Skip to main content
Advertisement

Main menu

  • Home
  • Content
    • Current Issue
    • Publication Preview--Ahead of Print
    • Past Issue Archive
    • Case of the Week Archive
    • Classic Case Archive
    • Case of the Month Archive
  • For Authors
  • About Us
    • About AJNR
    • Editors
    • American Society of Neuroradiology
  • Submit a Manuscript
  • Podcasts
    • Subscribe on iTunes
    • Subscribe on Stitcher
  • More
    • Subscribers
    • Permissions
    • Advertisers
    • Alerts
    • Feedback
  • Other Publications
    • ajnr

User menu

  • Subscribe
  • Alerts
  • Log in

Search

  • Advanced search
American Journal of Neuroradiology
American Journal of Neuroradiology

American Journal of Neuroradiology

  • Subscribe
  • Alerts
  • Log in

Advanced Search

  • Home
  • Content
    • Current Issue
    • Publication Preview--Ahead of Print
    • Past Issue Archive
    • Case of the Week Archive
    • Classic Case Archive
    • Case of the Month Archive
  • For Authors
  • About Us
    • About AJNR
    • Editors
    • American Society of Neuroradiology
  • Submit a Manuscript
  • Podcasts
    • Subscribe on iTunes
    • Subscribe on Stitcher
  • More
    • Subscribers
    • Permissions
    • Advertisers
    • Alerts
    • Feedback
  • Follow AJNR on Twitter
  • Visit AJNR on Facebook
  • Follow AJNR on Instagram
  • Join AJNR on LinkedIn
  • RSS Feeds
Research ArticleInterventional
Open Access

Short- and Long-Term Hemodynamic and Clinical Effects of Carotid Artery Stenting

B. Yang, W. Chen, Y. Yang, Y. Lin, Y. Duan, J. Li, H. Wang, F. Fu, Q. Zhuge and X. Chen
American Journal of Neuroradiology June 2012, 33 (6) 1170-1176; DOI: https://doi.org/10.3174/ajnr.A2930
B. Yang
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
W. Chen
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Y. Yang
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Y. Lin
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Y. Duan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
J. Li
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
H. Wang
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
F. Fu
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Q. Zhuge
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
X. Chen
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • References
  • PDF
Loading

Abstract

BACKGROUND AND PURPOSE: Stenosis of the carotid artery may cause reduced hemodynamic and neural function that may be ameliorated with CAS. The goal of this study was to evaluate short- and long-term hemodynamic and clinical effects after CAS.

MATERIALS AND METHODS: Hemodynamic parameters were acquired by PCT within 1 week before CAS and at 1 week and 1 year (10–13 months) after CAS. In ACA territory, MCA territory, PCA territory, basal ganglia, anterior and posterior CWS and IWS, the rCBF, rCBV, and rMTT were determined in 20 patients with unilateral carotid artery stenosis who underwent CAS. MR and noncontrast CT were performed within 1 week before CAS. Noncontrast CT and carotid arteriography were performed immediately after CAS. Carotid arteriography was performed 1 year after CAS. MRS was performed in 3 measurements. The variance analysis was performed to determine whether there were significant differences among the 3 measurements.

RESULTS: No significant differences were found among rCBV in any territory (P > .05). In the non-PCA territories, rMTT decreased and rCBF increased at 1 week after CAS (P < .01), but there was no significant difference between 1-week and 1-year effects (P > .05). For MR spectroscopy, no significant differences were found between 1 week after CAS and pretreatment (P > .05); the 1-year scores improved significantly (P < .01).

CONCLUSIONS: The long-term hemodynamic and clinical results after treatment validated that CAS is a durable procedure. The 1-week hemodynamic effects can predict long-term effects.

ABBREVIATIONS:

ACA
anterior cerebral artery
CAS
carotid artery stenting
CEA
carotid endarterectomy
CWS
cortical watershed
ISR
in-stent restenosis
IWS
internal watershed
PCA
posterior cerebral artery
PCT
perfusion CT
rCBF
relative cerebral blood flow
rCBV
relative cerebral blood volume
rMTT
relative mean transit time

Extracranial internal carotid artery stenosis accounts for 15%–20% of ischemic strokes, moreover, 14% and 23% of the patients with a TIA or stroke attributable to a high-grade intracranial stenosis had a further ipsilateral ischemic stroke over the next year, despite medical therapy.1⇓–3 CEA, as the treatment cornerstone, is of some benefit for patients with 50%–69% symptomatic stenosis and highly beneficial for those with 70% symptomatic stenosis or greater.4 CEA, although effective, does have limitations, such as the strict indications and contraindications. Thanks to the development of safe and effective protection systems that have helped reduce the periprocedural neurologic complications in recent years, CAS is increasingly used as an alternative method to CEA for treatment of ICA stenosis.5⇓–7 Moreover, among patients with symptomatic or asymptomatic carotid stenosis, the risk of the composite primary outcome of stroke, myocardial infarction, or death did not differ significantly in the group undergoing CAS and the group undergoing CEA.8

