(Circulation. 2006;113:2021-2030.)
© 2006 American Heart Association, Inc.
New Drugs and Technology |
From Lenox Hill Hospital, New York City, NY.
Correspondence to Dr Gary S. Roubin, Department of Cardiac and Vascular Interventional Services, Lenox Hill Heart and Vascular Institute, 9th Floor-Black Hall, Lenox Hill Hospital, 130E 77th St, New York, NY 10021.
| Abstract |
|---|
|
|
|---|
Key Words: carotid arteries prevention prognosis stents stroke
| Introduction |
|---|
|
|
|---|
| Historical Perspective |
|---|
|
|
|---|
Effective experimentation with carotid angioplasty began in the mid 1970s11,12 and rapidly developed during the subsequent 2 decades.1317 The contemporary era of carotid stenting began in 1994 when Roubin et al18 instigated the first rigorous, prospective study of carotid stenting entailing independent neurological evaluation at baseline and at 30 days after procedure. This study, and the experience of others,19 demonstrated that from the outset, carotid stenting performed by experienced operators produced acceptable outcomes. Although stenting compared with balloon angioplasty significantly enhanced the efficacy and safety of percutaneous carotid revascularization, the development of embolic protection methods provided the answer to the problem of atheroembolism from the intervention site. From the early description by Vitek et al20 of innominate artery angioplasty with occlusive balloon protection of the common carotid artery (CCA), through pioneering work by Theron et al21 and Henry et al,22 distal23 and proximal24 antiembolic protection technology has developed rapidly. The availability of multiple embolic protection systems has been shown in many single and multicenter registries to confer a remarkably low risk of embolic complications after carotid stenting.2529 Thus, the feasibility of carotid stenting, its simplicity compared with CEA, and the low morbidity afforded by distal protection devices have accelerated the acceptance and utilization of this procedure.
| Short-Term Outcomes and the Impact of Embolic Protection Devices |
|---|
|
|
|---|
| Long-Term Outcomes |
|---|
|
|
|---|
| Indications |
|---|
|
|
|---|
|
It is becoming evident that carotid stenting is particularly suitable for certain patient subsets characterized by specific clinical or anatomic features. The randomized, multicenter SAPPHIRE trial compared CEA with carotid stenting utilizing EPD in 334 patients considered at high risk for open surgical intervention because of coexistent vascular disease or nonvascular comorbidities.4 Enrollment required lesion diameter stenosis
50% in symptomatic patients or
80% in asymptomatic patients (the latter accounting for &71% of the trial population). By intention-to-treat analysis, 1-year rates of the individual major adverse event end points were lower with carotid stenting than with CEA (death [7.4% versus 13.5%, P=0.08], major ipsilateral stroke [0.6% versus 3.3%, P=0.09], and myocardial infarction [3.0% versus 7.5%, P=0.07]), although these differences did not attain statistical significance. However, the composite end point occurred significantly less frequently with carotid stenting than with CEA (12.2% versus 20.1%, respectively; P=0.053). At 1 year, the requirement for repeated carotid revascularization procedures was lower in patients treated with stenting than in those treated with CEA (0.6% versus 4.3%, P=0.04). Notably, carotid stenting was entirely devoid of cases of cranial nerve injury, which occurred in 5.3% of CEA patients. Recent prospective registries of carotid stenting in patients at high risk for CEA are consistent with the SAPPHIRE trial, with reports of 30-day major adverse event rates <8%.2,3 Thus, patients who have serious comorbid medical or anatomic conditions that increase the risk from an open surgical approach or general anesthesia should be primary candidates for carotid stenting. These conditions include advanced age, significant cardiac and pulmonary disease, prior neck irradiation or radical surgery, restenosis after endarterectomy, contralateral carotid occlusion, high lesions behind the mandible, and low lesions that would require thoracic exposure. Randomized trials comparing carotid stenting and CEA in patients at low surgical risk are in progress.
Carotid stenting has a number of notable relative contraindications. Patients who are intolerant to antiplatelet agents are more safely managed with CEA. Similarly, if the patient has a compelling reason to undergo a major surgical procedure within 3 to 4 weeks that will require the cessation of antiplatelet therapy, CEA may be a better option. A large thrombus burden and specific angiographic findings discussed in detail below should be excluded before carotid stenting. Intracranial arterial stenoses, arteriovenous malformations, or stable aneurysms are not necessarily contraindications for coronary artery stenting; however, in the latter case, stringent control of blood pressure and careful modulation of anticoagulation are mandatory. Although contrast nephropathy is an important consideration in patients undergoing carotid stenting, this seldom represents a contraindication, because experienced operators should rarely require
75 mL of contrast material to complete the procedure.
| Patient Selection |
|---|
|
|
|---|
Symptomatic Patients
Given the demonstrated benefit of revascularization over medical therapy in the management of severely stenotic lesions (70% to 99% diameter stenosis by the NASCET criteria39,43,44) clearly associated with symptoms attributable to the ipsilateral carotid distribution, CEA in these patients has been considered indicated when the periprocedural risk of death or stroke is <6%.38 The same is applicable to carotid stenting. Available data demonstrate that the rates of periprocedural death or disabling stroke after carotid stenting are generally below 6%, even without the universal use of EPDs1,45 and in patients at high risk for CEA.24
The risk of recurrent ipsilateral neurological events with medical management is much lower for moderate stenosis (50% to 69% by the NASCET criteria) than for severe carotid lesions.8 Because the potential benefit of any revascularization procedure is inversely related to angiographic lesion severity,40 in patients with lesions of moderate or borderline severity, the risk-benefit ratio of carotid stenting should be weighed accordingly.
