t-test or analysis of variance for continuous data and chi-squared or Fisher’s exact test for categorical data. We constructed prediction models using linear or logistic regression where appropriate. Survival probability was estimated using the
Annals of Vascular Surgery
Table I. Patient and stent characteristics Covariate
Total Age Male Diabetes Hypertension Hyperlipidemia CAD COPD CRI Current smoker Former smoker Statin use b-blocker Stent diameter Stent length Stent type Vivexx Acculink Prot eg e Cordis
ECA stenosis (%)
No ECA stenosis (%)
6 67 3 (50) 2 (33) 4 (67) 2 (33) 2 (33) 1 (17) 2 (33) 1 (17) 3 (50) 4 (67) 3 (50) 6.8 mm 38 mm
66 72 46 (70) 20 (31) 55 (85) 37 (57) 32 (49) 7 (11) 19 (29) 13 (20) 35 (54) 47 (72) 37 (57) 7.0 mm 34 mm
2 2 0 2
12 23 13 15
(33) (33) (0) (33)
P value
0.16 0.36 0.32 0.90 0.26 0.27 0.46 0.66 0.82 0.84 0.86 0.77 0.74 0.63 0.54 0.57
(18) (35) (20) (23)
CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; CRI, chronic renal insufficiency.
KaplaneMeier method. Univariable Cox proportional hazards models were constructed to describe the survival experience among time-dependent outcomes. All tests used were 2-sided with a P value 300 cm/sec), the 9 previously mentioned patients all had an ECA/CCA ratio of >4:1 with a mean of 9.7 (range 5e15), and in the group 4:1 ratio with at least an increase of 1 (mean increase in ratio of 5, range 3e9). There were 3 additional patients who met the criteria for poststent ECA stenosis for a total of 9 of 72 (12.5%) patients when comparing ECA/ CCA PSV ratios.
External carotid stenosis after carotid stenting 3
Fig. 1. Freedom from stenosis of the ECA after ICA stenting.
On univariate analysis, there were no demographic factors, comorbidities, stent characteristics, or medications that were predictive of long-term patency of the ECA. KaplaneMeier analysis demonstrated that 80% of the patients were free from stenosis at 5 years (Fig. 1). Interestingly, none of the patients with clinically significant stenosis had any meaningful neurological or extracranial symptoms such as jaw claudication, although, notably, none of these patients with a new ECA stenosis exhibited evidence of increase in PSV of the stented ICA (84 ± 5 postoperative PSV).
DISCUSSION Our study demonstrates an 8.3% rate of stenosis after coverage of the origin of the ECA while treating a lesion in the ICA distribution. None of the ECA stenoses progressed to complete occlusions over the study period and none of the patients with altered external carotid flow exhibited any clinically meaningful symptoms of hypoperfusion. No demographic variable, comorbid condition, stent characteristic, or disease-modifying medication was significantly associated with the development of ECA stenosis, including the traditional predictors of ICA in-stent restenosis such as female gender, advanced age, diabetes, stent width, and stent length. All patients maintained patency of their ICA over the study period, which did not allow us to assess the clinical significance of ECA stenosis in the presence of an ICA stenosis. Four prior studies have looked at external carotid flow after carotid stenting. Woo et al. identified an overall increase in velocities in the ECA after stenting compared with open endarterectomy, with 2 ECA occlusions noted in the stenting group only.6 This,
4 Siracuse et al.
however, looked at changes in velocities, but did not qualify whether these represented the development of a significant stenosis in each patient. de Borst et al. found increased ECA stenosis to be present in almost 74% of their patients; however, their cutoff for 50% stenosis was a PSV of 125 cm/sec. This value has been validated in existing literature for defining stenosis of ICA; however, using it to establish ECA stenosis has not been validated and it may overestimate the degree of stenosis.14 Therefore, we used a more stringent cutoff of 300 cm/sec, consistent with other peripheral vessels, with at least a 2-fold change required from prestenting PSV to account for patients who had elevated but compensated velocities before stenting.14 Casey et al. showed a higher rate of ECA stenosis/occlusion after stenting compared with endarterectomy using ECA/CCA criteria. In this series, all patients with poststenting ECA stenosis were asymptomatic as well.6 Brewster et al. did not look at stenosis but had an occlusion rate of 3.8%. Despite having a large amount of patients and longterm follow-up, they did not identify any patients with an ECA and ICA stenosis further showing that this is very uncommon. There are some limitations to our study. It is a single center, retrospective review, and our results should be evaluated with consideration for the inherent bias that exists with this design methodology. That being said, this is the largest study in the existing body of literature that focuses on significant (>50%) ECA stenosis defined according to rigorous objective criteria, as well as the only study that critically assesses factors that may be predictive or associated with this entity. The importance of the ECA as a collateral has previously been demonstrated in cases where there is severe stenosis of the ICA. Otherwise, ECA stenosis or even occlusion is typically asymptomatic. In our study, only one patient had a significant restenosis of the ICA, and this individual did not have ECA stenosis. While ECA stenosis or occlusion may be a cause for concern in patients with ICA in-stent restenosis, we did not have significant statistical power to definitely establish this beyond speculation. Larger studies with greater sample sizes are needed to further evaluate this phenomenon. On the basis of our analysis, we can conclude, however, that in patients with patent ICA stents, ECA stenosis is not common and most likely of little consequence. Therefore, placement of stents across ECA origin appears to be safe and may be customarily utilized in endovascular procedures to treat stenotic common and internal carotid arteries. However, the clinical significance in association with an ICA stenosis remains unclear.
