Abstract
Non-ipsilateral ischemic lesions after carotid artery stenting are considered to arise from emboli originating in the aortic arch, but the quantitative contribution of aortic arch calcification to post-carotid artery stenting ischemic lesions remains unclear. This study aimed to investigate the association between volumetric aortic arch calcification and non-ipsilateral diffusion-weighted imaging hyperintense lesions after transfemoral carotid artery stenting.
We retrospectively analyzed 99 consecutive transfemoral carotid artery stenting procedures performed between January 2018 and December 2023. Aortic arch calcification volume was quantified using preoperative computed tomography angiography using threshold-based segmentation. Postprocedural diffusion-weighted imaging performed within 48 h was assessed for hyperintense lesions in the contralateral hemisphere or cerebellum. Variables were evaluated using univariate and multivariate logistic regression analyses. Receiver operating characteristic curve analysis was used to determine the optimal cut-off value for predicting non-ipsilateral lesions.
Non-ipsilateral high-intensity diffusion-weighted imaging lesions occurred in 14 patients (14.1%), who showed significantly higher aortic arch calcification volumes than did those without lesions (median 2.2 vs. 1.0 mL, p = 0.005). Receiver operating characteristic analysis identified an optimal cutoff of 1.3 mL (sensitivity 78.6%, specificity 62.3%, area under the curve 0.73). Both age (odds ratio 1.1 per year, p = 0.039) and aortic arch calcification volume (odds ratio 1.3 per mL, p = 0.040) were independently associated with non-ipsilateral lesions. Aortic arch type and guiding catheter size showed no significant associations. Quantitative aortic arch calcification on preoperative computed tomography angiography was independently associated with non-ipsilateral ischemic lesions after transfemoral carotid artery stenting. Incorporating calcification volume into preprocedural assessments may assist in selecting alternative access routes or protective strategies for patients at high risk.
Keywords: carotid artery stenting, aortic arch calcification, diffusion-weighted imaging, embolic complication, endovascular treatment
Introduction
Carotid artery stenting (CAS) has become an established alternative to carotid endarterectomy, particularly in patients with high surgical risk.1-3) However, periprocedural ischemic complications, most frequently detected as new lesions on diffusion-weighted imaging (DWI), remain a major concern. Although most lesions occur in the ipsilateral hemisphere, non-ipsilateral DWI lesions are also observed and are presumed to originate from emboli dislodged from the aortic arch during catheter manipulation.4,5) These lesions are clinically relevant because they cannot be prevented by conventional distal embolic protection devices and may be associated with cognitive decrease and silent cerebral infarction.
In addition, qualitative assessment of aortic arch calcification has revealed an association with peri-procedural embolic events. However, previous studies were based on subjective grading or thickness measurements,5-7) and no studies have quantitatively evaluated the calcification burden using volumetric analysis. Furthermore, it is unclear whether the calcification volume is independently associated with non-ipsilateral ischemic lesions after transfemoral CAS, beyond age-related atherosclerotic changes or carotid plaque morphology.
Recent advances in 3-dimensional computed tomography angiography (CTA) and semi-automated plaque analysis software have enabled objective measurement of aortic calcification volume. Quantitative volumetric assessment provides an objective and reproducible measure of the overall calcified plaque burden, which may better reflect embolic risk during catheter manipulation than conventional qualitative grading or thickness-based evaluation. This approach may provide a reproducible imaging biomarker to better stratify patients at risk of embolic complications, and may potentially guide procedural strategies, including the selection of alternative access routes such as transcarotid artery revascularization.
Therefore, we hypothesized that the aortic arch calcification volume would be associated with the occurrence of non-ipsilateral DWI high lesions after transfemoral CAS. This study aimed to evaluate this association and determine a clinically applicable cut-off value for risk stratification, thereby contributing to more appropriate therapeutic decision-making for carotid stenosis.
Materials and Methods
Study design and patient population
This retrospective observational study was approved by the Hiroshima Prefectural Hospital Ethics Review Committee (R5-13-1) on June 27, 2023, and an opt-out consent process was implemented. A total of 115 consecutive CAS procedures performed between January 2018 and December 2023 were reviewed.