Asymptomatic Patients
Stroke prevention in asymptomatic patients requires special consideration. The risk of stroke in the territory of an asymptomatic carotid stenosis has been shown to be strongly dependent on angiographic lesion severity.41 In the European Carotid Surgery Trial (ECST), the 3-year rates of ipsilateral stroke with asymptomatic lesions of less than or greater than 70% stenosis were approximately 2% and 5.7%, respectively.41 (It is noteworthy in this regard that the methods for the measurement of the degree of carotid stenosis have varied among trials, so that application of the ECST methodology results in greater degrees of stenosis for a given lesion than the NASCET methodology.39,44) In the medical treatment arms of the ACAS and ACST, 5-year rates of death or ipsilateral stroke were similar at &12%.6 Thus, for clinical benefit to be derived by an asymptomatic patient with a severely stenotic carotid lesion, periprocedural rates of death or stroke after carotid revascularization must not exceed 3%.5 Given the high prevalence of asymptomatic carotid disease,46,47 the optimal application of carotid stenting in this patient subset must be defined rigorously (see "The 3% Rule" below).
Owing to the very low event rates in patients with asymptomatic lesions of moderate severity (<60% diameter stenosis), it is unknown whether currently available interventional techniques can improve long-term outcomes over those achievable with optimal medical management. Also unresolved are the indications for carotid stenting in asymptomatic individuals with contralateral carotid occlusion48 and those undergoing major cardiac or vascular surgery.49
| The 3% Rule |
|---|
|
|
|---|
3%.5 With the widespread availability of CEA and carotid stenting, candidates for carotid revascularization have generally been selected for either procedure on the basis of the presumed surgical risk (the "conventional paradigm," depicted in Figure 1). Low-risk surgical patients would usually be referred for CEA or be enrolled in a randomized clinical trial of surgery versus stenting. Patients considered at high risk for open surgery were often referred for carotid stenting, arbitrarily considered a low-risk intervention because little attention had been given to definition of the risks associated with the latter procedure. However, it is of crucial importance to recognize the risks of carotid stenting and to realize that in certain patients (easily identified by readily available clinical and angiographic features), particularly those with asymptomatic lesions, the risks of procedure-related major adverse events might exceed the long-term risk of ipsilateral stroke with medical therapy. We believe that for the full clinical potential of carotid stenting to be realized, a paradigm shift needs to be implemented in the process of procedural risk stratification and selection of patients for revascularization. This applies both to everyday clinical practice and to the design of randomized trials. Clinical decision making that incorporates these principles is depicted in Figure 1.
|
Implementing the 3% Rule
In determining the risk of death or stroke associated with carotid stenting, it is of critical importance to recognize 4 factors that have been associated with increased procedural complications (Table 2). The most important of these factors is advanced age. In the lead-in phase of the multicenter CREST trial, the risk of 30-day stroke or death among 749 patients was directly related to age (<60 years, 1.7%; 60 to 69 years, 1.3%; 70 to 79 years: 5.3%; and >80 years, 12.1%; P=0.006).50 Although the risk attributable to advanced age in this analysis appeared to be independent of other clinical (eg, gender or symptom status), angiographic (eg, lesion severity), or procedural (eg, use of distal protection devices) factors,50 it is likely that the increasing prevalence of the other factors listed in Table 2 with advanced age accounts, at least in part, for this association. Decreased cerebral reserve is another important factor when one considers the risk of carotid stenting. Carotid revascularization (carotid stenting or CEA) is usually associated with some degree of cerebral embolization that is generally well tolerated in patients with good cerebral reserve; however, patients with prior strokes, lacunar infarcts, microangiopathy, or dementia of varying stages are much more likely to experience neurological deficits after carotid stenting. This risk is markedly amplified in the presence of an isolated hemisphere with lack of good collateral support.
|
Although some lesion characteristics (eg, degree of stenosis and length) indicate potential technical difficulties, the 2 most important anatomic findings portending an increased procedural risk are vascular tortuosity and heavy concentric calcification. Excessive tortuosity is defined as
2 bend points that exceed 90°, within 5 cm of the lesion, including the takeoff of the ICA from the CCA (Figure 2). Excessive tortuosity increases the difficulty of access to the lesion, may not permit device delivery, and can prevent distal positioning of an EPD with a "landing zone" sufficient for stent placement. These factors expose the patient to the risks of atheroembolism from the arch, air embolism, excessive contrast administration, bifurcation plaque disruption, and ICA dissection. Importantly, tortuosity should be assessed after the sheath (or guide catheter) has been placed in the CCA, because forces by the catheter directed toward the unyielding base of the cranium tend to exaggerate ICA tortuosity (Figure 3). Finally, heavy calcification is an important predictor of complications. This is defined as concentric calcification,
3 mm in width and deemed by at least 2 orthogonal views to be circumferentially situated around the lesion (Figure 4).
