(Stroke. 2001;32:479.)
© 2001 American Heart Association, Inc.
Original Contributions |
Role of the Distal Balloon Protection Technique in the Prevention of Cerebral Embolic Events During Carotid Stent Placement
Presented at the Radiological Society of North America Annual Meeting; November 29–December 4, 1998; Chicago, Ill.
From the Department of Radiology (J-B.M., K.J.M., P.G., K.S., D.A.R.), Division of Clinical Pathology (J-C.P., E.P.), Surgical Intensive Care Unit (M.T-V.), and Neuropathology Unit (G.P.), Geneva University Hospital, Geneva, Switzerland; Division of Neuroradiology, Johns Hopkins Hospital, Baltimore, Md (K.J.M., P.G.); Diagnostic and Therapeutic Neuroangiography, Hospital General de Cataluña, Sant Cugat del Valles, Spain (K.J.M., P.G.); and Department of Radiology, Caen University Hospital, Caen, France (J.T.).
Correspondence to J-B. Martin, MD, Department of Radiology, Geneva University Hospital, Rue Micheli-du-Crest 24, CH-1211 Geneva 14, Switzerland. E-mail Jean-Baptiste.Martin{at}dim.hcuge.ch
 |
Abstract |
|---|
 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Background and Purpose—We sought to quantitatively and qualitatively evaluate the release of atheromatous plaque debris induced by carotid stenting procedures.
Methods—Eight patients with severe carotid atheromatous stenoses were treated by stent implantation under distal balloon protection. Blood samplings were obtained after stent deployment in the blood pooled below the inflated protection balloon. The samples were centrifuged and evaluated for plaque debris with the use of light microscopy. The debris release was quantitatively estimated by dividing the total volume of debris obtained by the mean debris size. Five patients without endovascular procedure were used as a control group.
Results—The 2 main debris types found were nonrefringent cholesterol crystals (4 to 389 µm; 115 to 8697 in number) and lipoid masses (7 to 600 µm; 341 to 34 000 in number). There was a statistically significant difference compared with the samples obtained in the control group (P=0.017).
Conclusions—Blood samples collected during stent implantation procedures contain a large quantity of atheromatous plaque debris. This emphasizes the role of distal protection techniques in avoiding migration of this plaque material into the cerebral circulation.
Key Words: atherosclerosis • carotid stenosis • protection device • stents
|
Introduction |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
The carotid bifurcation is the most common location of craniocervical atheromatous disease,1 accounting for 20% to 30% of strokes.2 Carotid stenoses may result in brain ischemia either through direct hemodynamic impact on the cerebral blood circulation or as a source of thromboembolic material.3 The tendency of atheromatous lesions to produce thromboembolic events is linked to their morphological characteristics, in particular the presence of plaque ulceration.4 The benefits of carotid atheromatous disease treatment by carotid endarterectomy have been established by several large studies.5 6 7 Carotid angioplasty and stenting recently emerged as a therapeutic alternative derived from the extensive experience gained in peripheral endovascular procedures. Initially, carotid angioplasty was associated with embolic complication rates ranging from 4% to 33%.8 9 10 11 12 13 14 15 16 17 This high propensity to produce embolic plaque debris led to the development of distal protection techniques to be used during endovascular procedures performed for lesions of the carotid bifurcation.18 Balloon angioplasty with or without stent placement using a distal protection technique involving transitory balloon occlusion of the cervical internal carotid artery (ICA) has been shown to be safe and effective.19 Diffusion of the balloon protection technique has been limited by the lack of device availability and large-scale studies. With the advent of commercially available protection devices, the role of protection techniques may rapidly increase.20 21
The purpose of the present study was to prospectively evaluate the amount and type of plaque debris released during endovascular stent placement in patients with carotid bifurcation atheromatous disease.
|
Subjects and Methods |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Carotid Stent Patients
Nine consecutive carotid bifurcation stent placements performed in 8 patients with severe carotid atheromatous disease were prospectively evaluated. In all cases, self-expandable stents (Wallstent, BSC) were deployed and performed after dilatation via a triple coaxial system.19 Eight lesions were symptomatic, and 1 lesion, a postradiotherapy stenosis with 95% lumen reduction, was asymptomatic (procedure 9 in the Table
).