Before or after CAS, PET, SPECT, PCT, and MR imaging have all been applied in the study of brain hemodynamics.9 However, the scarce availability in most radiology departments is considered as a large obstacle in the choice of PET and SPECT. In addition, difficulty in obtaining a quantitative measurement by MR imaging has drawn attention for many years. PCT, applied more and more widely, can be easily performed and has further simplified the approach to brain perfusion evaluation.10 Furthermore, PCT can be used to quantitatively estimate cerebral perfusion changes, such as an asymmetry in the hemisphere corresponding to the affected ICA, in patients with unilateral severe ICA stenosis.11

Some studies have investigated short-term hemodynamic effects after CAS by hemodynamic parameter measurement in the hemisphere on the side of the carotid stenosis,9,12 but few studies have been designed to evaluate short- and long-term hemodynamic effects after CAS in the territories of main cerebral arteries, and few studies have evaluated not only hemodynamic but also clinical effects after CAS. The aim of our study was to evaluate short- and long-term hemodynamic and clinical changes after CAS, and to analyze the relevance between the 2 changes.

Materials and Methods

We included 20 patients (17 men, 3 women; mean age 64 ± 8 years; range 46–75 years) in this study between April 2006 and March 2009. Inclusion criteria were as follows: 1) patients with unilateral ICA stenosis (≥60%) and without contralateral ICA steno-occlusive disease who met criteria for CAS and who were treated with CAS; 2) carotid DSA performed within 1 week before CAS to investigate the stenosis vessel and degree; cerebral PCT performed within 1 week before CAS to evaluate hemodynamic changes attributable to a high-grade carotid stenosis; cerebral MR imaging and noncontrast CT performed within 1 week before CAS to define the intracranial diseases, such as cerebral infarction or any other diseases affecting cerebral perfusion; 3) cerebral noncontrast CT performed immediately after CAS to define intracranial complications, such as intracranial hemorrhage; PCT performed at 1 week and at 1 year (10–13 months) after CAS; carotid arteriography performed immediately after CAS to define the residual stenosis and at 1 year (10–13 months) after treatment to define ISR if present; 4) neural function testing performed with MR spectroscopy in the 3 measurements; and 5) possible complications of CAS and the adverse effects of radiographic examinations were fully explained to every patient, and all patients in this study signed informed consent for research.

Exclusion criteria were as follows: 1) in addition to ICA, any other intracranial artery steno-occlusive diseases, such as contralateral ICA; 2) except cerebral infarction, any other diseases affecting cerebral perfusion, such as brain tumor; 3) cerebral MR imaging, noncontrast CT, or cerebral PCT not performed in 1 week before CAS; and 4) patients who were lost to follow-up at 1 week or 1 year after treatment.

MR imaging examination was performed on a Signa Excite 1.5 MR scanner (GE Healthcare; Milwaukee, Wisconsin) with the following scanning sequences: 1) (FLAIR) T1WI: TR 2100 ms, TE 27 ms, TI 750 ms, FOV 24 cm × 24 cm; 2) T2WI: TR 4400 ms, TE 102 ms, FOV 24 cm × 18 cm, matrix 256 × 192; and 3) DWI: TR 5000 ms, TE 100 ms, b-value of 1000 seconds/mm2.

DSA examination was performed with the Allura Xper FD 20 angiographic unit (Philips Medical Systems, Best, the Netherlands). On the angiograms of each patient (contrast medium 10 mL, bolus 3.5 ∼ 4.0 mL/s, pressure 150 ∼ 200 psi, 80 kVp, 20 mAs), the principal neuroradiologist measured the degree of carotid stenosis by percent diameter ratios.13⇓⇓–16

All CT scans were performed on a 16-section multidetector CT scanner (Light Speed 16; GE Healthcare). Noncontrast CT scans of the whole brain in an orientation parallel to the orbito-meatal line were obtained (5-mm section thickness, 5-mm section interval, 80 kVp, 120 mAs). From these images, 4 target sections for PCT examination were selected, which were judged from the level of the basal ganglia to the level of the upper portion of the lateral ventricles. Once the target cross-sections were selected, a bolus of 50 mL nonionic iodinated contrast agent was injected into the antecubital vein at an injection rate of 4.0 mL/s. Dynamic CT scans were then initiated 7 seconds after the start of injection with the following acquisition parameters: 80 kVp, 200 mAs, 50-second scanning time, and 50 images per section.