To ensure a homogeneous cohort undergoing transfemoral navigation across the aortic arch, we included only cases treated through the transfemoral approach, with available preoperative CTA and postoperative DWI obtained within 48 h. Of the 115 procedures initially reviewed, 16 cases treated through alternative access routes (transbrachial approach) were excluded. The remaining 99 transfemoral CAS cases were included in the final analysis.
CTA acquisition and quantitative aortic arch calcification analysis
All patients underwent contrast-enhanced CTA from the aortic arch to the intracranial artery. Calcified plaques of the aortic arch (from the ascending aorta to the origin of the left subclavian artery), representing the aortic segment potentially involved in embolic events during transfemoral CAS, were identified using a window width of 500-900 HU and window level of 100-250 HU.
Quantification of calcification volume was performed using threshold-based automated segmentation with SYNAPSE VINCENT (FUJIFILM Medical systems, Tokyo, Japan). Volume data were recorded in milliliters (mL). This semi-automated method has been validated previously, showing high intra- and interobserver reproducibility for thoracic aortic plaque quantification (intraclass correlation coefficient >0.9) (Figure 1).
Figure 1.
Quantification of aortic arch calcification on computed tomography angiography.
(A) Three-dimensional reconstruction of the supra-aortic vessels and aortic arch.
(B) Volume-rendered image showing segmented calcified plaques within the aortic arch.
(C-E) Axial (C), sagittal (D), and coronal (E) computed tomography angiography images with calcification areas highlighted in green. Segmentation was performed to quantify the calcification volume.
Magnetic resonance imaging and DWI lesion assessment
Postoperative brain magnetic resonance imaging, including DWI, was obtained within 48 h post-CAS. Two board-certified neurologists, blinded to the aortic plaque data, assessed the DWI lesions. Only non-ipsilateral lesions (in the contralateral hemisphere or cerebellum) were considered, to isolate embolic sources from the aortic arch. The primary end point of this study was the occurrence of non-ipsilateral DWI high-intensity lesions (contralateral hemisphere or cerebellum) within 48 h after transfemoral CAS.
Clinical, carotid imaging, and procedural variables
The clinical data included age, sex, hypertension, diabetes mellitus, dyslipidemia, smoking status, coronary artery disease, chronic kidney disease, and symptomatic carotid artery disease.
Carotid imaging findings comprised the degree of stenosis rate (using the North American Symptomatic Carotid Endarterectomy Trial method),8) ulceration, calcified plaque presence, and contralateral carotid stenosis. Procedural variables included guiding catheter size (8 or 9 Fr) and a type III aortic arch configuration.
CAS procedure
The indications were symptomatic stenosis ≥50% or asymptomatic stenosis ≥70%.9) Dual antiplatelet therapy was administered for at least 2 weeks before the procedure. CAS was performed with dual protection (distal filter plus flow reversal with aspiration) using an 8 or 9 Fr balloon-tipped guiding catheter placed in the common carotid artery by the coaxial method.10)
Statistical analysis
Associations between non-ipsilateral DWI lesions and clinical, imaging, and procedural factors were first assessed using the Mann-Whitney U test for nonparametric comparisons or the Wilcoxon signed-rank test for continuous variables and χ2 or Fisher's exact test for categorical variables. Subsequently, univariate analyses were conducted to identify the factors associated with the volume of aortic arch calcification. Spearman's rank correlation coefficient was used to evaluate the relationship between aortic arch calcification volume and age, in addition to the degree of carotid stenosis.
Variables that were significant in the univariate analysis, along with those associated with the calcification burden, were entered into multivariate logistic regression. Receiver operating characteristic (ROC) curve analysis was used to determine the optimal calcification volume cutoff, and the area under the curve (AUC), sensitivity, and specificity were calculated. Patients were stratified into the high- and low-calcification groups on the basis of this cutoff, and subgroup analyses were conducted to evaluate the effect of arch type and catheter diameter.
Calcification volume was also categorized into quartiles for testing the linear trend in risk using logistic regression. Statistical analyses were performed using JMP version 16 (SAS Institute, Cary, NC, USA). p < 0.05 was considered statistically significant.