Endovascular treatment was performed 1 to 5 months after
presentation of neurological symptoms. The degree of
stenosis ranged from 70% to 95%, with a mean percentage of
stenosis measured at 84% according to the criteria of the
North American Symptomatic Carotid
Endarterectomy Trial. Plaque ulcers were found in 7
of 9 cases (procedures 1 to 4 and 6 to 8). One patient was treated for
a recurrent stenosis secondary to neointimal
hyperplasia after previous stent implantation (procedure 8). Protection
was used in this case for a redilatation procedure without introduction
of another stent.
|
All procedures were performed under distal balloon
protection with the technique described by Théron et
al.19 This technique
involved temporary occlusion of the cervical ICA by a nondetachable
latex balloon (BC 17, Nycomed) fixed on a 2.6F and 300-cm-long
microcatheter (tubing with distal end collar, catalog No. 5RE-658,
Cordis Europe N.V.) by latex ligatures (Nycomed). All stenotic
lesions were passed with the protection balloon system and the stent
delivery device together, with the deflated protection balloon system
used as a guide. There was no need for predilatation in any of the
procedures. After stent deployment, the stent delivery device was
removed, and a postdilatation procedure with angioplasty balloons of 5
to 8 mm diameter and 2 cm in length (Smash, BSC) was performed.
Subsequently, after removal of the dilatation balloon, the 9F guiding
catheter (Vistabritetip, Cordis) was gently advanced under fluoroscopic
control within the stent lumen to reach the level of angioplasty, and
blood was aspirated with a 50-mL syringe. This aspiration occurred
through the large side port of a valve adapter (adjustable hemostasis
valve, Cordis) fixed to the hub of the 9F guide catheter, which allowed
for easy withdrawal of large blood samples. The space between the 9F
guide catheter lumen and the coaxial 2.6F microcatheter allows for
unconstrained fluid exchange. The remaining blood pooled below the
balloon was then flushed into the external carotid circulation by the
injection of 30 mL saline at a rate of 2 mL/s with a power injector
(Figures 1 and 2). The protection system was then withdrawn,
and a postprocedural angiographic control was obtained
(Figures 1 and 2). All patients received a bolus injection of
heparin (150 IU/kg) at the beginning of the procedure for
anticoagulation purposes. Atropine 1 mg IV was given immediately before
angioplasty to prevent bradycardia. Aspirin 300 mg/d (Bayer) was
started 3 days before the procedure and continued indefinitely.
Ticlopidine 1 mg (Ticlid, Sanofi Winthrop) was given immediately before
the procedure and continued for 3 months.
|
|
Analysis of Blood Samples Obtained
During Endovascular Procedures
All patients gave informed consent for blood
analysis. The blood samples were obtained by aspirating a total
of 30 to 50 mL with a 50-mL syringe, as described above, and were used
systematically in our procedures. The blood was heparinized and
centrifuged immediately after withdrawal. The sediment was
separated and weighed with a micrometric scale. To evaluate the quality
of the sediment, 3 samples were taken at 3 different gravity levels
(top, middle, and bottom parts of the sediment) and evaluated under the
microscope after coloration (Oil Red O and Papanicolaou). The quantity
of material analyzed in the 3 samples was extrapolated to the
total volume of the sediment, allowing for estimation of the total
number of plaque debris collected.
Control Group
As control, we elected to sample blood aspirated from
different patients of a similar age group, either with similar disease
but no endovascular treatment or similar disease at another location
receiving endovascular treatment. For the carotid stenosis
lesions, 3 symptomatic patients with similar
atheromatous lesions were sampled during
diagnostic angiography evaluation before
endarterectomy surgery. For the endovascular
treatment group receiving a stent for another
atheromatous lesion, we chose 2 patients with
symptomatic lesions of the distal ICA and vertebral artery
origin. The first patient underwent angioplasty and stenting of an
atheromatous stenotic lesion at the C5 segment
of the ICA siphon. The blood was collected after postdilatation of the
stent with a coaxial guide catheter reaching above the carotid
bifurcation. The second patient was treated for an
atheromatous stenosis of the right vertebral
artery origin by angioplasty followed by stenting. In this case, the
blood was collected in the subclavian artery at the level of the
atheromatous lesion, just after
postdilatation.