Postprocessing was performed by 1 neuroradiologist (with 6 years' experience in generating and interpreting PCT) from our institution, and he had no other involvement in the study. The image data were transferred to a dedicated workstation (Advantage Window 4.2; GE Healthcare) for postprocessing. In each patient, for the manual method, an arterial input ROI was placed in the ACA contralateral to the stenosis, and the venous input ROI was placed in the superior sagittal sinus.17 By calculation of the software, he got the maps that could show the absolute parameter values: CBF (expressed in mL per 100 g brain per minute), CBV (expressed in mL per 100 g brain), and MTT (expressed in seconds).

To quantify changes in perfusion parameters in all the territories, the rater chose ROIs on the 2 slabs, the level of the basal ganglia, and the level of the body lateral cerebral ventricle. In consideration of perfusion differences between gray matter and white matter, the rater chose ROIs including only gray matter, except IWS ROIs, and ensured the exclusion of bone tissue, CSF, large vessels, and cerebral infarction from the ROIs. Because long-term variability increased with the use of a small ROI, though improved with the averaging of more pixel values,17 the rater obtained some small ROIs in the same territory for the average parameter values. On the level of the basal ganglia (Fig 1A), the rater defined 5 ROIs in unilateral cerebral hemisphere as ACA territory, PCA territory, basal ganglia, anterior CWS, and posterior CWS, and, in view of many vessels in MCA territory, defined 2 ROIs as MCA territory. On the level of the body lateral cerebral ventricle (Fig 1B), the rater defined 4 ROIs in unilateral cerebral hemisphere corresponding to ACA territory, PCA territory, and anterior and posterior CWS, and, respectively, chose 3 ROIs as IWS and MCA territory. To the greatest extent possible, the rater kept the ROI size of every patient consistent in the same territory (basal ganglia ROI approximately 120 mm2 in size, IWS ROI approximately 40 mm2, any other ROI approximately 70 mm2). Through this method, the rater obtained 7 territories and 17 ROIs in the unilateral cerebral hemisphere, and, except in the basal ganglia, calculated the average absolute values of CBF, CBV, and MTT in any other territory. In the analysis, to avoid the impact of intersubject variation, the rater chose relative perfusion values (the symptomatic hemisphere to asymptomatic hemisphere ratios), and then, respectively, obtained rCBF, rCBV, and rMTT. The rater assessed the imaging independently, blinded to clinical information.

Fig 1.
  • Download figure
  • Open in new tab
  • Download powerpoint
Fig 1.

The ROIs of the 2 slabs in bilateral hemispheres. ROI maps show the level of the basal ganglia (A), including ACA territory (1–2), MCA territory (3–6), PCA territory (7–8), basal ganglia (9–10), anterior CWS (11–12), and posterior CWS (13–14); and also show the level of the body lateral cerebral ventricle (B), including ACA territory (15–16), MCA territory (17–22), PCA territory (23–24), anterior CWS (25–26), posterior CWS (27–28), and IWS (29–34).

Within 1 week before CAS, and at 1 week and 1 year after CAS, MR spectroscopy was performed by 1 neurologist (with 6 years' clinical experience) who had no other involvement in the study.

All of the statistical analyses were performed by SPSS statistical software (Version 17.0, SPSS, Chicago, Illinois). A P value < .05 was considered to indicate statistical significance. The variance analysis was performed to determine whether there were significant differences among 3 PCT parameters in all territories and among MR spectroscopy in the 3 measurements, and the least significant difference t test was used between any 2 measurements.

Results

The main MR imaging findings of 14 patients were multiple lacunar infarcts; 6 patients were observed with infarcts in the territory of stenosis of the ICA (the frontal lobe, 312 mm2; the parietal lobe, 338 mm2; the temporal lobe, 432 mm2, 552 mm2; and the basal ganglia, 112 mm2, 120 mm2). All 20 patients enrolled in this study did not present with any other diseases.

The mean stenosis degree of the ICAs in the 20 patients was 87% (range: 80 ∼ 95%) before CAS (Fig 2A). In 17 patients, ICAs immediately restored to normal, according to arteriography after CAS (Fig 2B), and the residual stenosis range of 3 patients was 10 ∼ 20%. The mean ICA stenosis degree of the 20 patients decreased to 2.5% (range: 0 ∼ 20%). At 1 year after CAS, the carotid arteriography indicated that none of the 20 patients underwent significant ISR.

Fig 2.
  • Download figure
  • Open in new tab
  • Download powerpoint
Fig 2.

