| | Patterns of in-stent restenosis after carotid artery stenting: Classification and implications for long-term outcomePresented at VASCULAR 2007, Annual Meeting of the Society for Vascular Surgery, Baltimore, Md, June 7-10, 2007. Received 21 June 2007; accepted 17 July 2007. ObjectivesFactors predicting in-stent restenosis (ISR) and future need for target lesion revascularization (TLR) after carotid artery stenting (CAS) remain undetermined. We hypothesized that the patterns of restenotic lesions may provide prognostic information. In this study, we developed an ultrasound classification scheme for ISR based on lesion length and distribution and assessed factors that may predict the need for TLR. MethodsPatients were followed up after CAS with B-mode ultrasound imaging, and ISR lesions (≥40% stenosis) were classified into type I (focal ≤10 mm end-stent lesions), II (focal ≤10 mm, intrastent), III (diffuse >10 mm, intrastent), IV (diffuse >10 mm proliferative, extending outside the stent), and V (total occlusion). The frequency of lesion types was assessed. Accuracy of the ultrasound classification was confirmed with angiography. We recorded patient (age, gender, comorbidities), lesion (severity, etiology, symptomatic status) and procedural features (type, number, length of stents), and the need for TLR. ResultsEighty-five ISR lesions developed after 255 CAS procedures. Their percentage distribution was type I, 40; type II, 25.9; type III, 12.9; for type IV, 20; and type V, 1.2. Accuracy of the ultrasound classification was confirmed by angiography (r2 = 0.82). Inter-rater agreement for the assignment of lesion type based on ultrasound was 0.88 (very good). TLR was performed in 13 that were ≥80% diameter reducing. On univariate analysis, the need for TLR was highest in type IV lesions (0%, 0%, 27.3%, and 58.8% [types I to IV, respectively]; P = .001). History of ISR (2.9%, 0%, 0%, and 41.2% [types I to IV]; P = .003) and diabetes mellitus (20.6%, 22.7%, 45.5%, and 52.9% [types I to IV]; P = .02) occurred more frequently with type IV ISR lesions. On multivariate analysis of all patient, lesion, and procedural characteristics, only the type of ISR (odds ratio, 5.1) and a history of diabetes (odds ratio, 9.7) were independent predictors of TLR. ConclusionsThe proposed classification accurately grades the magnitude of intimal hyperplasia after CAS and provides important prognostic information. Diffuse proliferative (type IV) ISR lesions and diabetes are important determinants of long-term outcome after CAS. This classification will facilitate a standardized description of recurrence after CAS and enable early identification of high-risk patients for additional monitoring, treatment, and investigation. Carotid artery stenting (CAS) has emerged as a less invasive alternative to carotid endarterectomy (CEA) for revascularization of extracranial carotid occlusive disease. Our institution1, 2, 3, 4, 5 and others6, 7, 8, 9, 10 have reported that CAS can be performed with low periprocedural morbidity. On long-term follow-up, we have observed in-stent restenosis (ISR) of ≥40% diameter reduction in 42.7% of our patients, and of ≥60% diameter reduction in 16.4% at 5 years of follow-up.5 Similarly, the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) investigators reported ISR in 19.7% of patients at 1 year of follow-up.11 Therefore, ISR will become increasingly prevalent due to the exponential increase in the use of carotid stents. Post-CAS ISR is currently treated at a threshold of ≥80% diameter reduction (6.4% incidence at 5 years5). However, factors that predict target vessel failure remain undetermined. Primary stenting prevents carotid artery recoil and constrictive remodeling.12 Post-CAS ISR can threfore be primarily attributed to neointimal hyperplasia,12, 13 and studies of coronary ISR indicate that long neointimal hyperplasia lesions diffusely involving the stent surface correlate with the highest recurrence and reintervention rates.14 The patterns of ISR developing after carotid artery stenting have not been described, and their prognostic utility has not been studied. We therefore developed an ultrasound classification scheme for post-CAS ISR based on the length and distribution of the lesion with respect to the stent and verified its accuracy with carotid angiography. We then assessed long-term clinical follow-up to determine whether the classification system predicted the need for future therapeutic reintervention in the form of