Results
Table 1 lists the baseline characteristics of the study population and comparison of variables with and without non-ipsilateral high-intensity DWI lesions.
Table 1.
Comparison of Patient Parameters, Radiological Findings, Procedural Factors and Anatomical Factors Between Patients with and without Non-Ipsilateral DWI High Lesions
| Total | Non-ipsilateral DWI high + | Non-ipsilateral DWI high − | p-Value | |
|---|---|---|---|---|
| (n = 99) | (n = 14, 14.1%) | (n = 85, 85.9%) | ||
| Patient parameters | ||||
| Age median [IQR] | 75.0 [70.0-79.9] | 79.5 [73.5-84.5] | 74.0 [69.5-78.0] | 0.13 |
| Female, n (%) | 15 (15.2) | 0 (0.0) | 15 (100.0) | 1 |
| Symptomatic lesion, n (%) | 37 (37.4) | 4 (28.6) | 33 (38.8) | 0.34 |
| Contralateral lesion, n (%) | 48 (48.5) | 8 (57.1) | 40 (47.1) | 0.34 |
| Hypertension, n (%) | 75 (75.8) | 10 (71.4) | 65 (76.5) | 0.78 |
| Dyslipidemia, n (%) | 97 (98.0) | 14 (100.0) | 83 (97.7) | 0.74 |
| Diabetes mellitus, n (%) | 45 (45.5) | 6 (42.9) | 39 (45.9) | 0.69 |
| Coronary disease, n (%) | 15 (15.2) | 2 (14.3) | 13 (15.3) | 0.67 |
| Smoking, n (%) | 79 (79.8) | 12 (85.7) | 67 (78.8) | 0.45 |
| Kidney failure, n (%) | 8 (8.1) | 1 (7.1) | 7 (8.2) | 0.72 |
| Radiological findings | ||||
| Ulceration, n (%) | 44 (44.8) | 7 (50.0) | 37 (44.1) | 0.45 |
| Calcified, n (%) | 81 (81.8) | 12 (85.7) | 69 (81.2) | 0.51 |
| Degree of stenosis rate median [IQR] | 67.0 [56.0-80.0] | 70.0 [62.5-80.0] | 66.0 [55.0-79.0] | 0.44 |
| Procedural factor | ||||
| 8 Fr Guiding catheter, n (%) | 85 (85.9) | 13 (92.9) | 72 (84.7) | 0.37 |
| Anatomical factor | ||||
| Aortic arch type III, n (%) | 17 (17.2) | 3 (17.7) | 14 (82.4) | 0.45 |
| Aortic arch calcified volume median [IQR] | 1.1 [0.5-2.3] | 2.2 [1.3-4.7] | 1.0 [0.4-1.9] | 0.0053 |
DWI: diffusion-weighted imaging; IQR: interquartile range
The median age of the 99 patients included in this analysis was 75.0 years [range, 53-92; interquartile range, 70.0-79.9], and 15 (15.2%) were women. Symptomatic carotid stenosis was present in 37 cases (37.4%). Non-ipsilateral high-intensity DWI lesions occurred in 14 patients (14.1%). In none of the patients with non-ipsilateral DWI high lesions did permanent neurological deficits develop, and no deterioration in the modified Rankin Scale (mRS) score at discharge was observed.
Patients with non-ipsilateral high-intensity DWI lesions had significantly greater aortic arch calcification volumes (median 2.2 vs. 1.0 mL, p = 0.005) (Figure 2), and were older (median, 79.5 vs. 74.0 years, p = 0.013) than those without lesions. No significant association was evident between contralateral lesions and other clinical, procedural, or carotid imaging factors. Although aortic arch calcification volume was significantly associated with non-ipsilateral DWI high lesions, the mere presence of calcified plaque showed no such association.
Figure 2.
Comparison of aortic arch calcification volume according to the presence of non-ipsilateral diffusion-weighted imaging (DWI) high lesions.