95% stenosis (A) of right carotid artery in a patient aged 71 years and basically normal (B) after CAS.

Hyperperfusion is classically defined as >100% increase in CBF compared with preoperative values,18 so none was observed with hyperperfusion after CAS (Fig 3). The results showed the comparison of cerebral hemodynamics (Figs 3–5) and the comparison of relative perfusion parameters among the 3 measurements (Table 1). In the 3 measurements, no significant differences were found among rCBVs in any territory (P > .05). In the non-PCA territories, rMTT decreased and rCBF increased at 1 week after CAS (P < .01), but there was no significant difference between 1-week and 1-year effects after CAS (P > .05).

Fig 3.
  • Download figure
  • Open in new tab
  • Download powerpoint
Fig 3.

On the level of the basal ganglia (left) and the body lateral cerebral ventricle (right), CBF is decreased before CAS in the right hemisphere (A, B); CBF in the affected hemisphere is improved significantly at 1 week after CAS (C, D); at 1 year after CAS, CBF is similar to that shown at 1 week after CAS (E, F).

Fig 4.
  • Download figure
  • Open in new tab
  • Download powerpoint
Fig 4.

On the level of the basal ganglia (left) and the body lateral cerebral ventricle (right), MTT is increased before CAS in the right hemisphere compared with the left hemisphere (A, B). This hemispheric difference disappeared at 1 week after CAS (C, D); compared with 1 week after CAS, no hemodynamic changes were found at 1 year after CAS (E, F).

Fig 5.
  • Download figure
  • Open in new tab
  • Download powerpoint
Fig 5.

On the level of the basal ganglia (left) and the body lateral cerebral ventricle (right), CBV is decreased before CAS in the right hemisphere (A, B); this hemispheric difference has not disappeared at 1 week after CAS (C, D) or at 1 year after CAS (E, F).

View this table:
  • View inline
  • View popup
Table 1:

Comparison of relative perfusion parameters among pretreatment, 1 week, and 1 year groups

The results showed the comparison of MR spectroscopy among the 3 measurements (Table 2). No significant differences were found between 1 week after CAS and pretreatment (P > .05); at 1 year after CAS, the scores improved significantly (P < .01).

View this table:
  • View inline
  • View popup
Table 2:

Comparison of MRS among pretreatment, 1 week, 1 year groups

Discussion

In the presence of ICA stenosis, protective collateral circulation could rapidly open to maintain normal CBF.19 In cases of severe ICA stenosis and deficient collateral circulation, hemispheric perfusion pressure is severely reduced, thus leading to maximal dilation of resistance vessels and chronic cerebral hypoperfusion,20 which may cause cerebral autoregulation dysfunction.21 Cerebral autoregulation protects the brain against changes in systemic blood pressure.21 The normal autoregulator response following a change in systemic blood pressure is rapid, and is initiated and completed within 15–30 seconds.22 After restoration of normal perfusion pressure after CAS, impaired autoregulatory mechanisms may adjust to the new steady state.20 However, in the absence of cerebral autoregulation due to critical hypoperfusion, CBF is directly dependent on the systemic blood pressure, so correction of critical stenosis causes rapid and large changes in CBF leading to hyperperfusion and intracranial hemorrhage.21

Ogasawara et al23 found that the onset of hyperperfusion peaked within a period of 12 hours postoperation in those who had undergone CAS. According to Abou-Chebl et al,24 hyperperfusion symptoms developed between 6 hours and 4 days postoperatively. Several authors have demonstrated, after surgery, maximal blood flow may occur in 3–4 days and fall to a steady state by day 7.25,26 According to these conclusions, we analyzed that blood flow could achieve steady state by 1 week after CAS. In addition, long-term results in a large cohort of patients validated that the ISR rate was acceptable and the need for reintervention was low, unrelated to the characteristics of the device.8 Progression of ISR after 6–12 months is uncommon over a 2- to 3-year period.27 In view of long-term clinical outcomes, we evaluated 1-year (10–13 months) hemodynamic and clinical changes after CAS to predict long-term effects and analyzed the relevance between 1-week and 1-year changes.

In our study, except in PCA territory, rCBF increased significantly in other territories at 1 week after CAS (P < .01). Our data indicated that CBF improved significantly after amelioration of ICA stenosis, and the conclusion of Markus and Cullinane28 was similar: there was no significant difference between rCBF measured at 1 week after CAS and that measured at 1 year after CAS (P > .05). The possible reason was that CBF could achieve a steady state at 1 week and 1 year after CAS.