target lesion-site revascularization (TLR). Methods  Patient population and treatment We performed 255 CAS procedures from January 1, 1996, through December 31, 2006. Lesions were treated with a WallStent (Boston Scientific Corp, Natick, Mass) or ACCULINK stent (Guidant Corp, St. Paul, Minn). Procedural details for CAS at our institution have been published in detail by our group previously.1, 2, 3, 4, 5 All patients received aspirin (325 mg daily) and clopidogrel (75 mg twice daily) for at least 48 hours before the procedure. Clopidogrel (75 mg daily) was continued for 30 days after the procedure, and aspirin was continued indefinitely. Patients early in our experience underwent CAS without embolic protection. The ACCUNET (Abbot, Menlo Park, Calif) antiembolic device was used in all subsequent patients. At last follow-up, 85 arteries developed ISR of ≥40% and constitute the cohort for the current study. Patients underwent endovascular retreatment when their ISR reached a threshold of ≥80%, regardless of neurologic symptoms. Devices used to treat ISR included balloon angioplasty, cutting balloon angioplasty, and restenting and were selected at the discretion of the treating physician. No patient required surgical revascularization for ISR. Lesions after the first recurrence were excluded from the primary analysis to avoid introducing any statistical bias in the multivariate model. Demographics and follow-up Clinical demographics and laboratory results were collected in a prospective registry. Risk factors that were tabulated included coronary artery disease (currently or previously symptomatic, requiring intervention), medically treated diabetes mellitus, medically treated hypertension, medically treated hypercholesterolemia (or if serum cholesterol was >180 mg/dL), and smoking (current or prior smoker). Clinical follow-up was performed with office visits and duplex ultrasound examinations. The occurrence of TLR events was recorded. Ultrasound examination Duplex ultrasound examinations, including Doppler velocity measurements and B-mode imaging studies, were performed in our noninvasive vascular laboratory, which is approved by the Inter-societal Commission on Accreditation of Vascular Laboratories,15 before and after CAS within 3 days of the procedure and during each annual follow-up visit. The studies were performed with a 7-13 MHz linear array transducer (Sequoia 512, Acuson, Mountain View, Calif). Doppler velocities were obtained with appropriate angle correction according to standard techniques used by our group previously4, 5, 16 to estimate the degree of stenosis. Velocity criteria for native carotid arteries (peak systolic velocity >130 cm/s) were used to identify potential patients with ISR. These underwent detailed B-mode imaging with power Doppler to select arteries with any ISR ≥40%. These lesions were finally included in the present analysis; therefore, only patients with confirmed visible restenotic lesions were included in the study. This strategy ensured that we did not miss any patients with ISR. B-mode imaging studies during follow-up were further used to define the morphology of the ISR lesions according to the length and distribution of the lesion with respect to the stent. Standard imaging techniques used previously by our group were applied to obtain grayscale images of the ipsilateral cervical carotid artery.5 The transducer was placed directly over the stented carotid artery segment to obtain a longitudinal image. It was then swept from the base of the neck to the angle of the mandible to obtain multiple cross-sectional images of the entire common and internal carotid arteries. The images were recorded on magneto-optical (MO) disks and analyzed off-line with a computer-assisted image-analysis program (Metamorph 6.1, Universal Imaging Corp, Downingtown, Pa) by independent observers blinded to clinical findings. The longitudinal image was used to measure the length of the lesion, defined as the distance from the proximal shoulder to the distal shoulder of the lesion, and to determine its location with respect to the stent. The cross-sectional views were used to determine the luminal diameters. Classification of in-stent restenosis B-mode images in longitudinal and serial cross sections were reviewed by two independent observers who classified the lesions on separate occasions (Fig 1). Disagreements were resolved by consensus. •Type I (focal end-stent group): Lesions are ≤10 mm long and are positioned at the proximal or