Annals of Vascular Surgery
CONCLUSION The rate of ECA stenosis after endovascular ICA and CCA stenting was 8% in our population, with no incidences of progression to total occlusions. ECA stenosis was not associated with symptomatic cerebral ischemia. Patient characteristics, comorbidities, stent characteristics, and medication profile were not associated with stenosis. Potential for ECA stenosis should not deter stenting across the ECA origin if necessary.
REFERENCES 1. Zarins CK, DelBeccaro EJ, Johns L, et al. Increased cerebral blood flow after external carotid artery revascularization. Surgery 1981;89:730e4. 2. Fokkema M, Reichmann B, den Hartog A, et al. Selective external endarterectomy in patients with ipsilateral symptomatic internal carotid artery occlusion. J Vasc Surg 2013;58:145e51. 3. Fearn SJ, Picton AJ, Mortimer AJ, et al. The contribution of the external carotid artery to cerebral perfusion in carotid disease. J Vasc Surg 2000;31:989e93. 4. Dalainas I, Avgerinos ED, Daskalopoulos ME, et al. The critical role of the external carotid artery in cerebral perfusion of patients with total occlusion of the internal carotid artery. Int Angiol 2012;31:16e21. 5. Abbas SM, Adams D, Vanniasingham P. What happens to the external carotid artery following carotid endarterectomy? BMC Surg 2008;8:20. 6. Casey K, Zhou W, Tedesco MM, et al. Fate of the external carotid artery following carotid interventions. Int J Angiol 2009;18:173e6. 7. Woo EY, Karmacharya J, Velazquez OC, et al. Differential effects of carotid artery stenting versus carotid endarterectomy on external carotid artery patency. J Endovasc Ther 2007;14:208e13. 8. de Borst GJ, Vos JA, Reichmann B, et al. The fate of the external carotid artery after carotid artery stenting. A follow-up study with duplex ultrasonography. Eur J Vasc Endovasc Surg 2007;33:657e63. 9. Brown K, Itum DS, Preiss J, et al. Carotid artery stenting has increased risk of external carotid artery occlusion compared with carotid endarterectomy. J Vasc Surg 2014 [Epub ahead of print]. 10. Reichmann BL, Hellings WE, van der Worp HB, et al. Flow velocities in the external carotid artery following carotid revascularization. Eur J Vasc Endovasc Surg 2013;46: 411e7. 11. Willfort-Ehringer A, Ahmadi R, Gruber D, et al. Effect of carotid artery stenting on the external carotid artery. J Vasc Surg 2003;38:1039e44. 12. Wasser K, Schnaudigel S, Wohlfahrt J, et al. Clinical impact and predictors of carotid artery in-stent restenosis. J Neurol 2012;259:1896e902. 13. Zierler RE, Strandness DE. Duplex Scanning in Vascular Disorders. 4th ed. Philadelphia: Lippincott, Williams & Wilkins, 2010. 14. Grant EG, Benson CB, Moneta GL, et al. Carotid artery stenosis: gray-scale and Doppler US diagnosisdSociety of Radiologists in Ultrasound Consensus Conference. Radiology 2003;229:340e6.