Box-and-whisker plot showing the distribution of aortic arch calcification volume in patients with (+) and without (−) non-ipsilateral high-intensity DWI lesions after carotid artery stenting. Patients with non-ipsilateral lesions showed significantly higher calcification volumes than those without lesions.
ROC analysis identified an optimal cutoff of 1.3 mL calcification volume for predicting non-ipsilateral DWI high lesions, with a sensitivity of 78.6%, specificity of 62.3%, and an AUC of 0.73 (Figure 3).
Figure 3.
Receiver operating characteristic (ROC) curve analysis of aortic arch calcification volume for predicting non-ipsilateral DWI high lesions.
The ROC curve reveals the discriminative ability of aortic arch calcification volume to predict the occurrence of non-ipsilateral high-intensity DWI lesions after carotid artery stenting. The optimal cut-off value was 1.3 mL, yielding a sensitivity of 78.6% and specificity of 62.3%. The area under the curve was 0.73.
DWI: diffusion-weighted imaging
Aortic arch calcification volume was significantly associated with diabetes mellitus (median 1.8 vs. 0.8 mL, p = 0.0036), calcified carotid plaque (median 1.2 vs. 0.6 mL, p = 0.037), and advanced age (Spearman's ρ = 0.44, p < 0.0001). There were no significant associations with other clinical, procedural, or carotid imaging factors (Table 2).
Table 2.
Univariate Analysis of Factors Associated with Aortic Arch Calcification Volume
| Variable | Category/Test | Calcification (median [IQR])/ρ | p value |
|---|---|---|---|
| Patient parameters | |||
| Age | Spearman’s ρ | 0.44 | <.0001 |
| Sex | Male | 1.2 [0.5-2.3] | 0.42 |
| Female | 1.0 [0.3-1.9] | ||
| Symptomatic lesion | symptomatic | 1.2 [0.6-2.4] | 0.54 |
| asymptomatic | 1.1 [0.5-2.3] | ||
| Contralateral lesion | Yes | 1.2 [0.5-3.2] | 0.17 |
| No | 1.0 [0.5-1.9] | ||
| Hypertension | Yes | 1.2 [0.6-2.7] | 0.08 |
| No | 0.7 [0.2-2.1] | ||
| Dyslipidemia | Yes | 1.1 [0.5-2.3] | 0.43 |
| No | 0.7 [0.3-1.1] | ||
| Diabetes mellitus | Yes | 1.8 [0.9-2.9] | 0.0036 |
| No | 0.8 [0.3-1.8] | ||
| Coronary disease | Yes | 1.9 [1.0-2.7] | 0.14 |
| No | 1.1 [0.4-2.2] | ||
| Smoking | Yes | 1.1 [0.5-2.3] | 0.87 |
| No | 1.4 [0.4-2.3] | ||
| Kidney failure | Yes | 2.1 [1.2-3.3] | 0.07 |
| No | 1.1 [0.4-2.2] | ||
| Radiological findings | |||
| Ulceration | Yes | 1.3 [0.6-2.6] | 0.35 |
| No | 1.1 [0.5-2.0] | ||
| Calcified | Yes | 1.2 [0.6-2.7] | 0.037 |
| No | 0.6 [0.2-1.7] | ||
| Degree of stenosis rate | Spearman’s ρ | −0.09 | 0.38 |
| Procedural factor | |||
| 8-Fr Guiding catheter | Yes | 1.2 [0.5-2.5] | 0.15 |
| No | 0.8 [0.2-1.9] | ||
| Anatomical factor | |||
| Aortic arch type III | Yes | 1.2 [0.5-2.5] | 0.83 |
| No | 1.1 [0.5-2.4] | ||
| Non-ipsilateral DWI high | Yes | 2.2 [1.3-4.7] | 0.0054 |
| No | 1.0 [0.4-1.9] |
DWI: diffusion-weighted imaging; IQR: interquartile range
In the multivariate logistic regression analysis including age, aortic arch calcification volume, calcified carotid plaque, and diabetes, both age (p = 0.0395, odds ratio [OR] 1.1, 95% confidence interval [CI] 1.0-1.3) and aortic arch calcification volume (p = 0.0398, OR 1.3, 95% CI 1.0-1.7) were independently associated with non-ipsilateral DWI high lesions (Table 3).