distal margin (but not both) of the stent. Lesions ≤10 mm long at both ends of the stent are defined as type I, multifocal end-stent. •Type II (focal intrastent group): Lesions are ≤10 mm long and are confined to within the stent(s) without extending outside the margins. Two or more discrete lesions ≤10 mm in length located within the stent are defined as type II, multifocal intrastent. •Type III (diffuse intrastent group): Lesions are >10 mm long and are confined to within the stent(s) without extending outside the margins. •Type IV (diffuse proliferative group): Lesions are >10 mm long and extend beyond the margin(s) of the stent(s). •Type V (occlusion group). Lesions have no prograde flow and no lumen is identified. Angiographic analysis The angiographic percentage of stenosis was measured before and after stent deployment in all patients undergoing CAS and was based on standard techniques using multiple projections. All angiograms were analyzed off-line with a computer-assisted quantitative edge-detection algorithm (MDQM; MEDCON Telemedicine Technology, Inc, Livingston, NJ) by an independent observer who was blinded to the ultrasound and clinical findings. In 13 arteries, ISR ≥80% was found and they underwent TLR. In 15 additional ISR lesions, confirmatory angiography was done for progressively increasing velocity measurements on ultrasound imaging and these were found to be <80% diameter-reducing lesions. Preprocedural B-mode imaging was compared with angiography in these patients to test the accuracy of our classification scheme. Angiographic stenosis was determined using North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria.17 The in-stent least luminal diameter was compared with the distal nontapering portion of the internal carotid artery, which served as the reference segment. Lesion length was measured as the distance from the proximal shoulder to the distal shoulder of the lesion. The angiographic lesion length was compared with that obtained by B-mode imaging. Statistical analysis Statistical analysis was performed using GraphPad Prism 3.00 software (GraphPad Software Inc, San Diego, Calif) and SPSS software (SPSS Inc, Chicago, Ill). Categoric data are presented as percentages and continuous data as mean ± SD. Categoric data were compared using the χ2 test, and continuous data were compared using analysis of variance with the Tukey post-test. P ≤ .05 was considered significant. The primary end point of the analysis was the association of lesion classification with TLR. Univariate variables with P < .2 were entered into the multivariate logistic regression model; forward stepping was used to determine the independent predictors of TLR. Independent variables were considered significant risk factors at P ≤ .05. To confirm the accuracy of the classification scheme, ISR lesion length measurements derived from duplex ultrasound imaging were compared with angiographic measurements using linear regression. Inter-rater agreement on the ultrasound classification was assessed by calculating the κ statistic; a score of 0.81 to 1.0 was defined as very good agreement. Results Patient characteristics Of the 255 CAS procedures performed, ISR developed in 85 arteries during a mean follow-up of 19.3 months. Of these 85 ISR lesions classified according to our proposed scheme, 40% (n = 34) were focal end stent (type I), 25.9% (n = 22) were focal intrastent (type II), 12.9% (n = 11) were diffuse intrastent (type III), 20% (n = 17) were diffuse proliferative, and 1.2% (n = 1) developed an occlusion. Inter-rater agreement for the assignment of lesion type based on ultrasound imaging was 0.88 (very good). Baseline patient characteristics are presented in Table I. None of the patients had neurologic symptoms in association with the development of ISR. All groups were well matched with respect to age and sex and for associated comorbidities such as a history of hypertension, coronary artery disease, hypercholesterolemia, and smoking. However, increasing levels of ISR classification were associated with an increasing prevalence of diabetes mellitus (20.6%, 22.7%, 45.5%, and 52.9% for types I to IV, respectively; χ2 trend, 5.4; P = .02). Lesion characteristics The severity (degree of stenosis) of the original lesion treated with CAS was comparable in all ISR classes, as indicated in Table II. The proportion of lesions treated for neurologic symptoms, the number of stents used per lesion, and the mean stent length used were also similar across