Background: The external carotid artery (ECA) can be an important collateral for cerebral perfusion in the presence of severe internal carotid artery (ICA) disease. ICA stenting that covers the ECA origin may put the ECA at increased risk of stenosis. Our objective was to determine the rate of ECA stenosis secondary to ICA stenting, determine predictive factors, and describe any subsequent associated symptoms. Methods: We retrospectively reviewed clinical data on all ICA stents crossing the origin of the ECA placed by vascular surgeons at our institution. We analyzed patient demographics, comorbidities, stent type and sizes, as well as medication profile to determine predictors of ECA stenosis. Results: Between 2005 and 2013, there were 72 (out of 119 total ICA stenting) patients (mean age 71, 68% male) who underwent placement of ICA stents that also crossed the origin of the ECA. Six patients (8.3%) had a significantly increased ECA stenosis postprocedure. There were no occlusions. All patients with ECA stenosis maintained patency of their ICA stent and were asymptomatic. Age, gender, comorbidities, stent type and size, and medication profile were not associated with ECA stenosis after stenting. Conclusions: ECA stenosis after ICA stenting covering the ECA origin is uncommon and not clinically significant in patients with patent ICA stents. The clinical significance of concurrent ECA and ICA stenosis after stenting is unclear as it is not captured here. The potential for ECA stenosis should not deter stenting across the ECA origin if necessary. Patient and stent factors are not predictive of ECA stenosis.
INTRODUCTION Although the external carotid artery (ECA) normally does not contribute significantly to cerebral blood flow, in cases where there is a stenosis or occlusion of the internal carotid artery (ICA), the ECA can be an important source of collateral perfusion.1e3 This is particularly important for flow in the middle cerebral artery distribution.4
Section of Vascular Surgery and Endovascular Interventions, New York-Presbyterian Hospital, Columbia University, College of Physicians and Surgeons, New York, NY. Correspondence to: Jeffrey J. Siracuse, MD, Department of Surgery, Boston University, Boston Medical Center, 732 Harrison Avenue, Boston, MA 02218, USA; E-mail: [email protected] Ann Vasc Surg 2015; -: 1–4 http://dx.doi.org/10.1016/j.avsg.2014.08.030 Ó 2015 Elsevier Inc. All rights reserved. Manuscript received: July 15, 2014; manuscript accepted: August 30, 2014; published online: ---.
After interventions for common carotid artery (CCA) and ICA disease that involves the origin of the ECA, the ECA can become stenotic or even occluded. ECA stenosis can occur in 5e11% of cases after carotid endarterectomy.5,6 In contrast, higher rates of stenosis and progression of preexisting stenosis have been seen in the ECA after ICA stenting; however, the rates of occlusion remain low.6e8 In other studies, patients who underwent carotid stenting were observed to have a significantly greater mean increase in peak systolic velocities (PSVs) of the ECA and higher rate of occlusion when compared with patients who underwent open carotid procedures.7,9,10 Interestingly, however, this group of patients did not have evidence of progression to full occlusion at 2-year follow-up.10 These patients in general remain asymptomatic with regard to their cerebral circulation, although jaw claudication has been associated with ECA stenosis after stenting.11 1
2 Siracuse et al.
There are no data predicting stenosis of the ECA after stenting based on either the type of or size of stent, patient characteristics and comorbidities, or periprocedural medications. Analysis of ICA instent restenosis shows female gender, advanced age, diabetes, stent width, stent length, smoking, and low high-density lipoprotein levels as predictive factors of postprocedure occlusion; however, it is unknown whether these factors affect the ECA patency poststenting as well.12 Our objective was therefore to describe the natural history of ECA patency after ICA stenting that crosses the ECA origin, as well as to identify any factors predictive of long-term ECA stenosis, using internal data from our institution. Our second goal was to determine the clinical significance of ECA stenosis in this setting.