|
|
|
Heavy calcification, especially in combination with arterial tortuosity, causes difficulties in tracking devices, lesion dilation, stent positioning, and achieving adequate stent expansion. In our experience in more than 1500 cases, the presence of 2 or more of the risk factors listed in Table 2 is an important adverse prognosticator in patients undergoing carotid stenting. Although special techniques generally result in a satisfactory angiographic outcome, the risk of neurological adverse events exceeds the 3% rule and is thus prohibitive.
| Procedural Considerations |
|---|
|
|
|---|
Periprocedural Monitoring and Management
With respect to preprocedural therapy, adequately dosed dual-antiplatelet therapy is key. Patients must receive either a combination of clopidogrel 75 mg and aspirin 325 mg for 5 days before carotid stenting or, alternatively, loading doses of clopidogrel (600 mg) and aspirin (650 mg) at least 4 hours before the procedure. On the day of the procedure, oral antihypertensive therapy is withheld, and adequate volume status is ensured. Mild sedation may be offered to anxious patients, but for the vast majority, reassurance and adequate local anesthesia are all that is necessary. The avoidance of sedatives enhances neurological monitoring and limits hypotension. Continuous monitoring of pulse oximetry, intra-arterial pressure, and heart rhythm is essential, as is meticulous control of hemodynamics. Intravenous atropine (0.6 to 1.0 mg) should be administered after placement of the sheath in the CCA to suppress bradycardic responses to balloon inflation and stent implantation. Hypotension is invariably noted after balloon dilation of the stent, particularly in elderly patients with heavily calcified stenoses, and is generally benign. However, aggressive volume expansion, intravenous phenylephrine, and occasionally dopamine infusions are sometimes necessary. Blood pressure elevation after the relief of the stenosis can also occur and should be treated with intravenous nitroglycerine, nitroprusside, or labetalol. If distal protection is with an occlusion-aspiration system, blood pressure should be lowered before the occlusive balloon is deflated to prevent the potential consequences of hyperperfusion.52 Anticoagulation therapy with carotid stenting is vital, but it is equally important to note that modest anticoagulation levels should be targeted. Either heparin (70 IU/kg initial bolus, targeting an activated clotting time of 200 to 250 seconds) or bivalirudin (0.75 mg · kg1 bolus, followed by a maintenance infusion of 1.75 mg · kg1 · h1) is administered immediately with sheath insertion. Prolonged infusion of anticoagulant drugs is unnecessary, and these are stopped immediately after stent deployment. Glycoprotein IIb/IIIa antagonists are not routinely used.53
The use of 6F femoral sheaths and arteriotomy closure devices allows for early ambulation. This counteracts the bradycardia and hypotension commonly associated with carotid stenting. Postprocedural intensive care monitoring is unnecessary, although patients should be followed up in a monitored environment by staff familiar with the postprocedural course and with groin access site management. Remaining sheaths should be removed as early as possible, once the activated clotting time has fallen below 150 seconds. Hypotension should be treated aggressively, and causes unrelated to baroreceptor responses (eg, retroperitoneal hemorrhage) should be considered and managed promptly.
Procedural Stages
The extent of diagnostic angiography is determined by the anatomic information obtained by preprocedural noninvasive studies but should at the very least include an accurate evaluation of lesion severity, the carotid bifurcation, ipsilateral intracranial anatomy, and the anatomy of the CCA. If a balloon-occlusive EPD is to be used, it is mandatory to ensure adequate collateral flow from the contralateral carotid or posterior circulations. For diagnostic angiography, a double-curved 5F catheter (VTK, Cook Inc, Bloomington, Ind) and a 0.038-inch angled-tip hydrophilic coated wire are used.54 In >98% of patients, this system enables safe selective catheterization of the CCA, ICA, and external carotid artery (ECA), both subclavian arteries, and at least 1 vertebral artery. The same catheterization technique is used to introduce a 6F 90-cm sheath (Shuttle, Cook Inc) into the CCA, generally delivered over a soft-tipped, stiff, 0.035-inch guidewire (eg, Supracore, Guidant Inc, Indianapolis, Ind) positioned in the ECA. The tip of the sheath is positioned in the distal CCA. Guiding shots of the lesion immediately after sheath placement are performed, because ICA tortuosity might be more pronounced by the sheath (Figure 3). Next, the lesion is crossed with a 0.014-inch guidewire, usually that of the EPD. The EPD is deployed in a distal segment of the cervical ICA. Next, the lesion is dilated with an undersized coronary balloon ("predilation"). The stent is the deployed and subsequently "postdilated" with a conservatively sized, low-profile balloon. Finally, the EPD is removed, and final angiography is performed. With contemporary rapid-exchange ("monorail") systems, the entire process should take as little as 10 to 15 minutes.
Special Considerations
Catheter Placement
Modifications of the catheter placement technique may be required when the lesion is located in the distal segments of the CCA or if the ECA cannot be catheterized. In these cases, the tip of the 5F catheter and guidewire (Amplatz Super Stiff J-wire, MediTech, Natick, Mass) assembly over which the 6F sheath is placed in the CCA is kept below the lesion or bifurcation. In cases of significant aortic arch elongation or CCA tortuosity, inability to access the ECA might result in insufficient support for sheath placement. Placing guidewires and catheters at or across the lesion to provide adequate support markedly increases the risk of embolic complications.