ISR types. Technical success was achieved in all patients and no differences were noted in the angiographic residual stenosis after therapy across all ISR types. In this cohort, 37 patients had been treated with a WallStent and 48 with an Acculink stent. The incidence of ISR did not vary with the type of stent used or the type of lesion treated. Univariate analysis indicated a difference in the patterns of ISR between stent types. Intrastent ISR patterns (types II and III) occurred more frequently after placement of Acculink stents compared with WallStents (P = .03). Univariate analysis also indicated that focal intrastent (type II) lesions occurred more frequently after treatment of primary atherosclerotic carotid stenosis compared with treatment for post-CEA restenosis (P = .02). Finally, 13 patients had recurrent ISR, of which three were type III lesions and the remaining 10 were type IV. On univariate analysis, higher levels of ISR classification were associated with prior ISR (2.9%, 0%, 0%, and 41.2% for types I to IV, respectively; χ2 trend, 13.3; P = .003). Target lesion revascularization Endovascular retreatment was required in three of 11 patients with type III ISR, and in 10 of 17 patients with type IV ISR (Table III). The mean interval between CAS and TLR was 18.2 months. We observed a significant increase in TLR in association with increasing levels of ISR classification (0%, 0%, 27.3%, and 58.8% for types I to IV, respectively; χ2 trend, 29.4; P = .001). Modalities used to treat ISR included balloon angioplasty, stenting, and cutting balloon angioplasty alone or in conjunction with stenting. Procedural success was achieved in all these cases, without evidence of any abrupt arterial closure or neurologic events. Endovascular treatment of ISR afforded similar percentage diameter residual stenoses in all instances and was not influenced by ISR class (Table III). | | |  | Variables⁎ | Patterns of in-stent restenosis by type | |
|---|
| I, focal end-stent (n = 34) | II, focal intrastent (n = 22) | III, diffuse intrastent (n = 11) | IV, diffuse proliferative (n = 17) | |
|---|
| Incidence of TLR, %⁎ | 0 | 0 | 27.3 | 58.8 | | | Devices used for ISR, No. | | | | | | |  Balloon angioplasty | 0 | 0 | 1 | 3 | | | Stent | 0 | 0 | 1 | 5 | | | Cutting balloon | 0 | 0 | 0 | 1 | | | Cutting balloon + stent | 0 | 0 | 1 | 1 | | | Post-treatment result, % residual stenosis | N/A | N/A | 10.4±6.9 | 11.9±6.1 | | | | |
Quantitative angiography vs B-mode imaging results Twenty-eight pairs of quantitative angiographic and B-mode ultrasound measurements were available for comparative analysis of the geographic distribution of the ISR lesions. The quantitative angiographic results verified the accuracy of our proposed ultrasound classification of ISR based on lesion length measurements (r2 = 0.82, linear regression; Fig 2). Multivariate analysis We introduced diabetes, coronary artery disease, neurologic symptom status, recurrent ISR and primary atherosclerosis etiologies, stent type, stent number, and the pattern of ISR according to the introduced B-mode ultrasound classification in a stepwise multiple logistic regression model to identify independent predictors of TLR. The only variables that independently predicted TLR after CAS were a worsening pattern of ISR according to our proposed ultrasound classification (odds ratio, 5.1; P = .003) and the presence of diabetes (odds ratio, 9.7; P = .04). Coronary artery disease, neurologic symptoms status, recurrent ISR and primary atherosclerosis etiologies, stent type, and stent number were not significant predictors of TLR in this model. Discussion In this study we have described for the first time, to our knowledge, the various anatomic patterns of ISR observed after carotid stenting. We have proposed a classification of these patterns that uses B-mode ultrasound imaging. The scheme depends on the length and the geographic location of the intimal hyperplasia response in relation to the stent. The B-mode definition of these patterns correlated with angiographic assessment, confirming that transcutaneous ultrasound imaging allowed accurate recognition of the patterns of ISR occurring after CAS. The proposed classification (Fig 1) is noninvasive and can be conveniently applied during each follow-up examination within a few minutes. It uses straight-forward B-mode imaging with power Doppler to outline the intimal hyperplastic lesions, with length measurements performed on-screen using standard software provided