METHODS All patients who underwent carotid stenting by vascular surgeons at New York-Presbyterian Hospital/Columbia University Medical Center between 2005 and 2013 were reviewed in detail. Patients in whom the ECA origin was not covered with the stent were excluded from the analysis. Patient demographics, comorbidities, symptoms, stent type and size, and medications were recorded. Our cutoff for stenosis of the ECA was a PSV of 300 cm/sec or greater.13 We chose to treat the ECA more as an independent peripheral vessel and 300 cm/sec has also been used as a cutoff for ECA stenosis.13 Some studies have used ECA/CCA ratio as a measure of ECA stenosis; however, this has not been validated as it has for the ICA.6 We did however include it as a comparison to our criteria. We also used a 2fold increase in PSV as the cutoff for a significant change in the velocity pre- and poststenting. This is to take into account prestenting PSV values that approach or are above 300 cm/sec to more accurately see if there was a change between the 2 samplings rather than detecting a new stenosis with a small increase in velocity. All patients were started on aspirin and clopidogrel at completion of the stenting procedure if they were not already on antiplatelet therapy. Follow-up was initially performed for all patients at 1 month and then at every 6 months thereafter with assessment of symptoms, physical examination, and duplex ultrasonography. Preoperative variables were analyzed using Student’s t-test or analysis of variance for continuous data and chi-squared or Fisher’s exact test for categorical data. We constructed prediction models using linear or logistic regression where appropriate. Survival probability was estimated using the
Annals of Vascular Surgery
Table I. Patient and stent characteristics Covariate
Total Age Male Diabetes Hypertension Hyperlipidemia CAD COPD CRI Current smoker Former smoker Statin use b-blocker Stent diameter Stent length Stent type Vivexx Acculink Prot eg e Cordis
ECA stenosis (%)
No ECA stenosis (%)
6 67 3 (50) 2 (33) 4 (67) 2 (33) 2 (33) 1 (17) 2 (33) 1 (17) 3 (50) 4 (67) 3 (50) 6.8 mm 38 mm
66 72 46 (70) 20 (31) 55 (85) 37 (57) 32 (49) 7 (11) 19 (29) 13 (20) 35 (54) 47 (72) 37 (57) 7.0 mm 34 mm
2 2 0 2
12 23 13 15
(33) (33) (0) (33)
P value
0.16 0.36 0.32 0.90 0.26 0.27 0.46 0.66 0.82 0.84 0.86 0.77 0.74 0.63 0.54 0.57
(18) (35) (20) (23)
CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; CRI, chronic renal insufficiency.
KaplaneMeier method. Univariable Cox proportional hazards models were constructed to describe the survival experience among time-dependent outcomes. All tests used were 2-sided with a P value 300 cm/sec), the 9 previously mentioned patients all had an ECA/CCA ratio of >4:1 with a mean of 9.7 (range 5e15), and in the group 4:1 ratio with at least an increase of 1 (mean increase in ratio of 5, range 3e9). There were 3 additional patients who met the criteria for poststent ECA stenosis for a total of 9 of 72 (12.5%) patients when comparing ECA/ CCA PSV ratios.
External carotid stenosis after carotid stenting 3
Fig. 1. Freedom from stenosis of the ECA after ICA stenting.
On univariate analysis, there were no demographic factors, comorbidities, stent characteristics, or medications that were predictive of long-term patency of the ECA. KaplaneMeier analysis demonstrated that 80% of the patients were free from stenosis at 5 years (Fig. 1). Interestingly, none of the patients with clinically significant stenosis had any meaningful neurological or extracranial symptoms such as jaw claudication, although, notably, none of these patients with a new ECA stenosis exhibited evidence of increase in PSV of the stented ICA (84 ± 5 postoperative PSV).
DISCUSSION Our study demonstrates an 8.3% rate of stenosis after coverage of the origin of the ECA while treating a lesion in the ICA distribution. None of the ECA stenoses progressed to complete occlusions over the study period and none of the patients with altered external carotid flow exhibited any clinically meaningful symptoms of hypoperfusion. No demographic variable, comorbid condition, stent characteristic, or disease-modifying medication was significantly associated with the development of ECA stenosis, including the traditional predictors of ICA in-stent restenosis such as female gender, advanced age, diabetes, stent width, and stent length. All patients maintained patency of their ICA over the study period, which did not allow us to assess the clinical significance of ECA stenosis in the presence of an ICA stenosis. Four prior studies have looked at external carotid flow after carotid stenting. Woo et al. identified an overall increase in velocities in the ECA after stenting compared with open endarterectomy, with 2 ECA occlusions noted in the stenting group only.6 This,