The aspirated material was evaluated by the previously described quantification technique, ie, analysis of 3 samples of the sediment and extrapolation to the total sediment volume.
Statistical Analysis
The 2-sample unequal variance
t test, with a value of
P<0.05 considered significant,
was used to evaluate differences in material collected by aspiration
during carotid stenting procedures (studied population) and during
diagnostic angiograms (control
group).
|
Results |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Types of Plaque Debris Found
The types of plaque debris found included cholesterol crystals and lipoid masses (Figures 3
and 4).
|
|
Carotid Stent Patients
Therapeutic carotid stent placement was successfully
performed in the 8 patients (9 stents), without periprocedural or
postprocedural complications (Table
).
No or minimal vasospasm (lumen reduction of <50%) at the level of the
protection balloon position was observed in 7 lesions, and a moderate
vasospasm (lumen reduction of 50% to 70%) with flow reduction was
observed in 2 lesions. The latter were treated with nimodipine (60 µm
IA, Nimotop, Bayer), with relief of vasospasm and improvement of the
circulation within a few minutes. The blood samples were positive for
cholesterol crystal in 7 of the 9 procedures (procedures 1
to 7 in the Table)
and positive for lipoid masses in all instances. By extrapolating the
values obtained with 3 samples to the total centrifuged
material for each collected blood specimen, the number of
cholesterol debris was found to range from 115 to 8697
(mean, 3100; SD, 3003; median, 3480). The size of the aspirated
cholesterol debris varied from 3.7 to 389 µm (mean, 102.5
µm; SD, 81.5 µm). By the same technique, the number of calculated
lipoid masses ranged from 341 to 34 333 (mean, 9726; SD, 12 723;
median, 3933). Their size varied from 7.4 to 594 µm (mean, 128
µm; SD, 90.7). The results are summarized in the Table.
Because of the small sample size, a correlation of the type
and the number of debris observed with symptoms or imaging studies was
not performed. It should be noted, however, that 6 of 7 ulcerated
lesions showed cholesterol crystals in the debris
(procedures 1 to 4, 6, and 7 in the Table).
Another lesion with 90% stenosis had cholesterol
crystals without visualization of ulceration (procedure 5).
No crystals were observed in 1 of the 7 ulcerated lesions
with 70% stenosis (procedure 8 in the Table)
and in 1 lesion with 80% stenosis without ulceration but
occurring after radiotherapy (procedure 9).
Control Group
The blood specimens obtained in 2 of the 3
diagnostic angiographic control cases were negative
(control cases 3 and 5 in the Table).
In the third patient the sampling showed a small quantity of
cholesterol crystals (number, 130; mean size, 51.3
µm; control case 4). The results are summarized in the Table.
The 2 control patients treated for atheromatous
stenoses by angioplasty and stenting underwent successful
procedures without periprocedural or postprocedural complications. The
sample obtained in the vertebral stent case was positive only for
lipoid masses (number, 364; mean size, 66.4 µm; control case 2). The
sample obtained in the intracranial stent case was positive for both
types of debris (220 cholesterol crystals; mean size, 145.3
µm; 73 lipoid masses; mean size, 535 µm; control case
1).