on most current ultrasound machines. Results can be printed and saved for future comparisons during follow-up. The classification incorporates prior observations that geographic location and lesion length are important measures of the severity of the intimal hyperplastic response to coronary stenting.14 We observed that the higher level pattern (diffuse proliferative, type IV) of ISR after CAS predicted subsequent TLR. Therefore, the intimal hyperplastic response was most severe in patients who presented with the higher level of the classification (type IV). We infer that the classification adequately captures the magnitude of the intimal hyperplastic response to CAS. In a previous study, we reported that ISR occurs in a significant proportion of patients after CAS.5 Although most lesions were moderate in severity (40% to 79% stenosis), 6.4% were hemodynamically significant (≥80% stenosis) and required reintervention. There is currently no way to predict which of the low-grade or moderate-grade lesions will progress to need reintervention. The present investigation demonstrates that a classification of ISR patterns can independently predict the development of high-grade ISR necessitating reintervention. The only other independent predictor was diabetes, which is a well-known predictor of early and aggressive intimal hyperplasia and ISR after coronary stenting.14, 18 One report has observed an increased incidence of ISR in diabetic patients undergoing carotid stenting.19 However, the relationship between diabetes and the need for repeat carotid revascularization was not evaluated. Our study confirms that diabetes is associated with severe ISR (type IV, Table I) and that it is an independent predictor of target vessel failure and subsequent reintervention. Prior ISR has been hypothesized to predict future severe recurrent ISR,5 but this has been refuted by others.20 Our study provides evidence that prior ISR predisposes to severe recurrent ISR (type IV, Table II). The reason for this exaggerated intimal hyperplastic response to a reintervention is unknown. In the laboratory, a severe intimal hyperplastic response can, however, be reproducibly stimulated in animal models by inducing vascular injury.21 The continuing presence of an intravascular stent may afford a similar injury stimulus for intimal hyperplasia in patients. The most frequently occurring pattern of ISR in our cohort was the focal end-stent type (type I, Table I). On univariate analysis, we observed that most of the intrastent ISR lesions (76.2%, type II, Table II) occurred in patients undergoing CAS for primary atherosclerotic lesions (P = .02). Conversely, there was a trend towards fewer intrastent ISR lesions contributed by patients undergoing CAS for post-CEA restenosis. To our knowledge, this is the first observation that ISR patterns may differ according to the etiology of the primary lesion being treated in the carotid artery. We have previously reported that stenting of the carotid artery alters arterial wall biomechanical and hemodynamic properties.4 It is possible that stenting alters wall properties differently in patients with calcified atherosclerotic lesions compared with more compliant fibrotic post-CEA restenotic lesions, thereby inducing differing patterns of ISR. On univariate analysis, the type of stent used for CAS was also observed to influence the pattern of ISR (P = .03, Table II). Intrastent patterns of ISR (both focal and diffuse, types II and III) occurred more often in patients treated with the Acculink stent compared with the WallStent. We believe this is the first observation that ISR patterns may vary according to the type of stent deployed in the carotid artery. The results will require substantiation with a larger number of patients. Stent biomechanical properties vary according to their material, geometric design, and dimensions before and after deployment. These factors may induce variable changes in carotid arterial wall biomechanics,22 thereby influencing ISR patterns. Findings from the current investigation may therefore impact future stent designs and material selection. Despite optimal endovascular treatment with similar final diameter stenosis, some individuals had an enhanced intimal hyperplastic response to carotid stenting. As stated, univariate analysis demonstrated that several factors could influence the magnitude of the intimal hyperplastic response and subsequent need for reintervention. These included the pattern of ISR after