Crossing the Lesion
Wiring the lesion and device delivery can be technically challenging. It is critical to minimize the number and volume of contrast injections into the brain, because this alone predisposes to neurological events. At times, because of extreme angulation at its takeoff, the ICA might not be amenable to wiring. In more complex and calcified lesions, a 7F sheath will provide superior support. At all times, the position of the sheath should be monitored to prevent its prolapse back into the arch. Appropriately shaped 5F catheters (125-cm right Judkins or internal mammary catheters) can be advanced through the guiding sheath so that the tip points into the ostium of the ICA, facilitating wire entry. The EPD must be placed at least
2 cm cephalad to the stenosis to accommodate the tip of the stent delivery system and to provide satisfactory coverage of the lesion. With heavy calcification, it can be technically difficult or even impossible to advance the EPD beyond the lesion. In these situations, placement of a second ("buddy") wire and gentle dilation of the lesion with an undersized balloon can facilitate delivery of the system. Anticipating this situation and having the necessary equipment available minimizes cerebral ischemia. Frequently used for this purpose are 0.014-inch coronary guidewires (eg, Balance, Guidant Inc, Santa Clara, Calif) through an over-the-wire low-profile angioplasty balloon (eg, Maverick, 2.0x40 mm, Boston Scientific, Natick, Mass). After inflation, the balloon catheter is used to exchange the wire for a more supportive type (eg, Stabilizer-Plus, Cordis Inc, Miami, Fla). This guidewire will usually straighten the ICA to permit delivery of the EPD beyond the lesion, although it might result in significant spasm that reduces flow (Figure 3). The tip of any wire used is placed close to the skull base, so the operator must ensure its control to avoid distal vessel trauma. Depending on the severity of ICA tortuosity, "buddy wires" can be removed after the protection device has been placed. Alternatively, the buddy wire can be withdrawn after the stent has been positioned, after stent deployment and postdilation ("jailed buddy wire"), or even after retrieval of the protection device. This can be important, because resistance to stent delivery might cause the sheath to prolapse into the arch, a problem that can be eliminated by the buddy wire.
Predilation
Lesion dilation before stenting is strongly recommended. Experimental work has shown that more debris is liberated from the lesion site when predilation is not performed,26 and clinical experience is concordant.36 Atheroembolism is increased when predilation is performed with large (0.035-inch compatible) balloons, so low-profile coronary balloons should be selected. When full deflation is ensured, these balloons "rewrap" well without residual winging, so that the risk of vessel-wall trauma during balloon withdrawal is reduced. If the lesion is preocclusive, it is preferable to gradually step up the balloon size to minimize plaque disruption and distal embolization. In these situations, predilation is first performed with a 2.0-mm balloon followed by a second inflation of a 3.5- to 4.0-mm balloon. In rare cases, mainly in heavily calcified lesions, a 5-mm balloon might be required to enable stent delivery. Long balloons (30 to 40 mm in length) are preferred to avoid a "watermelon seed" effect.
Stent Selection and Deployment
Self-expanding stents are routinely used because balloon-expandable stents are prone to deformation by external compression. The nominal diameter of the self-expanding stent chosen should be at least 1 to 2 mm larger than the largest diameter of the treated segment, usually the CCA, and 10-mm stents are used in almost all cases (oversizing the stent relative to the diameter of the ICA produces no adverse effects and provides effective trapping of plaque, thereby reducing the risk of embolization). Stent length should be adequate to cover the entire lesion, typically located at the origin or proximal segment of the ICA, such that it usually extends from the distal CCA to a healthy segment of the ICA, covering the origin of the ECA. For the vast majority of cases, a stent 30 mm in length by 10 mm in diameter will provide complete lesion coverage and facilitates facile, accurate placement with "road mapping" or bone landmarks. The use of contrast injections for stent positioning should be avoided, because embolic events from air trapping may occur.
Positioning the distal end of the stent in kinks and tortuosities of the ICA should be avoided. These tortuosities can rarely be eliminated and tend to be displaced distally and to be exaggerated by the stiff stent. Covering the origin of the ECA with the stent is not associated with adverse clinical consequences. Follow-up arteriograms have shown that the ECA remains patent with only few exceptions.
Postdilation
This is a critical step and requires careful attention, because it is at this stage that embolic events are most likely to develop. The risk of embolization is minimized by conservative sizing of the balloon (5 mm) and by performing a single inflation. The balloon should be deflated slowly. Mild residual stenoses (10% to 20%) or persistence of an ulcer at the lesion site should be accepted, because overzealous stent dilation driven by these findings can worsen embolization.
EPD Removal
Removal of balloon-occlusive EPDs is preceded by aspiration of 50 to 60 mL of blood with a dedicated catheter. Filter-based EPDs are removed with a dedicated retrieval catheter. Rarely, the filter can become obstructed by large amounts of embolic material, and blood flow in the ICA is interrupted. Facile technique and optimal antiplatelet therapy prevent this complication in most cases.
Final Angiographic Assessment
Careful attention must be paid to the segment of the ICA that contained the EPD. Occasionally (1% to 5% of cases), the embolic protection device can cause dissection in the ICA. The risk of this eventuality is greater with balloon-occlusive devices than with filter-based devices. It is not unusual to encounter spasm and kinks in the cephalad segment of the ICA, particularly in tortuous vessels. These are generally alleviated by guidewire removal and withdrawal of the guiding sheath to the proximal CCA. A small dose of intra-arterial nitroglycerine (100 to 200 µg) is occasionally needed. Stent-related distal edge dissections are rare.