Table 3.
Multivariate Logistic Regression Analysis for Predictors of Non-Ipsilateral DWI High Lesions after Carotid Artery Stenting
| Odd ratio | 95% CI | p-Value | |
|---|---|---|---|
| Age (per year) | 1.1 | 1.0-1.3 | 0.0395 |
| Aortic arch calcification volume (per mL) | 1.3 | 1.0-1.7 | 0.0398 |
| Diabetes mellitus | 0.7 | 0.2-2.3 | 0.51 |
| Calcified carotid plaque | 0.7 | 0.1-6.2 | 0.79 |
CI: confidence interval; DWI: diffusion-weighted imaging
When stratified by high (≥ 1.3 mL) and low (< 1.3 mL) calcification volume, no significant association emerged between non-ipsilateral lesions and the presence of aortic arch type III anatomy (high group: p = 0.67; low group: p = 0.42) or guiding catheter diameter (high group: p = 0.73; low group: p = 0.55) (Table 4). There was a nonsignificant but suggestive trend toward an increasing risk of non-ipsilateral DWI high lesions with higher quartiles of aortic arch calcification (p for trend = 0.072).
Table 4.
Distribution of Non-Ipsilateral DWI High Lesions by Guiding Catheter Size and Aortic Arch Type III, According to Calcification Volume
| Stratum by calcification | Predictor | Category | non-ipsilateral DWI high (+) | non-ipsilateral DWI high (−) | p-Value |
|---|---|---|---|---|---|
| (n = 14, 14.1%) | (n = 85, 85.9%) | ||||
| High calcification (n = 43) | Guiding catheter size | 8 Fr | 10/39 25.6% | 29/39 74.4% | 0.73 |
| 9 Fr | 1/4 25.0% | 3/4 75.0% | |||
| Aortic arch type III | Yes | 2/8 25.0% | 6/8 75.0% | 0.67 | |
| No | 9/35 25.7% | 26/32 74.3% | |||
| Low calcification (n = 56) | Guiding catheter size | 8 Fr | 3/46 6.5% | 43/46 93.5% | 0.55 |
| 9 Fr | 0/10 0.0% | 10/10 100% | |||
| Aortic arch type III | Yes | 1/9 11.1% | 8/9 88.9% | 0.42 | |
| No | 2/47 4.3% | 45/47 95.7% |
DWI: diffusion-weighted imaging
Discussion
In this study, quantitative aortic arch calcification measured using preoperative CTA was significantly associated with the occurrence of non-ipsilateral DWI high lesions after transfemoral CAS. This association persisted after adjustment for major clinical and carotid imaging factors, suggesting that the calcification burden may play an important role in the risk of embolism during CAS. Nevertheless, the results should be interpreted with caution given the number of outcome events was limited, and potential model overfitting cannot be excluded.
To our knowledge, this is the first study to evaluate aortic calcification using volumetric analysis and to identify a clinically applicable cut-off value for predicting remote embolic lesions after CAS.
Previous studies have suggested that aortic arch plaque morphology, ulceration, or calcification thickness may contribute to cerebral embolization during CAS.11) Kastrup et al.6) and Gröschel et al.7) reported that arch calcification visible on plain radiography or CTA was associated with increased perioperative embolic events, particularly in older patients. However, these assessments were qualitative or semiquantitative in nature. More recently, Ito et al.5) indicated that contralateral DWI lesions after CAS were associated with aortic arch plaque, although the calcification burden was not quantitatively assessed. Our findings build on those of these studies using CTA-based volumetric measurements, which provide an objective, reproducible parameter that better reflects total embolic risk than qualitative grading. A larger volume of aortic arch calcification may reflect a more extensive and rigid atherosclerotic burden, which can increase the risk of plaque disruption and microembolization during catheter manipulation. Heavily calcified plaques may also reduce vascular compliance, leading to greater mechanical stress when devices are advanced through the arch, thereby facilitating embolic release into the cerebral circulation.11)
Importantly, we found that a calcification volume of ≥1.3 mL was associated with non-ipsilateral DWI lesions with moderate accuracy (AUC, 0.73). This threshold may provide practical guidance for preprocedural risk stratification. In patients with extensive aortic calcification, alternative strategies―such as transcarotid artery revascularization (TCAR), brachial or radial access, or minimizing arch manipulation―may be considered to reduce embolic risk. Conversely, patients with low calcification volumes may safely undergo transfemoral CAS with standard protection devices. Although the discriminative performance of calcification volume was moderate (AUC, 0.73), and dichotomization did not yield significant group differences, volumetric assessment may remain more informative when analyzed as a continuous variable and may serve as a useful parameter for risk stratification rather than a definitive predictive marker.