CAS, diabetes, prior ISR, the etiology of the original lesion, and the type of stent used (Table I, Table II). On multivariate analysis, however, the pattern of ISR, reflecting the severity of the intimal hyperplastic response to injury, independently predicted future target vessel failure (odds ratio, 5.1; P = .003). Prior ISR did not independently predict subsequent TLR. This observation is different from findings in the coronary artery.18 Because prior ISR does result in more severe ISR after CAS, we infer that the pattern of ISR, influenced by several mechanisms, determines the risk for target vessel failure and TLR in the carotid artery. The proposed classification will facilitate the identification of patients with severe patterns of ISR (type IV) noninvasively by ultrasound imaging. This will enable early selection of these patients for aggressive monitoring or additional therapy in conjunction with stenting. Endovascular treatment was successfully achieved without complications in all instances of reintervention for high-grade (≥80%) ISR (Table III). We have previously reported that post-CAS ISR is a neointimal hyperplastic lesion that is not associated with the same risk of atheroembolic complications as in primary atherosclerotic lesions.5 The multiple modalities used (plain/cutting balloon angioplasty, primary stenting or a combination of these) indicate an absence of consensus on the optimal method of treatment. Intravascular radiation23 and local24 or systemic25 pharmacologic agents are under active investigation in high-risk coronary ISR patients and may prove beneficial in their treatment. Early and appropriate identification and treatment of these high-risk ISR patients using our ultrasound classification may improve cost-effective patient management and help develop novel revascularization strategies. Limitations This retrospective analysis is subject to the limitations related to such an investigation. Data were retrieved from our CAS Quality Assurance Database. The database is updated prospectively and incorporates the same information for all carotid stenosis patients undergoing endovascular interventions, regardless of clinical indications and outcomes. Because selective carotid angiography is associated with a risk of atheroembolic stroke,26 this modality was not used for routine follow-up. Duplex ultrasonography is readily available at our certified vascular laboratory. It produces high-resolution images of this relatively superficial artery, is inexpensive,12, 27 and is therefore ideally suited for the follow-up of patients undergoing CAS.5 Only persistently high velocities indicative of ISR ≥80%, or a recent rapid increase in velocities, were indications for diagnostic angiography. Although intravascular ultrasonography may provide accurate information on intimal hyperplastic lesions, the risk of atheroembolic stroke from additional instrumentation across the treated arterial segment has resulted in limited use of this modality for follow-up by most CAS operators. This analysis includes 14 patients that underwent CAS without antiembolic protection early in our experience. To the best of our knowledge, however, use of an antiembolic device does not alter ISR and should therefore not influence results of this study. Carotid occlusion is a rare outcome after CAS5 and occurred in only one patient from this series of 255 CAS procedures; therefore, it is not possible to determine predictors for this outcome. Of note, this patient remained asymptomatic despite the occlusion. Conclusion ISR after CAS presents with various ultrasound patterns that provide important prognostic information. As determined by the classification introduced in this study, focal end-stent, focal intrastent, diffuse intrastent, diffuse proliferative, and occluded ISR represent a spectrum of increasing intimal hyperplastic response to CAS. The pattern of ISR and a history of diabetes are important determinants of long-term outcome after CAS. In contrast, other comorbidities, prior neurologic symptom status, and immediate technical results appear to be less important. These observations imply that intrinsic biologic characteristics (ISR pattern and diabetes) have more influence over the long-term results of CAS than the immediate technical results of the treatment. The classification also offers an opportunity for the early identification of high-risk patients for intensive monitoring and treatment. By providing a standardized method of describing restenotic lesions, it will also facilitate further investigations into adjunctive treatments for ISR and improved stent design. Author contributions Conception and design: BL Analysis and interpretation: BL, EK, RH Data collection: BL, EK, SC, IK, RH Writing the article: BL, RH Critical revision of the article: BL, EK, SC, IK, RH Final approval of the article: BL, EK, SC, IK, RH Statistical analysis: BL Obtained funding: BL, RH Overall responsibility: BL References 1. 1Hobson RW, Goldstein JE, Jamil Z, Lee BC, Padberg FT, Hanna AK, et al. Carotid restenosis: operative and endovascular management. J Vasc Surg. 1999;29:228–235. Abstract | Full Text |