Statistical Analysis
The statistical evaluation of the results revealed a
significant difference for both types of debris between the samples
obtained below the protection balloon during carotid stenting
procedures and the samples obtained in the control group
(P=0.017).
|
Discussion |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Although the complication rate related to endovascular treatment methods of carotid stenosis has decreased with the evolution of therapeutic devices,8 10 the risk of cerebral embolic events secondary to plaque debris migration during angioplasty and stent deployment remains of concern.9 16 Previous in vitro experimentation on isolated specimens of carotid atheromatous plaques has demonstrated the fragility of the plaque and the risk of debris release during stent placement.22 In vitro studies have, on the other hand, emphasized the ability of the distal balloon technique to protect against migration of plaque debris into the cerebral circulation.23 The purpose of our study was to confirm in vivo the role of this technique by sampling and analyzing the blood pooled below the protection balloon in 9 carotid stenting procedures. Two types of debris (cholesterol crystals and lipoid masses) were found in these samples. Atheromatous plaques are composed of a mixture of cholesterol crystals and atheromatous material; both can be released in the circulation when the plaque is broken.24 Cholesterol crystals were defined as geometric, angulated unstained structures, and lipoid masses were identified as aggregates of amorphous, granular, compact material stained with Oil Red O coloration.
The amount of collected debris was significantly higher in the carotid stent patients than in the 5 control patients (P=0.017), confirming that debris release occurs during angioplasty and stent deployment.
High numbers of cholesterol crystals were seen mostly with ulcerated plaques and tight atheromatous stenosis, which may allow us to postulate that ulceration and degree of squeeze of the plaque during endovascular treatment could be considered risk factors for expulsion of cholesterol crystals.
In the present investigation, debris was collected during only one of the protection maneuvers, ie, the aspiration of the blood pooled below the balloon with a 50-mL syringe. The protection methodology implies that after this initial aspiration, the stagnant blood is flushed away toward the external carotid circulation by a brisk saline injection. This second part of the cleaning procedure was not evaluated in our study, which therefore likely underestimates the total amount of released debris. Another source of underestimation of the material accumulated below the protection balloon lies in the handling of the blood specimens: immediate heparinization of the samples precluded evaluation of potentially present thrombotic material, and centrifugation of the specimens probably fragmented the collected debris, explaining their relatively small size.
Although sampling below the carotid stenosis before treatment would have been a good option to perform control studies, we elected to use a different patient group for this purpose. Sampling in the control group was performed in less advanced or differently located vascular atheromatosis, which allowed for sampling in a proximity of the lesion that was similar to the one used after carotid stent implantation. This choice of control allowed us to avoid a potentially dangerous preprocedural catheter sampling close to the ulcerated carotid lesions.
This study did not evaluate the potential of plaque debris released during the first and last steps of the endovascular procedure, ie, during initial introduction of the protection balloon system through the stenotic lesion and during removal of the same system at the end of the procedure.
Continuous sonographic Doppler controls at the level of the middle cerebral artery have shown presence of embolic events for the first step of the procedure in previous studies.25 26 We have occasionally performed similar Doppler controls at the level of the middle cerebral artery, and during both of these procedural steps we have recorded a small number of Doppler signals, indicating embolic events that were asymptomatic. We believe that protection from embolic events is difficult to avoid during both of these steps. However, our observation during introduction of the protection system together with the stent delivery device indicates important flow reduction as soon as the stenotic segment is passed. This flow arrest keeps potential debris close to the lesion while the protection balloon is inflated higher up in the ICA.
Our study confirms that uncovered stents do not provide protection against plaque debris release. It is interesting to note that all the samples collected during carotid stenting procedures were positive for lipoid masses. The case of intimal hyperplasia that developed over a previously placed stent and was treated by angioplasty and restenting was positive for lipoid masses as well, showing that this particular indication carried comparable embolic risks.
Whether lipoid masses or cholesterol crystals would have different embolic effects cannot be concluded from this study. The maximal sizes of 0.389 mm for crystals and 0.594 mm for lipoid masses indicate that both may exist in sizes that are enough large to occlude small cerebral arteries. Depending on location, this might lead to a neurological event.27 If the high number of smaller pieces of debris observed in our study is representative of endovascular procedures, then there needs to be an explanation for the few symptomatic events observed in the clinical cases treated without protection. It may be that the cerebral circulation tolerates a high number of silent embolic events if they are small enough to permit collateral supply.
The study shows that there are a significant number of large pieces of debris produced during endovascular stent application; however, the period when most debris is produced cannot be indicated because the samples were not drawn in a fractionated manner over the different steps of the procedure. We currently believe that the steps most likely to produce larger pieces of debris are during stent postdilatation procedures with balloon squeeze of the plaque and during shear forces of stent struts produced by secondary stent deformation in contact with the atheromatous wall.