Our results demonstrated that, in the 3 measurements, no significant differences were found between rCBV in all territories (P > .05). Similarly, Soinne et al29 quantitatively evaluated hemodynamic changes before surgery and 3 and 100 days afterward, and then showed, for CBV values, that there were no significant interhemispheric differences at any stage. However, Waaijer et al12 reported that rCBV was increased after treatment. We suggest this may be because, first, our ROIs were different from Waaijer et al's,12 who chose ROIS only in MCA territory. Second, CBV, as a complex physiologic parameter,30 depends on arterial, capillary, and venous compartments as well as parenchymal and pial components.

Except in PCA territory, rMTT decreased significantly in other territories at 1 week after CAS (P < .01). The results indicate that cerebral perfusion obviously improved after CAS. There was no significant difference between rMTT in any territory measured at 1 week after CAS and that measured at 1 year after CAS (P > .05). The conclusion shows the coherence of results between 1 week and 1 year, and, consequently, validated CAS as a durable procedure for amelioration of ICA stenosis. Our conclusion agrees with the study published by Soinne et al,29 where, partly, they concluded rMTT decreased significantly in 3 and 100 days after surgery. However, Kluytmans et al31 demonstrated that no significant alterations in MTT were observed in the hemisphere ipsilateral to the stenosed ICA 2–6 months after treatment. One reason might be that the variability of relative MTT was significantly lower than absolute MTT.32

In ACA territory, rCBF increased and rMTT decreased after CAS (P < .01). The absence or hypoplasia of the proximal ACA in 10% of subjects may allow similar perfusion parameters in both ACA distributions, even in tandem with a unilateral ICA stenosis. But in addition to the arterial segments of the circle of Willis, the ophthalmic artery, leptomeningeal vessels, and anastomoses between distal segments of the major cerebral arteries constitute secondary collaterals, and the number and size of these anastomotic vessels are greatest between the anterior and middle cerebral arteries.33 Secondary collateral pathways are presumed to be recruited once primary collaterals at the circle of Willis have failed, and increasing severity of carotid stenosis has been correlated with a greater extent of collateralization,33 so anastomoses between anterior and middle cerebral arteries may lead to differences between both ACA distributions in conjunction with unilateral ICA stenosis. In addition, absence of the anterior communicating artery could cause significant differences between both ACA distributions. However, rCBF and MTT changed nonsignificantly in PCA territory in the 3 measurements (P > .05). The results indicated that the influence of ICA stenosis in the territory is extremely small. The possible reasons for this are as follows: first, the number and size of these anastomotic vessels are smaller and fewer between the middle and posterior cerebral arteries, with even fewer between the posterior and anterior cerebral arteries;33 second, the absence or hypoplasia of either posterior communicating artery in 30% may allow similar perfusion parameters in both PCA distributions.

For MR spectroscopy, no significant differences were found between 1 week after CAS and pretreatment (P > .05)—a possible reason for this is the short recovery time. However, at 1 year after CAS, the scores improved significantly (P < .01). The 1-year results showed long-term improvements in neural function in patients treated with CAS, and the results were similar in Turk et al,34 who analyzed 3-month follow-up scores.

Our study analyzed hemodynamic and clinical effects before and after CAS, and evaluated the coherence of hemodynamic effects between 1 week and 1 year after CAS, emphasizing that 1-week hemodynamic follow-up has great value for predicting long-term effects and can help to avoid additional radioactive examinations. Moreover, we were able to evaluate cerebral hemodynamic changes after CAS in different cerebral artery territories. We chose ROIs in ACA territory, MCA territory, PCA territory, basal ganglia, and anterior and posterior CWS and IWS in bilateral hemispheres. Especially with IWS, we emphasized its improvement in hemodynamics after CAS, because Momjian-Mayor and Baron35 demonstrated that severe hemodynamic compromise might underlie IWS infarction, and artery-to-artery embolism might play an important role in isolated CWS infarcts. Taking into consideration the influences of physiologic variations, individual differences, and postprocessing steps,36 we specifically chose relative perfusion parameters in our study.

A limitation of the technique used in this study is that the 16-section multidetector CT scan was performed on just 4 levels, including the 4 levels of the basal ganglia and the body of the lateral cerebral ventricle, so it was short of total brain parameters, especially the posterior circulation parameters. Furthermore, with only 20 patients in our study, there were not enough cases to reflect the parameter variation trends, and, for this reason, more patients should be enrolled to acquire more authoritative data. Otherwise, taking drugs might influence the measurement results to a certain extent. Also, we only analyzed patients with unilateral ICA stenosis rather than bilateral ICA steno-occlusive disease.

Conclusions

The long-term hemodynamic and clinical results after treatment validated CAS as a durable procedure for amelioration of unilateral ICA stenosis. In addition, the coherence of hemodynamic results between 1 week and 1 year indicated that the 1-week hemodynamic effects after CAS could predict long-term effects.