4 Siracuse et al.
however, looked at changes in velocities, but did not qualify whether these represented the development of a significant stenosis in each patient. de Borst et al. found increased ECA stenosis to be present in almost 74% of their patients; however, their cutoff for 50% stenosis was a PSV of 125 cm/sec. This value has been validated in existing literature for defining stenosis of ICA; however, using it to establish ECA stenosis has not been validated and it may overestimate the degree of stenosis.14 Therefore, we used a more stringent cutoff of 300 cm/sec, consistent with other peripheral vessels, with at least a 2-fold change required from prestenting PSV to account for patients who had elevated but compensated velocities before stenting.14 Casey et al. showed a higher rate of ECA stenosis/occlusion after stenting compared with endarterectomy using ECA/CCA criteria. In this series, all patients with poststenting ECA stenosis were asymptomatic as well.6 Brewster et al. did not look at stenosis but had an occlusion rate of 3.8%. Despite having a large amount of patients and longterm follow-up, they did not identify any patients with an ECA and ICA stenosis further showing that this is very uncommon. There are some limitations to our study. It is a single center, retrospective review, and our results should be evaluated with consideration for the inherent bias that exists with this design methodology. That being said, this is the largest study in the existing body of literature that focuses on significant (>50%) ECA stenosis defined according to rigorous objective criteria, as well as the only study that critically assesses factors that may be predictive or associated with this entity. The importance of the ECA as a collateral has previously been demonstrated in cases where there is severe stenosis of the ICA. Otherwise, ECA stenosis or even occlusion is typically asymptomatic. In our study, only one patient had a significant restenosis of the ICA, and this individual did not have ECA stenosis. While ECA stenosis or occlusion may be a cause for concern in patients with ICA in-stent restenosis, we did not have significant statistical power to definitely establish this beyond speculation. Larger studies with greater sample sizes are needed to further evaluate this phenomenon. On the basis of our analysis, we can conclude, however, that in patients with patent ICA stents, ECA stenosis is not common and most likely of little consequence. Therefore, placement of stents across ECA origin appears to be safe and may be customarily utilized in endovascular procedures to treat stenotic common and internal carotid arteries. However, the clinical significance in association with an ICA stenosis remains unclear.
Annals of Vascular Surgery
CONCLUSION The rate of ECA stenosis after endovascular ICA and CCA stenting was 8% in our population, with no incidences of progression to total occlusions. ECA stenosis was not associated with symptomatic cerebral ischemia. Patient characteristics, comorbidities, stent characteristics, and medication profile were not associated with stenosis. Potential for ECA stenosis should not deter stenting across the ECA origin if necessary.
REFERENCES 1. Zarins CK, DelBeccaro EJ, Johns L, et al. Increased cerebral blood flow after external carotid artery revascularization. Surgery 1981;89:730e4. 2. Fokkema M, Reichmann B, den Hartog A, et al. Selective external endarterectomy in patients with ipsilateral symptomatic internal carotid artery occlusion. J Vasc Surg 2013;58:145e51. 3. Fearn SJ, Picton AJ, Mortimer AJ, et al. The contribution of the external carotid artery to cerebral perfusion in carotid disease. J Vasc Surg 2000;31:989e93. 4. Dalainas I, Avgerinos ED, Daskalopoulos ME, et al. The critical role of the external carotid artery in cerebral perfusion of patients with total occlusion of the internal carotid artery. Int Angiol 2012;31:16e21. 5. Abbas SM, Adams D, Vanniasingham P. What happens to the external carotid artery following carotid endarterectomy? BMC Surg 2008;8:20. 6. Casey K, Zhou W, Tedesco MM, et al. Fate of the external carotid artery following carotid interventions. Int J Angiol 2009;18:173e6. 7. Woo EY, Karmacharya J, Velazquez OC, et al. Differential effects of carotid artery stenting versus carotid endarterectomy on external carotid artery patency. J Endovasc Ther 2007;14:208e13. 8. de Borst GJ, Vos JA, Reichmann B, et al. The fate of the external carotid artery after carotid artery stenting. A follow-up study with duplex ultrasonography. Eur J Vasc Endovasc Surg 2007;33:657e63. 9. Brown K, Itum DS, Preiss J, et al. Carotid artery stenting has increased risk of external carotid artery occlusion compared with carotid endarterectomy. J Vasc Surg 2014 [Epub ahead of print]. 10. Reichmann BL, Hellings WE, van der Worp HB, et al. Flow velocities in the external carotid artery following carotid revascularization. Eur J Vasc Endovasc Surg 2013;46: 411e7. 11. Willfort-Ehringer A, Ahmadi R, Gruber D, et al. Effect of carotid artery stenting on the external carotid artery. J Vasc Surg 2003;38:1039e44. 12. Wasser K, Schnaudigel S, Wohlfahrt J, et al. Clinical impact and predictors of carotid artery in-stent restenosis. J Neurol 2012;259:1896e902. 13. Zierler RE, Strandness DE. Duplex Scanning in Vascular Disorders. 4th ed. Philadelphia: Lippincott, Williams & Wilkins, 2010. 14. Grant EG, Benson CB, Moneta GL, et al. Carotid artery stenosis: gray-scale and Doppler US diagnosisdSociety of Radiologists in Ultrasound Consensus Conference. Radiology 2003;229:340e6.