Although more serious damage of the arterial wall due to application of a protection balloon may occur,28 such complications can be avoided by adequate training.
Conclusion
Our in vivo study clearly indicates that a large amount
of plaque debris, probably underestimated in both size and number by
our methodology, is released during the placement of a carotid stent.
It is our belief that this debris accounts for most of the embolic
complications related to carotid angioplasty and stenting. In the 9
uncomplicated carotid procedures reported here, potential embolic
material was collected in the blood pooled below the protection balloon
before it was washed out toward the external carotid circulation. Our
findings emphasize the capacity of the distal protection technique to
increase the safety of carotid angioplasty and stenting by preserving
the cerebral circulation from plaque debris
migration.
|
Acknowledgments |
|---|
This study was supported by a fellowship for prospective researchers from the Swiss National Science Foundation (Dr Gailloud).
Received June 15, 2000; revision received November 27, 2000; accepted November 27, 2000.
|
References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
1. Prati P, Vanuzzo D, Casaroli M, Di Chiara A, De Biasi F, Feruglio GA, Touboul PJ. Prevalence and determinants of carotid atherosclerosis in a general population. Stroke. 1992;23:1705–1711.
2. DeBakey ME. Carotid endarterectomy revisited. J Endovasc Surg. 1996;3:4.[Medline] [Order article via Infotrieve]
3.
Riles TS, Lieberman
A, Kopelman I, Imparato AM. Symptoms, stenosis, and bruit:
interrelationships in carotid artery disease.
Arch Surg. 1981;116:218–220.
4. Kerber CW, Heilman CB. Flow dynamics in the human carotid artery, I: preliminary observations using a transparent elastic model. AJNR Am J Neuroradiol. 1992;13:173–180.[Abstract]
5. Eliasziw M, Smith RF, Singh N, Holdsworth DW, Fox AJ, Barnett HJ, for the North American Symptomatic Carotid Endarterectomy Trial (NASCET) Group. Further comments on the measurement of carotid stenosis from angiograms. Stroke. 1994;25:2445–2449.[Abstract]
6. Eliasziw M, Streifler JY, Spence JD, Fox AJ, Hachinski VC, Barnett HJ, for the North American Symptomatic Carotid Endarterectomy Trial (NASCET) Group. Prognosis for patients following a transient ischemic attack with and without a cerebral infarction on brain CT. Neurology. 1995;45(pt 1):428–431.
7. Rothwell PM, Gibson RJ, Slattery J, Warlow CP, for the European Carotid Surgery Trialists’ Collaborative Group. Prognostic value and reproducibility of measurements of carotid stenosis: a comparison of three methods on 1001 angiograms. Stroke. 1994;25:2440–2444.[Abstract]
8.
Roubin GS. The
status of carotid stenting. AJNR Am J
Neuroradiol. 1999;20:1378–1381.
Letter.
9. Roubin GS, Yadav S, Iyer S, Vitek J. Carotid-stent supported angioplasty: a neurovascular intervention to prevent stroke. Am J Cardiol. 1996;78:8–12.
10. Henry M, Amor M, Masson I, Henry I, Tzvetanov K, Chati Z, Khanna N. Angioplasty and stenting of the extracranial carotid arteries. J Endovasc Surg. 1998;5:293–304.[Medline] [Order article via Infotrieve]
11. Mathias K, Jager H, Sahl H, Hennigs S, Gissler HM. Interventional treatment of arteriosclerotic carotid stenosis [in German]. Radiologe. 1999;39:125–134.[Medline] [Order article via Infotrieve]
12. Mathias KD. Angioplasty and stenting for carotid lesions: an argument for. Adv Surg. 1999;32:225–243.[Medline] [Order article via Infotrieve]
13. Wholey MH, Wholey M, Bergeron P, Dietrich EB, Henry M, Laborde JC, Mathias K, Myla S, Roubin GS, Shawl F, Theron JG, Yadav JC, Dorros G, Guimaraens L, Higashida R, Kumar V, Leon M, Lim M, Londero H, Mesa J, Ramee S, Rodriguez A, Rosenfield K, Teitelbaum G, Vozzi C. Current global status of carotid artery stent placement. Cathet Cardiovasc Diagn. 1998;44:1–6.[Medline] [Order article via Infotrieve]
14.