Acknowledgments

The authors appreciate the assistance of Hanming Wang, Haibo Huang, and Lianghao Fan in data acquisition, and express their sincere gratitude to the people and their families who participated in the study.

Footnotes

  • The project described was supported by grant numbers H20090009 and H20090012 from the Science and Technology Bureau of Wenzhou City, ZheJiang Province, China.

Indicates open access to non-subscribers at www.ajnr.org

References

  1. 1.↵
    1. Chimowitz MI,
    2. Lynn MJ,
    3. Howlett-Smith H,
    4. et al
    . Comparison of warfarin and aspirin for symptomatic intracranial arterial stenosis. N Engl J Med 2005; 352: 1305–16
    CrossRefPubMed
  2. 2.↵
    1. Gröschel K,
    2. Schnaudigel S,
    3. Pilgram SM,
    4. et al
    . A systematic review on outcome after stenting for intracranial atherosclerosis. Stroke 2009; 40: e340–e347
    Abstract/FREE Full Text
  3. 3.↵
    1. Chaturvedi S,
    2. Bruno A,
    3. Feasby T,
    4. et al
    . Carotid endarterectomy—an evidence based review. Neurology 2005; 65: 794–801
    Abstract/FREE Full Text
  4. 4.↵
    1. Rothwell PM,
    2. Eliasziw M,
    3. Gutnikov SA,
    4. et al
    . Analysis of pooled data from the randomised controlled trials of endarterectomy for symptomatic carotid stenosis. Lancet 2003; 361: 107–16
    CrossRefPubMed
  5. 5.↵
    1. Qureshi AI,
    2. Kirmani JF,
    3. Divani AA,
    4. et al
    . Carotid angioplasty with or without stent placement versus carotid endarterectomy for treatment of carotid stenosis: a meta-analysis. Neurosurgery 2005; 56: 1171–79
    CrossRefPubMed
  6. 6.↵
    1. Coward LJ,
    2. Featherstone RL,
    3. Brown MM
    . Safety and efficacy of endovascular treatment of carotid artery stenosis compared with carotid endarterectomy: a Cochrane systematic review of the randomized evidence. Stroke 2005; 36: 905–11
    Abstract/FREE Full Text
  7. 7.↵
    1. Gurm HS,
    2. Yadav JS,
    3. Fayad P,
    4. et al
    . Long-term results of carotid stenting versus endarterectomy in high-risk patients. N Engl J Med 2008; 358: 1572–79
    CrossRefPubMed
  8. 8.↵
    1. Brott TG,
    2. Hobson RW 2nd.,
    3. Howard G,
    4. et al
    . Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med 2010; 363: 11–23
    CrossRefPubMed
  9. 9.↵
    1. Gaudiello F,
    2. Colangelo V,
    3. Bolacchi F,
    4. et al
    . Sixty-four-section CT cerebral perfusion evaluation in patients with carotid artery stenosis before and after stenting with a cerebral protection device. AJNR Am J Neuroradiol 2008; 29: 919–23
    Abstract/FREE Full Text
  10. 10.↵
    1. Nabavi DG,
    2. Cenic A,
    3. Craen RA,
    4. et al
    . CT assessment of cerebral perfusion in man: experimental validation and early clinical experience. Radiology 1999; 213: 141–49
    CrossRefPubMed
  11. 11.↵
    1. Trojanowska A,
    2. Drop A,
    3. Jargiello T,
    4. et al
    . Changes in cerebral hemodynamics after carotid stenting: evaluation with CT perfusion studies. J Neuroradiol 2006; 33: 169–74
    CrossRefPubMed
  12. 12.↵
    1. Waaijer A,
    2. van Leeuwen MS,
    3. van Osch MJ,
    4. et al
    . Changes in cerebral perfusion after revascularization of symptomatic carotid artery stenosis: CT measurement. Radiology 2007; 245: 541–48
    CrossRefPubMed
  13. 13.↵
    1. Barnett HJ,
    2. Taylor DW,
    3. Haynes RB,
    4. et al
    . Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 1991; 325: 445–53
    CrossRefPubMed
  14. 14.↵
    1. Fox AJ
    . How to measure carotid stenosis. Radiology 1993; 186: 316–18
    CrossRefPubMed
  15. 15.↵
    1. Hobson RW,
    2. Weiss DG,
    3. Fields WS,
    4. et al
    . Efficacy of carotid endarterectomy for asymptomatic carotid artery stenosis. N Eng J Med 1993; 328: 221–27
    CrossRefPubMed
  16. 16.↵
    Endarterectomy for asymptomatic carotid artery stenosis. Executive Committee for the Asymptomatic Carotid Atherosclerosis study. JAMA 1995; 273: 1421–28
    CrossRefPubMed
  17. 17.↵
    1. Turk AS,
    2. Grayev A,
    3. Rowley HA,
    4. et al
    . Variability of clinical CT perfusion measurements in patients with carotid stenosis. Neuroradiology 2007; 49: 955–61
    CrossRefPubMed
  18. 18.↵
    1. Ogasawara K,
    2. Yukawa H,
    3. Kobayashi M,
    4. et al