Full-Text PDF (384 KB)
|
CrossRef
2. 2Hobson RW, Lal BK, Chakhtoura E, Goldstein J, Haser PB, Kubicka R, et al. Carotid artery stenting: analysis of data for 105 patients at high risk. J Vasc Surg. 2003;37:1234–1239. Abstract | Full Text |
Full-Text PDF (138 KB)
|
CrossRef
3. 3Hobson RW, Lal BK, Chakhtoura EY, Goldstein J, Kubicka R, Haser PB, et al. Carotid artery closure for endarterectomy does not influence results of angioplasty-stenting for restenosis. J Vasc Surg. 2002;35:435–438. Abstract | Full Text |
Full-Text PDF (119 KB)
|
CrossRef
4. 4Lal BK, Hobson RW, Goldstein J, Chakhtoura EY, Duran WN. Carotid artery stenting: is there a need to revise ultrasound velocity criteria?. J Vasc Surg. 2004;39:58–66. Abstract | Full Text |
Full-Text PDF (156 KB)
|
CrossRef
5. 5Lal BK, Hobson RW, Goldstein J, Geohagan M, Chakhtoura E, Pappas PJ, et al. In-stent recurrent stenosis after carotid artery stenting: life table analysis and clinical relevance. J Vasc Surg. 2003;38:1162–1168. Abstract | Full Text |
Full-Text PDF (144 KB)
|
CrossRef
6. 6Ohki T, Veith FJ. Carotid artery stenting: utility of cerebral protection devices. J Invasive Cardiol. 2001;13:47–55. MEDLINE 7. 7Roubin GS, New G, Iyer SS, Vitek JJ, Al-Mubarak N, Liu MW, et al. Immediate and late clinical outcomes of carotid artery stenting in patients with symptomatic and asymptomatic carotid artery stenosis: a 5-year prospective analysis. Circulation. 2001;103:532–537. 8. 8Vitek JJ, Roubin GS, New G, Al-Mubarek N, Iyer SS. Carotid angioplasty with stenting in post-carotid endarterectomy restenosis. J Invasive Cardiol. 2001;13:123–125. MEDLINE 9. 9Yadav JS, Wholey MH, Kuntz RE, Fayad P, Katzen BT, Mishkel GJ, et al. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med. 2004;351:1493–1501.
CrossRef
10. 10NACPTAR-Investigators. Update of the immediate angiographic results and in-hospitalcentral nervous system complications of cerebral percutaneous transluminal angioplasty. Circulation. 1995;92:383. 11. 11FDA. Circulatory system devices panel. Panel transcript. http://www.fda.gov/ohrms/dockets/ac/04/transcripts/4033t1.htm 2004. 12. 12Willfort-Ehringer A, Ahmadi R, Gruber D, Gschwandtner ME, Haumer A, Haumer M, et al. Arterial remodeling and hemodynamics in carotid stents: a prospective duplex ultrasound study over 2 years. J Vasc Surg. 2004;39:728–734. Abstract | Full Text |
Full-Text PDF (170 KB)
|
CrossRef
13. 13Piamsomboon C, Roubin GS, Liu MW, Iyer SS, Mathur A, Dean LS, et al. Relationship between oversizing of self-expanding stents and late loss index in carotid stenting. Cathet Cardiovasc Diagn. 1998;45:139–143. MEDLINE |
CrossRef
14. 14Mehran R, Dangas G, Abizaid AS, Mintz GS, Lansky AJ, Satler LF, et al. Angiographic patterns of in-stent restenosis: classification and implications for long-term outcome. Circulation. 1999;100:1872–1878. 15. 15ICAVL. The intersocietal commission for the accreditation of vascular laboratories: standards for accreditation in noninvasive vascular testing. Columbia, MD: ICAVL; 2005;. 16. 16Hobson RW, Strandness DE. Carotid artery stenosis: what’s in the measurement?. J Vasc Surg. 1993;18:1069–1070. Abstract | Full Text |
Full-Text PDF (163 KB)
|
CrossRef
17. 17North american symptomatic carotid endarterectomy trial collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325:445–453. MEDLINE 18. 18Abizaid A, Kornowski R, Mintz GS, Hong MK, Abizaid AS, Mehran R, et al. The influence of diabetes mellitus on acute and late clinical outcomes following coronary stent implantation. J Am Coll Cardiol. 1998;32:584–589. Abstract | Full Text |
Full-Text PDF (84 KB)
|
CrossRef
19. 19Willfort-Ehringer A, Ahmadi R, Gessl A, Gschwandtner ME, Haumer A, Lang W, et al. Neointimal proliferation within carotid stents is more pronounced in diabetic patients with initial poor glycaemic state. Diabetologia. 2004;47:400–406.