Postdischarge Monitoring and Treatment
Patients are discharged with instructions to take clopidogrel (75 mg/d) for 1 month, except for patients treated for lesions related to prior neck irradiation, in whom clopidogrel treatment is extended to 1 year. In the absence of contraindications, aspirin (325 mg/d) is prescribed indefinitely. Patients should have a baseline ultrasound duplex study within 1 month after carotid stenting. This serves as a reference for later follow-up evaluations. Not infrequently, flow velocities within the stent are elevated despite documented good angiographic results. Evidence to date suggests that this finding neither predicts excessive progression of neointimal proliferation nor restenosis.55 Magnetic resonance angiography is not useful for follow-up purposes because of signal dropout due to the metallic stent. Computed tomographic angiography has shown some promise56 and may prove to be the modality of choice for follow-up after carotid stenting. Significant angiographic restenosis (>80%) is an uncommon finding, occurring in 3% to 6% of patients.1,36,57 Restenosis is more common in patients initially treated for radiation-induced or post-CEA lesions and can usually be managed by balloon dilation or repeated stenting.
| Conclusions |
|---|
|
|
|---|
| Acknowledgments |
|---|
Dr Roubin has served as a consultant to or on the advisory board of Abbot Vascular Devices and the Kensey Nash Corporation. Dr Iyer has served as a consultant to or on the advisory board of Abbot Vascular Devices and the Boston Scientific Corporation. Dr Brennan has served as a consultant to Abbot Vascular Devices.
| References |
|---|
|
|
|---|
2. Gray WA. The ARCHeR trials: final one year results. Presented at: Annual American College of Cardiology Scientific Sessions; March 7, 2004; New Orleans, La.
3. Withlow P. Registry study to evaluate the Neuroshield Bare-Wire Cerebral Protection System and X-Act Stent in patients at high risk for carotid endarterectomy (SECuRITY]). Presented at: Annual Transcatheter Therapeutics Scientific Sessions; September 17, 2003; Washington, DC.
4. Yadav JS, Wholey MH, Kuntz RE, Fayad P, Katzen BT, Mishkel GJ, Bajwa TK, Whitlow P, Strickman NE, Jaff MR, Popma JJ, Snead DB, Cutlip DE, Firth BG, Ouriel K; Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy Investigators. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med. 2004; 351: 14931501.
5. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995; 273: 14211428.
6. Halliday A, Mansfield A, Marro J, Peto C, Peto R, Potter J, Thomas D. Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial. Lancet. 2004; 363: 14911502.[CrossRef][Medline] [Order article via Infotrieve]
7. North 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: 445453.[Abstract]
8. Randomised trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet. 1998; 351: 13791387.[CrossRef][Medline] [Order article via Infotrieve]
9. Paciaroni M, Eliasziw M, Kappelle LJ, Finan JW, Ferguson GG, Barnett HJ. Medical complications associated with carotid endarterectomy: North American Symptomatic Carotid Endarterectomy Trial (NASCET). Stroke. 1999; 30: 17591763.
10. Ferguson GG, Eliasziw M, Barr HW, Clagett GP, Barnes RW, Wallace MC, Taylor DW, Haynes RB, Finan JW, Hachinski VC, Barnett HJ. The North American Symptomatic Carotid Endarterectomy Trial: surgical results in 1415 patients. Stroke. 1999; 30: 17511758.
11. Mathias K. A new catheter system for percutaneous transluminal angioplasty (PTA) of carotid artery stenoses [in German]. Fortschr Med. 1977; 95: 10071011.[Medline] [Order article via Infotrieve]
12. Mathias K, Mittermayer C, Ensinger H, Neff W. Percutaneous catheter dilatation of carotid stenoses: animal experiments [authors translation]. Rofo. 1980; 133: 258261.[Medline] [Order article via Infotrieve]
13. Belan A, Vesela M, Vanek I, Weiss K, Peregrin JH. Percutaneous transluminal angioplasty of fibromuscular dysplasia of the internal carotid artery. Cardiovasc Intervent Radiol. 1982; 5: 7981.[CrossRef][Medline] [Order article via Infotrieve]
14. Bockenheimer SA, Mathias K. Percutaneous transluminal angioplasty in arteriosclerotic internal carotid artery stenosis. AJNR Am J Neuroradiol. 1983; 4: 791792.[Abstract]
15. Hasso AN, Bird CR, Zinke DE, Thompson JR. Fibromuscular dysplasia of the internal carotid artery: percutaneous transluminal angioplasty. AJR Am J Roentgenol. 1981; 136: 955960.