    . Prediction and monitoring of cerebral hyperperfusion after carotid endarterectomy by using single-photon emission computerized tomography scanning. J Neurosurg 2003; 99: 504–10
    CrossRefPubMed
  19. 19.↵
    1. Wu B,
    2. Wang X,
    3. Guo J,
    4. et al
    . Collateral circulation imaging: MR perfusion territory arterial spin-labeling at 3T. AJNR Am J Neuroradiol 2008; 29: 1855–60
    Abstract/FREE Full Text
  20. 20.↵
    1. Fukuda T,
    2. Ogasawara K,
    3. Kobayashi M,
    4. et al
    . Prediction of cerebral hyperperfusion after carotid endarterectomy using cerebral blood volume measured by perfusion-weighted MR imaging compared with single-photon emission CT. AJNR Am J Neuroradiol 2007; 28: 737–42
    Abstract/FREE Full Text
  21. 21.↵
    1. Adhiyaman V,
    2. Alexander S
    . Cerebral hyperperfusion syndrome following carotid endarterectomy. QJM 2007; 100: 239–44
    FREE Full Text
  22. 22.↵
    1. Strandgaard S,
    2. Paulson OB
    . Cerebral autoregulation. Stroke 1984; 15: 413–16
    FREE Full Text
  23. 23.↵
    1. Ogasawara K,
    2. Sakai N,
    3. Kuroiwa T,
    4. et al
    . Intracranial hemorrhage associated with cerebral hyperperfusion syndrome following carotid endarterectomy and carotid artery stenting: retrospective review of 4494 patients. J Neurosurg 2007; 107: 1130–36
    CrossRefPubMed
  24. 24.↵
    1. Abou-Chebl A,
    2. Yadav JS,
    3. Reginelli JP,
    4. et al
    . Intracranial hemorrhage and hyperperfusion syndrome following carotid artery stenting: risk factors, prevention, and treatment. J Am Coll Cardiol 2004; 43: 1596–601
    CrossRefPubMed
  25. 25.↵
    1. Naylor AR,
    2. Whyman MR,
    3. Wildsmith JA,
    4. et al
    . Factors influencing the hyperaemic response after carotid endarterectomy. Br J Surg 1993; 80: 1523–27
    PubMed
  26. 26.↵
    1. Jørgensen LG,
    2. Schroeder TV
    . Defective cerebrovascular autoregulation after carotid endarterectomy. Eur J Vasc Surg 1993; 7: 370–79
    CrossRefPubMed
  27. 27.↵
    1. Heck D
    . Incidence and time course of carotid in-stent restenosis in a consecutive series of 295 patients. J Neurointervent Surg 2009; 1: 44–47
    Abstract/FREE Full Text
  28. 28.↵
    1. Markus H,
    2. Cullinane M
    . Severely impaired cerebrovascular reactivity predicts stroke and TIA risk in patients with carotid artery stenosis and occlusion. Brain 2001; 124: 457–67
    Abstract/FREE Full Text
  29. 29.↵
    1. Soinne L,
    2. Helenius J,
    3. Tatlisumak T,
    4. et al
    . Cerebral hemodynamics in asymptomatic and symptomatic patients with high-grade carotid stenosis undergoing carotid endarterectomy. Stroke 2003; 34: 1655–61
    Abstract/FREE Full Text
  30. 30.↵
    1. Derdeyn CP,
    2. Videen TO,
    3. Yundt KD,
    4. et al
    . Variability of cerebral blood volume and oxygen extraction: stages of cerebral haemodynamic impairment revisited. Brain 2002; 125: 595–607
    Abstract/FREE Full Text
  31. 31.↵
    1. Kluytmans M,
    2. van der Grond J,
    3. Eikelboom BC,
    4. et al
    . Long-term hemodynamic effects of carotid endarterectomy. Stroke 1998; 29: 1567–72
    Abstract/FREE Full Text
  32. 32.↵
    1. Serafin Z,
    2. Kotarski M,
    3. Karolkiewicz M,
    4. et al
    . Reproducibility of dynamic computed tomography brain perfusion measurements in patients with significant carotid artery stenosis. Acta Radiol 2009; 50: 226–32
    Abstract/FREE Full Text
  33. 33.↵
    1. Liebeskind DS
    . Collateral circulation. Stroke 2003; 34: 2279–84
    Abstract/FREE Full Text
  34. 34.↵
    1. Turk AS,
    2. Chaudry I,
    3. Haughton VM,
    4. et al
    . Effect of carotid artery stenting on cognitive function in patients with carotid artery stenosis: preliminary results. AJNR Am J Neuroradiol 2008; 29: 265–68
    Abstract/FREE Full Text
  35. 35.↵
    1. Momjian-Mayor I,
    2. Baron JC
    . The pathophysiology of watershed infarction in internal carotid artery disease: review of cerebral perfusion studies. Stroke 2005; 36: 567–77
    Abstract/FREE Full Text
  36. 36.↵
    1. Fiorella D,
    2. Heiserman J,
    3. Prenger E,
    4. et al
    . Assessment of the reproducibility of postprocessing dynamic CT perfusion data. AJNR Am J Neuroradiol 2004; 25: 97–107
    Abstract/FREE Full Text
  • Received July 10, 2011.
  • Accepted after revision September 26, 2011.
  • © 2012 by American Journal of Neuroradiology
PreviousNext
Back to top