CrossRef
20. 20Setacci C, de Donato G, Setacci F, Pieraccini M, Cappelli A, Trovato RA, et al. In-stent restenosis after carotid angioplasty and stenting: a challenge for the vascular surgeon. Eur J Vasc Endovasc Surg. 2005;29:601–607. Abstract | Full Text |
Full-Text PDF (158 KB)
|
CrossRef
21. 21Clowes AW, Schwartz SM. Significance of quiescent smooth muscle migration in the injured rat carotid artery. Circ Res. 1985;56:139–145. MEDLINE 22. 22Garcia LA, Hosley SE, Baim DS, Carrozza JP. In vivo assessment of stent recoil in normal porcine arteries: evaluation of contemporary stent designs. Catheter Cardiovasc Interv. 2001;53:277–280. MEDLINE |
CrossRef
23. 23Bhargava B, Karthikeyan G, Tripuraneni P. Intravascular brachytherapy: indications and management of adverse events. Am J Cardiovasc Drugs. 2004;4:385–394. MEDLINE |
CrossRef
24. 24Kastrati A, Mehilli J, von Beckerath N, Dibra A, Hausleiter J, Pache J, et al. Sirolimus-eluting stent or paclitaxel-eluting stent vs balloon angioplasty for prevention of recurrences in patients with coronary in-stent restenosis: a randomized controlled trial. Jama. 2005;293:165–171.
CrossRef
25. 25Brito FS, Rosa WC, Arruda JA, Tedesco H, Pestana JO, Lima VC. Efficacy and safety of oral sirolimus to inhibit in-stent intimal hyperplasia. Catheter Cardiovasc Interv. 2005;64:413–418. MEDLINE |
CrossRef
26. 26Executive committee for the asymptomatic carotid atherosclerosis study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995;273:1421–1428. MEDLINE 27. 27Lal BK, Hobson RW, Pappas PJ, Kubicka R, Hameed M, Chakhtoura EY, et al. Pixel distribution analysis of b-mode ultrasound scan images predicts histologic features of atherosclerotic carotid plaques. J Vasc Surg. 2002;35:1210–1217. Abstract | Full Text |
Full-Text PDF (969 KB)
|
CrossRef
a Division of Vascular Surgery, University of Medicine and Dentistry, New Jersey-New Jersey Medical School, Newark, NJ b Department of Physiology, University of Medicine and Dentistry, New Jersey-New Jersey Medical School, Newark, NJ c Department of Biomedical Engineering, University of Medicine and Dentistry, New Jersey-New Jersey Medical School, Newark, NJ d Division of Vascular Surgery, St. Michaels Medical Center, Newark, NJ e Division of Vascular Surgery, University of Athens, Athens, Greece.  Reprint requests: Brajesh K Lal, MD, UMDNJ-New Jersey Medical School, 185 S Orange Ave, MSB-H570, Newark, NJ 07103.
Competition of interest: none. Supported by grants from the American Heart Association (RA5883, BKL) and the National Institutes of Health (NS38384, RWH). PII: S0741-5214(07)01182-2 doi:10.1016/j.jvs.2007.07.022 © 2007 The Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved. | |
|
FULL TEXT01182-2/journalimage?img=PIIS0741521407011822.gr1.lrg.gif&fig=fig1&kwhquery=&issn=0741-5214&ishighres=false&allhighres=false&free=yes','journalimage');)
01182-2/journalimage?img=PIIS0741521407011822.gr2.lrg.gif&fig=fig2&kwhquery=&issn=0741-5214&ishighres=false&allhighres=false&free=yes','journalimage');)