Yadav JS, Roubin
GS, Iyer S, Vitek J, King P, Jordan WD, Fisher WS. Elective stenting of
the extracranial carotid arteries.
Circulation. 1997;95:376–381.
15. Diethrich EB, Marx P, Wrasper R, Reid DB. Percutaneous techniques for endoluminal carotid interventions. J Endovasc Surg. 1996;3:182–202.[Medline] [Order article via Infotrieve]
16. Diethrich EB, Ndiaye M, Reid DB. Stenting in the carotid artery: initial experience in 110 patients. J Endovasc Surg. 1996;3:182–202.
17. Bergeron P, Chambran P, Bianca S, Benichou H, Massonat J. Endovascular treatment of arteries with cerebral destination: failures and limits [in French]. J Mal Vasc. 1996;21(suppl A):123–131.
18. Theron J, Courtheoux P, Alachkar F, Bouvard G, Maiza D. New triple coaxial catheter system for carotid angioplasty with cerebral protection. AJNR Am J Neuroradiol. 1990;11:869–874; comment 875–877.[Medline] [Order article via Infotrieve]
19.
Théron JG,
Payelle GG, Coskun O, Huet HF, Guimaraens L. Carotid artery
stenosis: treatment with protected balloon angioplasty and
stent placement. Radiology. 1996;201:627–636.
20.
Carlino M, De
Gregorio J, Di Mario C, Anzuini A, Airoldi F, Albiero R, Briguori C,
Dharmadhikari A, Sheiban I, Colombo A. Prevention of distal
embolization during saphenous vein graft lesion angioplasty: experience
with a new temporary occlusion and aspiration system.
Circulation. 1999;99:3221–3223.
21. Oesterle SN, Hayase M, Baim DS, Teirstein PS, Ramee SR, Whitlow PL, Webb J, Virmani R. An embolization containment device. Cathet Cardiovasc Intervent. 1999;47:243–250.[Medline] [Order article via Infotrieve]
22. Ohki T, Marin ML, Lyon RT, Berdejo G L, Soundararajan K, Ohki M, Yuan JG, Faries PL, Wain RA, Sanchez LA, Suggs WD, Veith FJ. Ex vivo human carotid artery bifurcation stenting: correlation of lesion characteristics with embolic potential. J Vasc Surg. 1998;27:463–471.[Medline] [Order article via Infotrieve]
23. Martin J-B, Sayegh Y, Gailloud P, Sugiu K, Spadola L, Khan H, Guimaraens L, Fasel JHD, Théron J, Rüfenacht DA. In-vitro models of human carotid atheromatous disease. In: Henry M, Amor M, Théron J, Roubin GS. Carotid Angioplasty and Stenting. 1st ed. Toulouse, France: Europa; 1998:199–204.
24.
Stary HC,
Chandler AB, Dinsmore RE, Fuster V, Glagov S, Insull W, Rosenfeld ME,
Schwartz CJ, Wagner WD, Wissler RW. A definition of advanced types of
atherosclerotic lesions and a histological
classification of atherosclerosis.
Circulation. 1995;92:1355–1374.
25. Benichou H, Bergeron P. Carotid angioplasty and stenting: will periprocedural transcranial Doppler monitoring be important? J Endovasc Surg. 1996;3:217–223.[Medline] [Order article via Infotrieve]
26. Bergeron P, Benichou H, Rudondy P, Jausseran JM, Fernandi M, Courbier R. Stroke prevention during carotid surgery in high risk patients (value of transcranial Doppler and local anesthesia). J Cardiovasc Surg (Torino). 1991;32:713–719.[Medline] [Order article via Infotrieve]
27. Lovblad KO, Plushke W, Remonda L, Gruber-Wiest D, Do D, Barth A, Kniemeyer H, Basseti C, Mattle H, Schroth G. Diffusion-weighted MRI for monitoring neurovascular interventions. Neuroradiology. 2000;42:134–138.[Medline] [Order article via Infotrieve]
28. Théron J, Guimaraens L, Coskun O, Sola T, Martin J-B, Ruefenacht DA. Complications of carotid angioplasty and stenting. Neurosurg Focus. 1998. Available at: http://www.neurosurgery.org/focus/dec98/5-6-4.html. Accessed November 18, 1998.