Quantification was performed using the validated SYNAPSE VINCENT software, which applies predefined Hounsfield thresholds to segment and calculate calcification volume with high intra- and interobserver reproducibility. This semi-automated approach is practical for routine use and may be readily applied to preoperative CTA data.12)
Age was also an independent predictor of non-ipsilateral DWI lesions, consistent with prior studies.13) Although age and calcification volume were moderately correlated, both retained significance in the multivariate analysis, suggesting that calcification contributes to the risk of embolism, independent of age-related vascular changes. The mechanisms linking calcification and embolization may involve plaque fragmentation, catheter scraping, or loss of aortic compliance; however, these pathways require further investigation.
This study showed that quantitative aortic arch calcification measured on preoperative CTA is independently associated with the occurrence of non-ipsilateral DWI high lesions after transfemoral CAS. A calcification volume of ≥1.3 mL was identified as a potential threshold for risk stratification of remote embolic events. These findings suggest that the aortic arch calcification burden is associated with non-ipsilateral ischemic lesions after transfemoral CAS and may serve as a useful parameter for preprocedural risk stratification.
Limitations
This study has several limitations. First, its retrospective design and single-center setting may limit the generalizability of the findings. Second, the sample size and number of ischemic events were relatively small, which may have yielded insufficient power to detect weaker associations, as suggested by the non-significant trend across calcification quartiles. Because only 14 patients experienced non-ipsilateral DWI high lesions, the multivariate model may be subject to overfitting, and the results should be interpreted cautiously. We did not evaluate the anatomical distribution of aortic arch calcification, which may also influence embolic risk. The potential role of optimized medical therapy, including antiplatelet or lipid-lowering treatment, in reducing embolic risk in patients with extensive aortic calcification was not evaluated in this study and should be addressed in future research. Third, procedural details such as the number of catheter manipulations or temporal improvements in technique were not systematically recorded.14) A prospective multicenter study with standardized imaging and procedural protocols is warranted to validate our findings.
Despite these limitations, our study highlights a practical and reproducible imaging biomarker that can be readily incorporated into routine CTA evaluations before CAS. Recognizing the vulnerability of transfemoral CAS to aortic arch-related embolic events may improve risk stratification and support more appropriate treatment selection from among CAS, carotid endarterectomy, and emerging approaches such as TCAR.
Conflicts of Interest Disclosure
All authors have no conflict of interest.
Acknowledgments
We thank Editage (www.editage.com) for its English language editing services.
Funding Statement
This work was supported by Grants-in-Aid for Scientific Research of the Japan Society for the Promotion of Science (Grant Number JP23K15678).