16. Wiggli U, Gratzl O. Transluminal angioplasty of stenotic carotid arteries: case reports and protocol. AJNR Am J Neuroradiol. 1983; 4: 793795.[Abstract]
17. Tsai FY, Matovich V, Hieshima G, Shah DC, Mehringer CM, Tiu G, Higashida R, Pribram HF. Percutaneous transluminal angioplasty of the carotid artery. AJNR Am J Neuroradiol. 1986; 7: 349358.[Abstract]
18. Roubin GS, Yadav S, Iyer SS, Vitek J. Carotid stent-supported angioplasty: a neurovascular intervention to prevent stroke. Am J Cardiol. 1996; 78: 812.[Medline] [Order article via Infotrieve]
19. Diethrich EB, Ndiaye M, Reid DB. Stenting in the carotid artery: initial experience in 110 patients. J Endovasc Surg. 1996; 3: 4262.[CrossRef][Medline] [Order article via Infotrieve]
20. Vitek JJ, Raymon BC, Oh SJ. Innominate artery angioplasty. AJNR Am J Neuroradiol. 1984; 5: 113114.[Medline] [Order article via Infotrieve]
21. 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: 869874.[Medline] [Order article via Infotrieve]
22. Henry M, Amor M, Henry I, Klonaris C, Chati Z, Masson I, Kownator S, Luizy F, Hugel M. Carotid stenting with cerebral protection: first clinical experience using the PercuSurge GuardWire system. J Endovasc Surg. 1999; 6: 321331.[CrossRef][Medline] [Order article via Infotrieve]
23. Ohki T, Veith FJ. Critical analysis of distal protection devices. Semin Vasc Surg. 2003; 16: 317325.[CrossRef][Medline] [Order article via Infotrieve]
24. Parodi JC, La Mura R, Ferreira LM, Mendez MV, Cersosimo H, Schonholz C, Garelli G. Initial evaluation of carotid angioplasty and stenting with three different cerebral protection devices. J Vasc Surg. 2000; 32: 11271136.[CrossRef][Medline] [Order article via Infotrieve]
25. Reimers B, Corvaja N, Moshiri S, Sacca S, Albiero R, Di Mario C, Pascotto P, Colombo A. Cerebral protection with filter devices during carotid artery stenting. Circulation. 2001; 104: 1215.
26. Ohki T, Marin ML, Lyon RT, Berdejo GL, 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: 463471.[CrossRef][Medline] [Order article via Infotrieve]
27. Jaeger H, Mathias K, Drescher R, Hauth E, Bockisch G, Demirel E, Gissler HM. Clinical results of cerebral protection with a filter device during stent implantation of the carotid artery. Cardiovasc Intervent Radiol. 2001; 24: 249256.[CrossRef][Medline] [Order article via Infotrieve]
28. Al-Mubarak N, Roubin GS, Vitek JJ, Iyer SS, New G, Leon MB. Effect of the distal-balloon protection system on microembolization during carotid stenting. Circulation. 2001; 104: 19992002.
29. Guimaraens L, Sola MT, Matali A, Arbelaez A, Delgado M, Soler L, Balaguer E, Castellanos C, Ibanez J, Miquel L, Theron J. Carotid angioplasty with cerebral protection and stenting: report of 164 patients (194 carotid percutaneous transluminal angioplasties). Cerebrovasc Dis. 2002; 13: 114119.[CrossRef][Medline] [Order article via Infotrieve]
30. Cremonesi A, Manetti R, Setacci F, Setacci C, Castriota F. Protected carotid stenting: clinical advantages and complications of embolic protection devices in 442 consecutive patients. Stroke. 2003; 34: 19361941.
31. Mas JL, Chatellier G, Beyssen B. Carotid angioplasty and stenting with and without cerebral protection: clinical alert from the Endarterectomy Versus Angioplasty in Patients With Symptomatic Severe Carotid Stenosis (EVA-3S) trial. Stroke. 2004; 35: e18e20.[CrossRef][Medline] [Order article via Infotrieve]
32. Weisz G. Distal protection devices improve the safety of carotid artery stenting. analysis of over 1350 procedures. Circulation. 2003; 108 (suppl IV): IV-605. Abstract.
33. Zahn R, Mark B, Niedermaier N, Zeymer U, Limbourg P, Ischinger T, Haerten K, Hauptmann KE, Leitner ER, Kasper W, Tebbe U, Senges J. Embolic protection devices for carotid artery stenting: better results than stenting without protection? Eur Heart J. 2004; 25: 15501558.
34. Kastrup A, Groschel K, Krapf H, Brehm BR, Dichgans J, Schulz JB. Early outcome of carotid angioplasty and stenting with and without cerebral protection devices: a systematic review of the literature. Stroke. 2003; 34: 813819.
35. Gray WA, White HJ Jr, Barrett DM, Chandran G, Turner R, Reisman M. Carotid stenting and endarterectomy: a clinical and cost comparison of revascularization strategies. Stroke. 2002; 33: 10631070.
36. Bosiers M, Peeters P, Deloose K, Verbist J, Sievert H, Sugita J, Castriota F, Cremonesi A. Does carotid artery stenting work on the long run: 5-year results in high-volume centers (ELOCAS Registry). J Cardiovasc Surg (Torino). 2005; 46: 241247.[Medline] [Order article via Infotrieve]
37. Goldstein LB, Adams R, Becker K, Furberg CD, Gorelick PB, Hademenos G, Hill M, Howard G, Howard VJ, Jacobs B, Levine SR, Mosca L, Sacco RL, Sherman DG, Wolf PA, del Zoppo GJ. Primary prevention of ischemic stroke: a statement for healthcare professionals from the Stroke Council of the American Heart Association. Circulation. 2001; 103: 163182.
38. Biller J, Feinberg WM, Castaldo JE, Whittemore AD, Harbaugh RE, Dempsey RJ, Caplan LR, Kresowik TF, Matchar DB, Toole J, Easton JD, Adams HP Jr, Brass LM, Hobson RW II, Brott TG, Sternau L. Guidelines for carotid endarterectomy: a statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke. 1998; 29: 554562.