This article has been cited by other articles:
 |
|
 |
|
  A. D. Talenfeld, R. B. Schwope, H. J. Alper, E. I. Cohen, and R. A. Lookstein MDCT Angiography of the Renal Arteries in Patients with Atherosclerotic Renal Artery Stenosis: Implications for Renal Artery Stenting with Distal Protection Am. J. Roentgenol., June 1, 2007; 188(6): 1652 - 1658. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. P. Liew and J. R Bartholomew Atheromatous embolization Vascular Medicine, November 1, 2005; 10(4): 309 - 326. [Abstract] [PDF]
|
|
|
|
 |
|
 R. Zahn, T. Ischinger, B. Mark, S. Gass, U. Zeymer, W. Schmalz, K. Haerten, K. E. Hauptmann, E.-R. von Leitner, W. Kasper, et al. Embolic Protection Devices for Carotid Artery Stenting: Is There a Difference Between Filter and Distal Occlusive Devices? J. Am. Coll. Cardiol., June 7, 2005; 45(11): 1769 - 1774. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. P. Lownie, D. M. Pelz, D. H. Lee, S. Men, I. Gulka, and P. Kalapos Efficacy of Treatment of Severe Carotid Bifurcation Stenosis By Using Self-Expanding Stents without Deliberate Use of Angioplasty Balloons AJNR Am. J. Neuroradiol., May 1, 2005; 26(5): 1241 - 1248. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Zahn, B. Mark, N. Niedermaier, U. Zeymer, P. Limbourg, T. Ischinger, K. Haerten, K. E. Hauptmann, E.-R. v. Leitner, W. Kasper, et al. Embolic protection devices for carotid artery stenting: better results than stenting without protection? Eur. Heart J., September 1, 2004; 25(17): 1550 - 1558. [Abstract] [Full Text]
|
|
|
|
 |
|
 I. Linfante, J. A. Hirsch, M. Selim, G. Schlaug, L. R. Caplan, and A. S. Reddy Safety of Latest-Generation Self-expanding Stents in Patients With NASCET-Ineligible Severe Symptomatic Extracranial Internal Carotid Artery Stenosis Arch Neurol, January 1, 2004; 61(1): 39 - 43. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Wittkugel, J. Fiehler, C. Koch, B. Eckert, E. Kilic, M. Frahm, and H. Zeumer Endovascular Treatment of Internal Carotid Artery Stenosis: Effect of Primary Stent Application on Debris Particle Release in Human Cadaveric Specimens Radiology, December 1, 2003; 229(3): 855 - 860. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Kastrup, K. Groschel, H. Krapf, B. R. Brehm, J. Dichgans, and J. B. Schulz Early Outcome of Carotid Angioplasty and Stenting With and Without Cerebral Protection Devices: A Systematic Review of the Literature Stroke, March 1, 2003; 34(3): 813 - 819. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. J. Fox Jr, C. J. Moran, D. T. Cross III, R. L. Grubb Jr, K. M. Rich, M. R. Chicoine, R. G. Dacey Jr, and C. P. Derdeyn Long-Term Outcome After Angioplasty for Symptomatic Extracranial Carotid Stenosis in Poor Surgical Candidates Stroke, December 1, 2002; 33(12): 2877 - 2880. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. H. Brooks, R. R. McClure, M. R. Jones, T. C. Coleman, and L. Breathitt Carotid angioplasty and stenting versus carotid endarterectomy: randomized trial in a community hospital J. Am. Coll. Cardiol., November 15, 2001; 38(6): 1589 - 1595. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||