References
- 1).Dumont TM, Mokin M, Wach MM, et al. Understanding risk factors for perioperative ischemic events with carotid stenting: is patient age over 80 years or is unfavorable arch anatomy to blame? J Neurointerv Surg. 2014;6(3):219-24. doi: 10.1136/neurintsurg-2013-010721 [DOI] [PubMed] [Google Scholar]
- 2).Naggara O, Touzé E, Beyssen B, et al. Anatomical and technical factors associated with stroke or death during carotid angioplasty and stenting: results from the endarterectomy versus angioplasty in patients with symptomatic severe carotid stenosis (EVA-3S) trial and systematic review. Stroke. 2011;42(2):380-8. doi: 10.1161/STROKEAHA.110.588772 [DOI] [PubMed] [Google Scholar]
- 3).Casana R, Bissacco D, Malloggi C, et al. Aortic arch types and postoperative outcomes after carotid artery stenting in asymptomatic and symptomatic patients. Int Angiol. 2020;39(6):485-91. doi: 10.23736/S0392-9590.20.04494-6 [DOI] [PubMed] [Google Scholar]
- 4).Burzotta F, Nerla R, Pirozzolo G, et al. Clinical and procedural impact of aortic arch anatomic variants in carotid stenting procedures. Catheter Cardiovasc Interv. 2015;86(3):480-9. doi: 10.1002/ccd.25947 [DOI] [PubMed] [Google Scholar]
- 5).Ito H, Uchida M, Sase T, et al. Risk factors of contralateral microembolic infarctions related to carotid artery stenting. Neurol Med Chir (Tokyo). 2018;58(7):311-9. doi: 10.2176/nmc.oa.2018-0023 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6).Kastrup A, Gröschel K, Schnaudigel S, et al. Target lesion ulceration and arch calcification are associated with increased incidence of carotid stenting-associated ischemic lesions in octogenarians. J Vasc Surg. 2008;47(1):88-95. doi: 10.1016/j.jvs.2007.09.045 [DOI] [PubMed] [Google Scholar]
- 7).Gröschel K, Pilgram SM, Ernemann U, et al. Aortic calcification on plain chest radiography predicts embolic complications during carotid artery stenting. Eur J Neurol. 2008;15(7):730-6. doi: 10.1111/j.1468-1331.2008.02183.x [DOI] [PubMed] [Google Scholar]
- 8).Barnett HJ, Taylor DW, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med. 1998;339(20):1415-25. doi: 10.1056/NEJM199811123392002 [DOI] [PubMed] [Google Scholar]
- 9).Brott TG, Halperin JL, Abbara S, et al. 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease: executive summary: a report of the American College of Cardiology Foundation, and the American Stroke Association, American Association of Neuroscience Nurses, American Association of Neurological Surgeons, American College of Radiology, American Society of Neuroradiology, Congress of Neurological Surgeons, Society of Atherosclerosis Imaging and Prevention, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of NeuroInterventional Surgery, Society for Vascular Medicine, and Society for Vascular Surgery. J Am Coll Cardiol. 2011;57(8):1002-44. doi: 10.1016/j.jacc.2010.11.005 [DOI] [PubMed] [Google Scholar]
- 10).Sakamoto S, Kiura Y, Okazaki T, et al. Usefulness of dual protection combined with blood aspiration for distal embolic protection during carotid artery stenting. Acta Neurochir (Wien). 2015;157(3):371-7. doi: 10.1007/s00701-014-2311-6 [DOI] [PubMed] [Google Scholar]
- 11).Szikra P, Boda K, Rarosi F, et al. Aortic arch and common carotid artery plaques with soft components pose a substantial risk of cerebral embolization during carotid stenting. Interv Neuroradiol. 2016;22(4):438-44. doi: 10.1177/1591019916633242 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12).Mizutani K, Torimoto I, Sekikawa Z, et al. Semiautomatic volumetry of low attenuation of thoracic aortic plaques on curved planar reformations using MDCT angiographic data with 0.5 mm collimation. BioMed Res Int. 2018;2018:3563817. doi: 10.1155/2018/3563817 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13).Bijuklic K, Wandler A, Varnakov Y, et al. Risk factors for cerebral embolization after carotid artery stenting with embolic protection: a diffusion-weighted magnetic resonance imaging study in 837 consecutive patients. Circ Cardiovasc Interv. 2013;6(3):311-6. doi: 10.1161/CIRCINTERVENTIONS.112.000093 [DOI] [PubMed] [Google Scholar]
- 14).Kim HJ, Lee HJ, Yang JH, et al. The influence of carotid artery catheterization technique on the incidence of thromboembolism during carotid artery stenting. AJNR Am J Neuroradiol. 2010;31(9):1732-6. doi: 10.3174/ajnr.A2141 [DOI] [PMC free article] [PubMed] [Google Scholar]