39. Albers GW, Hart RG, Lutsep HL, Newell DW, Sacco RL. AHA Scientific Statement: supplement to the guidelines for the management of transient ischemic attacks: a statement from the Ad Hoc Committee on Guidelines for the Management of Transient Ischemic Attacks, Stroke Council, American Heart Association. Stroke. 1999; 30: 25022511.
40. Barnett HJ, Taylor DW, Eliasziw M, Fox AJ, Ferguson GG, Haynes RB, Rankin RN, Clagett GP, Hachinski VC, Sackett DL, Thorpe KE, Meldrum HE, Spence JD; North American Symptomatic Carotid Endarterectomy Trial Collaborators. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med. 1998; 339: 14151425.
41. The European Carotid Surgery Trialists Collaborative Group. Risk of stroke in the distribution of an asymptomatic carotid artery. Lancet. 1995; 345: 209212.[Medline] [Order article via Infotrieve]
42. Mathur A, Roubin GS, Iyer SS, Piamsonboon C, Liu MW, Gomez CR, Yadav JS, Chastain HD, Fox LM, Dean LS, Vitek JJ. Predictors of stroke complicating carotid artery stenting. Circulation. 1998; 97: 12391245.
43. Eliasziw M, Smith RF, Singh N, Holdsworth DW, Fox AJ, Barnett HJ; North American Symptomatic Carotid Endarterectomy Trial (NASCET) Group. Further comments on the measurement of carotid stenosis from angiograms. Stroke. 1994; 25: 24452449.[Abstract]
44. Rothwell PM, Gutnikov SA, Warlow CP. Reanalysis of the final results of the European Carotid Surgery Trial. Stroke. 2003; 34: 514523.
45. Wholey MH, Wholey M, Mathias K, Roubin GS, Diethrich EB, Henry M, Bailey S, Bergeron P, Dorros G, Eles G, Gaines P, Gomez CR, Gray B, Guimaraens J, Higashida R, Ho DS, Katzen B, Kambara A, Kumar V, Laborde JC, Leon M, Lim M, Londero H, Mesa J, Musacchio A, Myla S, Ramee S, Rodriquez A, Rosenfield K, Sakai N, Shawl F, Sievert H, Teitelbaum G, Theron JG, Vaclav P, Vozzi C, Yadav JS, Yoshimura SI. Global experience in cervical carotid artery stent placement. Catheter Cardiovasc Interv. 2000; 50: 160167.[CrossRef][Medline] [Order article via Infotrieve]
46. Pujia A, Rubba P, Spencer MP. Prevalence of extracranial carotid artery disease detectable by echo-Doppler in an elderly population. Stroke. 1992; 23: 818822.
47. Ellis MR, Franks PJ, Cuming R, Powell JT, Greenhalgh RM. Prevalence, progression and natural history of asymptomatic carotid stenosis: is there a place for carotid endarterectomy? Eur J Vasc Surg. 1992; 6: 172177.[CrossRef][Medline] [Order article via Infotrieve]
48. Baker WH, Howard VJ, Howard G, Toole JF; ACAS Investigators. Effect of contralateral occlusion on long-term efficacy of endarterectomy in the asymptomatic carotid atherosclerosis study (ACAS). Stroke. 2000; 31: 23302334.
49. Paciaroni M, Caso V, Acciarresi M, Baumgartner RW, Agnelli G. Management of asymptomatic carotid stenosis in patients undergoing general and vascular surgical procedures. J Neurol Neurosurg Psychiatry. 2005; 76: 13321336.
50. Hobson RW II, Howard VJ, Roubin GS, Brott TG, Ferguson RD, Popma JJ, Graham DL, Howard G. Carotid artery stenting is associated with increased complications in octogenarians: 30-day stroke and death rates in the CREST lead-in phase. J Vasc Surg. 2004; 40: 11061111.[CrossRef][Medline] [Order article via Infotrieve]
51. Vitek JJ, Roubin GS, Al-Mubarek N, New G, Iyer SS. Carotid artery stenting: technical considerations. AJNR Am J Neuroradiol. 2000; 21: 17361743.
52. Coutts SB, Hill MD, Hu WY. Hyperperfusion syndrome: toward a stricter definition. Neurosurgery. 2003; 53: 10531058.[CrossRef][Medline] [Order article via Infotrieve]
53. Chan AW, Yadav JS, Bhatt DL, Bajzer CT, Gum PA, Roffi M, Cho L, Agah R, Topol EJ. Comparison of the safety and efficacy of emboli prevention devices versus platelet glycoprotein IIb/IIIa inhibition during carotid stenting. Am J Cardiol. 2005; 95: 791795.[Medline] [Order article via Infotrieve]
54. Vitek JJ. Femoro-cerebral angiography: analysis of 2,000 consecutive examinations, special emphasis on carotid arteries catheterization in older patients. Am J Roentgenol Radium Ther Nucl Med. 1973; 118: 633647.[Medline] [Order article via Infotrieve]
55. Roffi M, Chan A, Yadav J. Can ultrasound accurately predict restenosis after carotid artery stenting? Circulation. 2001; 104 (suppl II): II-583. Abstract.