In this issue

American Journal of Neuroradiology: 33 (6)
American Journal of Neuroradiology
Vol. 33, Issue 6
1 Jun 2012
  • Table of Contents
  • Index by author
Advertisement
Print
Download PDF
Email Article

Thank you for your interest in spreading the word on American Journal of Neuroradiology.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Short- and Long-Term Hemodynamic and Clinical Effects of Carotid Artery Stenting
(Your Name) has sent you a message from American Journal of Neuroradiology
(Your Name) thought you would like to see the American Journal of Neuroradiology web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Short- and Long-Term Hemodynamic and Clinical Effects of Carotid Artery Stenting
B. Yang, W. Chen, Y. Yang, Y. Lin, Y. Duan, J. Li, H. Wang, F. Fu, Q. Zhuge, X. Chen
American Journal of Neuroradiology Jun 2012, 33 (6) 1170-1176; DOI: 10.3174/ajnr.A2930

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Share
Short- and Long-Term Hemodynamic and Clinical Effects of Carotid Artery Stenting
B. Yang, W. Chen, Y. Yang, Y. Lin, Y. Duan, J. Li, H. Wang, F. Fu, Q. Zhuge, X. Chen
American Journal of Neuroradiology Jun 2012, 33 (6) 1170-1176; DOI: 10.3174/ajnr.A2930
del.icio.us logo Digg logo Reddit logo Twitter logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One
Purchase

Jump to section

  • Article
    • Abstract
    • ABBREVIATIONS:
    • Materials and Methods
    • Results
    • Discussion
    • Conclusions
    • Acknowledgments
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • References
  • PDF

Related Articles

  • No related articles found.
  • PubMed
  • Google Scholar

Cited By...

  • Carotid stenting for unilateral stenosis can increase contralateral hemispheric cerebral blood flow
  • Crossref
  • Google Scholar

This article has not yet been cited by articles in journals that are participating in Crossref Cited-by Linking.

More in this TOC Section

  • Flow Diversion for ICA Aneurysms with Compressive Neuro-Ophthalmologic Symptoms: Predictors of Morbidity, Mortality, and Incomplete Aneurysm Occlusion
  • The Safety and Efficacy of Flow Diversion versus Conventional Endovascular Treatment for Intracranial Aneurysms: A Meta-analysis of Real-world Cohort Studies from the Past 10 Years
  • ADC Level is Related to DWI Reversal in Patients Undergoing Mechanical Thrombectomy: A Retrospective Cohort Study
Show more INTERVENTIONAL

Similar Articles

Advertisement

News and Updates

  • Lucien Levy Best Research Article Award
  • Thanks to our 2021 Distinguished Reviewers
  • Press Releases

Resources

  • Evidence-Based Medicine Level Guide
  • How to Participate in a Tweet Chat
  • AJNR Podcast Archive
  • Ideas for Publicizing Your Research
  • Librarian Resources
  • Terms and Conditions

Opportunities

  • Share Your Art in Perspectives
  • Get Peer Review Credit from Publons
  • Moderate a Tweet Chat

American Society of Neuroradiology

  • Neurographics
  • ASNR Annual Meeting
  • Fellowship Portal
  • Position Statements

© 2022 by the American Society of Neuroradiology | Print ISSN: 0195-6108 Online ISSN: 1936-959X

Powered by HighWire