56. Leclerc X, Gauvrit JY, Pruvo JP. Usefulness of CT angiography with volume rendering after carotid angioplasty and stenting. AJR Am J Roentgenol. 2000; 174: 820822.
57. Bergeron P, Roux M, Khanoyan P, Douillez V, Bras J, Gay J. Long-term results of carotid stenting are competitive with surgery. J Vasc Surg. 2005; 41: 213221.[CrossRef][Medline] [Order article via Infotrieve]
This article has been cited by other articles:
![]() |
P. T.L. Chiam, G. S. Roubin, G. Panagopoulos, S. S. Iyer, R. M. Green, C. Brennan, and J. J. Vitek One-Year Clinical Outcomes, Midterm Survival, and Predictors of Mortality After Carotid Stenting in Elderly Patients Circulation, May 5, 2009; 119(17): 2343 - 2348. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Macdonald, R. Lee, R. Williams, G. Stansby, and on behalf of the Delphi Carotid Stenting Consensus Towards Safer Carotid Artery Stenting: A Scoring System for Anatomic Suitability Stroke, May 1, 2009; 40(5): 1698 - 1703. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Skjelland, K. Krohg-Sorensen, B. Tennoe, S. J. Bakke, R. Brucher, and D. Russell Cerebral Microemboli and Brain Injury During Carotid Artery Endarterectomy and Stenting Stroke, January 1, 2009; 40(1): 230 - 234. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. J. White, J. A. Beckman, R. P. Cambria, A. J. Comerota, W. A. Gray, R. W. Hobson II, S. S. Iyer, and for Writing Group 5 Atherosclerotic Peripheral Vascular Disease Symposium II: Controversies in Carotid Artery Revascularization Circulation, December 16, 2008; 118(25): 2852 - 2859. [Full Text] [PDF] |
||||
![]() |
M. Tsutsumi, H. Aikawa, M. Onizuka, M. Iko, T. Kodama, K. Nii, S. Hamaguchi, H. Etou, K. Sakamoto, and K. Kazekawa Carotid Artery Stenting for Calcified Lesions AJNR Am. J. Neuroradiol., September 1, 2008; 29(8): 1590 - 1593. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. K. Eskandari Preventable Complications of Carotid Stenting Perspectives in Vascular Surgery and Endovascular Therapy, March 1, 2008; 20(1): 17 - 25. [Abstract] [PDF] |
||||
![]() |
S. S. Iyer, C. J. White, L. N. Hopkins, B. T. Katzen, R. Safian, M. H. Wholey, W. A. Gray, R. Ciocca, W. B. Bachinsky, G. Ansel, et al. Carotid artery revascularization in high-surgical-risk patients using the Carotid WALLSTENT and FilterWire EX/EZ: 1-year outcomes in the BEACH Pivotal Group. J. Am. Coll. Cardiol., January 29, 2008; 51(4): 427 - 434. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. S. Gurm, B. K. Nallamothu, and J. Yadav Safety of carotid artery stenting for symptomatic carotid artery disease: a meta-analysis Eur. Heart J., January 1, 2008; 29(1): 113 - 119. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. K. Veeraswamy, B. G. Rubin, L. A. Sanchez, M. A. Curi, P. J Geraghty, J. C. Parodi, and G. A. Sicard Complications of Carotid Artery Stenting Are Largely Preventable: A Retrospective Error Analysis Perspectives in Vascular Surgery and Endovascular Therapy, December 1, 2007; 19(4): 403 - 408. [Abstract] [PDF] |
||||
![]() |
J. Van der Heyden, M. J. Suttorp, E. T. Bal, J. M. Ernst, R. G. Ackerstaff, J. Schaap, J. C. Kelder, M. Schepens, and H. W. Plokker Staged Carotid Angioplasty and Stenting Followed by Cardiac Surgery in Patients With Severe Asymptomatic Carotid Artery Stenosis: Early and Long-Term Results Circulation, October 30, 2007; 116(18): 2036 - 2042. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. A. Abbruzzese and R. P. Cambria Contemporary Management of Carotid Stenosis: Carotid Endarterectomy Is Here to Stay Perspectives in Vascular Surgery and Endovascular Therapy, September 1, 2007; 19(3): 248 - 256. [Abstract] [PDF] |
||||
![]() |
J. M. U-King-Im, M. J. Graves, J. J. Cross, N. J. Higgins, J. Wat, R. A. Trivedi, T. Tang, S. P. S. Howarth, P. J. Kirkpatrick, N. M. Antoun, et al. Internal Carotid Artery Stenosis: Accuracy of Subjective Visual Impression for Evaluation with Digital Subtraction Angiography and Contrast-enhanced MR Angiography Radiology, July 1, 2007; 244(1): 213 - 222. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. R. Bates, C. J. D. Babb, D. E. Casey, C. U. Cates, G. R. Duckwiler, T. E. Feldman, W. A. Gray, K. Ouriel, E. D. Peterson, K. Rosenfield, et al. ACCF/SCAI/SVMB/SIR/ASITN 2007 Clinical Expert Consensus Document on Carotid Stenting: A Report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents (ACCF/SCAI/SVMB/SIR/ASITN Clinical Expert Consensus Document Committee on Carotid Stenting) Vascular Medicine, February 1, 2007; 12(1): 35 - 83. [PDF] |
||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2006 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |