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The Supraaortic and Vertebral Endovascular Interventions
The Supraaortic and Vertebral Endovascular Interventions Mark H. Wholey, MD,* and Michael H. Wholey, MD, MBA†
W
ith few exceptions, most of the occlusive disease involving the great vessels off the aortic arch is no longer considered a surgical disease. For example, both the right and the left subclavian arteries, the left common carotid origin, the innominate origin, and the proximal divisions of the right and left vertebral arteries are all quite amenable to endovascular stenting. There are however exceptions and these may occur when either aneurysmal disease, sepsis, trauma, or total occlusions that may not be amendable to recanalization by endovascular techniques are present. The causes of stenotic lesions in these vessels are similar to other vessels, where the majority is caused by atherosclerotic disease, although other causes such as dissection, fibromuscular disease (FMD), and various vasculitidies are not infrequent. The majority of the supraaortic atherosclerotic occlusive lesions involves the left subclavian artery.1 Such disease results in a “subclavian steal,” which was first described in 1961 by Reivich and coworkers.2,3 By occluding the left subclavian artery, arterial flow is provided by the right subclavian artery with flow into the right vertebral artery and then retrograde flow into the left vertebral artery and subsequently into left subclavian artery. Additional collaterals also include the external carotid, the ascending cervical artery, and the thyrocervical trunk. Though present, the number of patients who become symptomatic are relatively uncommon; in a study of 1114 patients with disease involving the innominate and subclavian arteries, only 168 (15%) demonstrated signs and symptoms of subclavian stenosis.4 In Perler and Williams’ study of 6534 patients, only 17% were noted to have stenosis of 30% or more.5 Of these patients, only 24% had clinical and angiographic evidence of subclavian steal.5 The progression of the disease is also limited. Only 17% of 67 patients in Ackerman and coworkers study had progression of disease in 2 years.6 Only 4 of 55 asymptomatic patients developed vertebrobasilar symptoms in 4-year follow-up.6 The diagnosis of subclavian steal is based on having upper *Pittsburgh Vascular Institute, UPMC Presbyterian Shadyside, Pittsburgh, PA. †Department of Cardiovascular Interventional Radiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas. Address reprint requests to Mark H. Wholey, MD, Pittsburgh Vascular Institute, 5230 Centre Avenue, Pittsburgh, PA 15232. E-mail: [email protected].
1089-2516/05/$-see front matter © 2005 Elsevier Inc. All rights reserved. doi:10.1053/j.tvir.2005.02.007
extremity ischemia where a pressure gradient of 20 mm Hg is noted and symptoms of arm claudication, paresis, and atheroembolic digital ischemia are seen. Less commonly, there is vertebrobasilar insufficiency, which includes symptoms of ataxia, diploplia, syncope, vertigo, dizziness, nausea, and vomiting. Another syndrome, which has been increasing in frequency, includes coronary steal syndrome in which a stenosis proximal to internal mammary-coronary artery bypass may cause ischemic symptoms. The growing use of the left internal mammary artery (LIMA) for coronary bypass procedures has resulted in greater surveillance and treatment of the left subclavian artery (Fig. 1A-D). Though debatable, highgrade, proximal subclavian arterial stenoses in relatively asymptomatic patients are now considered appropriate therapy to maintain the capacity to use the LIMA. Similarly, there is the increased need to maintain subclavian patency for patients undergoing or expecting possible hemodialysis. Subclavian stenosis is frequently seen as a cause for failed hemodialysis fistulas. Doppler examinations of the brachiocephalic arteries usually confirm the diagnosis of subclavian steal by showing retrograde flow of the ipsilateral vertebral artery. MRA is increasingly being used to diagnose subclavian artery stenoses, although angiography has traditionally been the gold standard. Innominate artery stenosis is relatively uncommon. When the atherosclerotic disease involves the innominate artery, the symptoms may be more severe and include cerebral symptoms. The occlusion in the innominate artery causes retrograde flow from the vertebral and into the right common carotid and the right subclavian artery. Symptoms generally include vertebrobasilar insufficiency with ataxia, diploplia, syncope, vertigo, dizziness, nausea, and/or vomiting. It may also include upper extremity ischemia and atheroembolic digital ischemia. Indications to treat vertebral artery origin lesions include symptoms of vertebrobasilar insufficiency and more related to simple flow related stenoses, as opposed to embolic events.7 Vertebrobasilar symptoms may be related to head or neck position or the more classic patterns related to blood pressure and orthostatic factors.
Treatment The treatment modalities for occlusive disease involving subclavian, left common carotid, or innominate arteries has been 215
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Figure 1 (A) High-grade subclavian stenosis with significant decrease antegrade flow through LIMA. (B) Radionuclide study demonstrating reversible septal ischemia in the stress and resting phase study. (C) Following effective stenting of left subclavian and restoration of antegrade flow through LIMA. (D) Radionuclide stress examination postsubclavian stenting demonstrating no further septal ischemia following restoration of LIMA.
surgery, endovascular treatment, or medical therapy. Surgical options include endarterectomy or more common, bypass procedures. There has been a long history of subclavian bypass procedures; Parot and coworkers introduced carotidsubclavian transposition in 1964.8 Diethrich and coworkers introduced carotid subclavian bypass in 1967 reporting relief of 93% in 125 patients with operative mortality of 4.8%.9 The patency of such surgical procedures has been good with 5-year patency of 90% for surgical bypasses and 96% patency for transpositions.9 However, it is very invasive with its share of surgical morbidity and mortality. Direct carotid to ipsilateral artery bypass and transposition has been reported to have ⬍5% morbidity and ⬍2% mortality.10 Whether surgical or endovascular treatment, patient’s prognosis remains good. Because of the dramatic symptoms of upper extremity ischemia or cerebral ischemia, patients seek medical attention rather quickly. As a result, patients tend to have focal lesions in large vessels relatively early in
disease progression, so long-term results are good. There is generally excellent relief of ischemic symptoms. However, there are poor results (only 20%) of improving dizziness. Today, angioplasty and stent placement in the treatment of proximal arch vessel lesions is considered the treatment of choice by most interventionists.11 Dotter and Judkins have performed endovascular treatment of lesions involving the great vessels off the aortic arch since the original description in 1964.12 Early interventionalists have angioplastied lesions arising from the innominate, right subclavian, left common carotid, and left subclavian arteries. Angioplasty performed before 1989 alone on short stenotic lesions had a good technical success rate, high complication rate, and marginal primary patency. As Table 1 shows, early interventional radiologists had a technical success of 92%, complication rate of 5% with 1% CNS problems, and a restenosis rate of 19% at 2 years.12 With the advent of lower profile balloon catheters (from 7 to 5 French) and improved wire technology, compli-
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Table 1 Early Angioplasty (Prior to 1989) Results of Subclavian Artery Stenoses Author
Patients
Technical Success
Restenosis Rate
Complication Rate
Follow-up
Wholey/Erbstein Wilm’s et al
24 23
88% 91%
16% (4/24) 13% (3/23)
4% (1/24) 4% (1/23)
18-26 mos 25 mos
cation rates improved to 0 to 2%, but still restenosis remained high with rates of 4 to 22%. With the advent of stent technology, occlusive disease and long stenoses could now be treated successfully and the primary patency rates could be improved. The traditional indications for endovascular stent placement included suboptimal angioplasty results, recurrent or ⬎30% residual stenosis, gradient ⬎10 mm Hg, thromboemboli, or late restenosis after angioplasty. Because of superior patency results, however, almost all lesions are stented (refer to Table 2). Restenosis rates have been reduced to 0 to 18% for 2- to 4-year followups. Surprisingly, the neurologic complication rate of subclavian stent placement has been low. This may be due to the retrograde vertebral artery flow. Following angioplasty and stent placement, the vertebral artery retrograde flow does not reverse until 20 seconds to 4 minutes.13 With the advent of embolic protection filters and systems, complications should decrease further. The treatment of innominate artery stenosis is similar to that of subclavian stenoses except that extra attention must be made not to compress the nearby right common carotid artery. The treatment of the left common carotid artery is also similar to the subclavian technique, although great care must be taken to avoid disastrous neurocomplications.
Technique of Supraaortic Stenting Approach Deciding on which approach to employ is one of the first major decisions. It will dictate which type of sheaths, wires, and stents to be deployed. We generally prefer to come from the common femoral route because of long-term experience and because of the lower risk of hematoma complications that can occur from brachial approaches. Brachial approach is preferred in many subclavian and innominate artery occlusions, especially in those lesions lacking a characteristic nipple in the proximal segment of the artery. We will also use this approach when the takeoff of the subclavian or innominate artery is at such a steep angle to the aorta that traditional femoral access is foreboding (Fig. 2A, B). Also, if severe aor-
toiliac disease is present, we will naturally choose the brachial approach. When selected, we prefer the low brachial approach near the olecranon fossa because of the difficulty in holding pressure to brachial in the upper arm. We almost never use the axillary approach because of the brachial plexus injury that can result from an expanding hematoma. On occasion when there is combined internal carotid artery stenosis and left common carotid stenosis, we may consider endarterectomy followed by retrograde positioning of the common carotid stent.
Technique Left Subclavian Stenoses For subclavian artery lesions, we will select the targeted vessel with a 5-French diagnostic catheter either separately or through a long 6-French vascular sheath, or an 8-French guide catheter. Once arterial access is obtained, we will anticoagulate with either Heparin or initiate bivilarubin (weightrelated dosage). A LAO projection with the pigtail catheter in the aortic arch is first performed. Under roadmapping and under the best image angle, we will cross the lesion carefully. With the guidewire past the lesion, we then advance the guide just proximal to the lesion. We will predilate lesions that are severely diseased and pose a risk of stripping or impeding the passage of our balloon-mounted stents. Predilatation helps to reduce the risk of stent migration as well as allowing for a quick reference as to the vessel size and lesion length. We will recheck the images to see important vessel takeoffs as well as to assess possible dissections. For ostial lesions, we will occasionally use an RAO view to see the origin well. Rarely do we advance the sheath or guide over and past the lesion. If the sheath should go past the lesion, we will let the sheath backbleed before advancement of the balloonmounted stent. We will then advance the balloon-mounted stent to the lesion, being certain that important vessels such as the internal mammary and the vertebral arteries are not compromised. If the vertebral is at risk, we will leave a 0.014” guidewire as a safety wire in the vertebral artery during subclavian stenting. We then hold the balloon carefully because
Table 2 Endovascular Subclavian Stent Results Author
Patients
Tech Success
Restenosis Rate
Cx
Follow-up
Henry ’99 Sullivan ’98 Sueoka ’96 Kumar ’95
46 66 7 27
91% 94% 100% 100%
16% 15% 0 0
3% 17% 0 11%‡
4 years* 36 mos† 12 mos
*J Endovasc. Surg 1999, 6:33-41. †J Vasc Surg. 1998;28(6):1059-65. ‡Two brachial art. injury, one stent displacement.
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M.H. Wholey and M.H. Wholey protection device. At the present time the only available distal embolic protection devices available are the PercuSurge balloon (guidewire), the Boston Scientific EPI Filter wire (Natick, MA), and the Guidant Accunet. All are off-label indications for those applications. Left Subclavian Occlusions Gaining access through left subclavian total occlusions is somewhat more difficult and may require both a femoral and a brachial approach to get access. We will generally start from the femoral route and with manipulations of a diagnostic catheter, such as a headhunter or vertebral-shaped catheter, and with a torquable guidewire (regular or stiff Glidewire or Wholey 0.035” guidewire), we will get through most lesions (Fig. 4A-C). Attention must be made, especially with the stiff glide wire, not to dissect or perforate the subclavian artery. Also, care must be made with the wire crossing the subclavian artery ostium, to be gentle with wire manipulations for fear that the wire will dissect across the ostium with manipulations. Once across the lesion, predilation and balloon-mounted
Figure 2 (A, B) Total occlusion of the innominate artery. Recanalization with balloon-expandable stent resulting in no residual stenosis and improvement in antegrade flow through the right common carotid as well as the right subclavian and right vertebral.
of the aortic arch pulsations and deploy the stent quickly to approximately 8 atm. We will then perform a poststenting angiogram and assess the stent apposition to the vessel diameter. The origin of the subclavian artery maybe fragile, so we are cautious not to overdilate for fear of dissection. When dissection occurs during stent deployment, it may require an additional overlapping stent. If possible, it is best not to cover either the vertebral or the internal mammary artery. If this is necessary, it is fortunate that the stent cell size allows adequate flow and rarely results in junctional occlusion (Fig. 3A, B). Frequently with a high-grade lesion in the subclavian artery, we will protect the vertebral artery with an embolic
Figure 3 (A) Subclavian stenosis with stenting in a diabetic patient that resulted in edge dissection just proximal to the origin of the internal mammary. (B) Precise positioning of a stent at the dissection site resulted in improved flow with correction of the dissection. Note the internal mammary is preserved along with the left vertebral artery.
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Figure 4 (A) Total occlusion of the left subclavian artery with visible retrograde flow from the left vertebral to reconstitute the subclavian. (B) Dynamic study showing the shunt reversal from the right vertebral to the left vertebral. (C) Reestablishment of antegrade flow in the vertebral and the subclavian following effective stenting of the totally occluded segment.
stent placement proceeds similar to stenotic lesions. Caution, however, is also recommended in the initial dilation of those patients with total occlusion. Frequently the rigid dystrophic calcification results in excessive dissection and occasionally a false aneurysm. For these reasons in total occlusions, it is best to initially underdilate after establishing a minimal lumen and subsequently positioning a balloon expandable stent. In
the event a false aneurysm does develop, it may then be necessary to position a covered stent at that site. Distal Subclavian/Axillary Lesions We are encountering more patients, especially those on hemodialysis, who present with mid and distal subclavian stenosis. We frequently discuss these cases with our vascular
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surgery colleagues for possible surgical options on a case-bycase basis. When we intervene, we will generally prefer to angioplasty alone those lesions at crucial areas such as between the first rib and clavicle as well as at the subclavian/ axillary junction where there is bending and compression. When the lesion does not respond to angioplasty, we will use self-expanding stents such as Wallstents and the nitinol stents. We will oversize the stent 1 to 2 mm greater than the vessel diameter. Through a long 8-French guide, we will deliver and deploy the stent. During deployment, care must be taken to watch the proximal end of the stent, which has a tendency to jump or shrink further distally than planned. Maintain gentle posterior pressure when deploying self-expanding stents. Left Common Carotid Stenoses For left common carotid artery lesions, we will use guiding catheters (usually 8 French) for positioning at the vessel ostium. We will use 0.035” wires with torquability and support to cross the lesion. If the vessel comes off the aorta at a steep angle or is a bovine arch, you may need to take the guidewire farther up into the common carotid or even the external carotid for needed support. We have on occasion used embolic protection devices for these lesions for preventing embolic complications. Like subclavian lesions, we will predilate severe lesions to allow for easy advancement of the balloon-mounted stent. When ready and properly visualized, we will deploy the stent. Again, aortic arch pulsations could lead to errors in placement. Ideally, we like to have the edge of the stent extend approximately 1 mm into the aorta for ostial lesions. Innominate Artery Lesions For innominate artery lesions, technique is similar to that of stenting the left subclavian and the left common carotid artery. Attention must be given to the bifurcation of the right common carotid and the right subclavian arteries. Even if the subclavian is mildly stenotic, the stent in the right common carotid could result in a significant lesion of the unaffected subclavian (Fig. 5A, B). Kissing stents may then be required. Innominate and right subclavian lesions are frequently managed from the brachial approach.
Decision of Which Stent For lesions involving the proximal segments of the left subclavian, left common carotid, and especially the innominate artery, we use a balloon-mounted stent. The chance for compression and deformation of the stent is low. Self-expandable stents are not chosen because of the inability to be exactly precise in a region where millimeters count. Furthermore, there is the possibility of stent migration with the self-expandable stents. We will use self-expandable stents for lesions in the mid subclavian in or near the region of the clavicle and first rib or where the stent is externally exposed to compression. We measure the lesion and a normal arterial segment to determine stent length and diameter. We will use QCA from the angiographic images to determine vessel size and lesion length. The predilatation balloon catheter provides a quick reference point in terms of lesion length and also vessel diameter. Never place a balloon-mounted stent
Figure 5 (A) Total occlusion of the innominate with no visible antegrade flow in either the carotid or the right subclavian artery. (B) Six-months post follow-up examination demonstrating the innominate to be widely patent with excellent flow in the subclavian and vertebral as well as the right common carotid. Note the intimal hyperplasia that exists in the 6-month follow-up but does not compromise innominate artery dimensions.
larger than the normal vessel diameter. As a matter of fact, in total occlusions we will purposely slightly undersize.
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Figure 6 (A) High-grade stenotic lesion of the proximal right vertebral. (B) Balloon-expandable stent positioned just at the ostium at the target lesion site and restoring the right vertebral to basically normal dimensions. Note distal protection device in the right vertebral.
Decision of Which Guidewire Guidewire selection depends on the approach, lesion characteristics, and type of stent chosen and availability of equipment. For most proximal subclavian stenoses, coming from the femoral route, a 0.035” torquable guidewire is sufficient. A Glidewire (Terumo, Boston Scientific) may also be used for crossing. Five-French-long balloon catheters can course through most 6-French-long vascular sheaths or 8-French guiding catheters. For more diseased subclavian arteries and for those requiring a brachial approach, we may generally use 0.014” guidewires and 6-French sheaths.
Decision of Guiding Catheter versus Sheath Whether you chose a guiding catheter or sheath, it is important never to compromise your ability to inject contrast to visualize the lesion in relation to the balloon catheter. Likewise, it is essential to obtain the best angle to see the takeoff of the vessel in relation to the aorta. It is also crucial to have the best angle to visualize the takeoff of key vessels (vertebral, common carotid, or internal mammary arteries). Because of respiration, roadmap images are not often helpful. Another feature to be aware of is dramatic aortic pulsations
when deploying a stent. If there is a large gap in diastolic and systolic blood pressures, there can be an excess of pulsations of the vessels. These pulsations can cause large motions (1 cm or more) in the position of the lesion relative to the balloon catheter or self-expanding stent when trying to deploy. Blood pressure control is essential in these patients as well as the need for slightly longer stents. For subclavian and innominate artery lesions, we prefer to use a long 8-French guide or 6-French sheath. For left common carotid lesions, where support against the aortic wall is important, we prefer guiding catheters. When coming from a brachial approach, we use as small a sheath as possible; we generally use a long 6-French sheath. Sheath and guide catheter sizes are also dependent on stent selection. Generally, we will use a stent mounted on a 7- to 8-mm balloon catheter, which can be advanced through an 8-French guide. Larger stent sizes, those mounted on 9- to 10-mm balloon catheters, may require larger sheaths.
Proximal Vertebral Artery Stent Placement The proximal vertebral vessels are also considered a part of the brachial cephalic group and in fact the anomalous origin of the left vertebral from the aortic arch occurs in 5 to 10% of
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Figure 7 (A) High-grade stenosis in the proximal basilar artery in a patient with symptomatic basilar artery insufficiency being managed medically. (B) Total occlusion of the basilar artery at its origin with failed anticoagulation therapy. Note patency of the posterior inferior cerebella artery. (C) 3.5 mm over 014 wire at the target lesion site in the basilar artery. (D) Postdilation demonstrates normal dimensions of the basilar artery at the target lesion site with restoration of flow in both posterior cerebrals and in the left superior cerebellar. The right superior cerebella remains occluded. (E) Tenmonth follow-up examination demonstrating patency of the basilar artery with satisfactory posterior inferior cerebellar and superior cerebellar flow but with 50% restenosis that did not warrant additional adjunctive angioplasty considering the patient was essentially asymptomatic.
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Figure 8 (A) Total occlusion of the left subclavian artery. (B) Recanalization of the total occlusion following 4-mm balloon angioplasty. Progressive expansion resulted in focal extravasation at the target lesion site.
the patient population. In the vertebral multicenter registry reported by Jain and coworkers,14 54 patients were evaluated with a technical success of 98% and a restenosis at 1 year of 5.5%. The predominant stent utilized in those patients was the balloon-expandable Palmaz stent (Fig. 6A, B). Chastain and coworkers15 reported in the Journal of Neurosurgery in 50 patients 98% technical success in 55 vertebral arteries with no procedural-related complications. A 25-month follow-up did demonstrate two patients with recurrence of vertebrobasilar artery insufficiency and a 6-month angio-restenosis rate of 10%. Schumacher and coworkers16 reported a 1% incidence of vertebroembolic events with 5% overall compli-
cations and a 13% restenosis rate at 2 years when angioplasty alone was utilized. At the present time most vertebral artery stenotic lesions are being managed with balloon-expandable stents considering that the stent does eliminate the potential for dissection in addition to eliminating the elastic recoil that frequently follows the angioplasty procedure. In those patients being evaluated for vertebrobasilar insufficiency, an MRA study to include both extra- and intracranial circulation is a satisfactory screening procedure. When endovascular intervention is necessary, however, that procedure is preceded by a detailed selective vertebral arteriogram to evaluate the entire vasculature in the posterior fossa. Occasionally in
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Figure 8 continued (C) Extravasation resulted in extraplural hematoma that required evacuation and positioning a PTFE covered stent at the target lesion site that controlled further extravasation.
those patients with multivessel occlusive disease, one can clearly demonstrate the segmental atherosclerotic change also present in the cerebellar circulation. Selective examination of the vertebral artery may demonstrate basilar artery stenotic lesions. Unfortunately endovascular management of the basilar artery is attendant with a relatively high complication rate, which can be as variable as 15 to 20%. The medical management of these patients with symptomatic disease also has its limitations considering that recurrent stroke will occur in 14% and the mortality at 15 months as been described as high as 21%.16 Basilar artery complications that might occur during vertebral interventions are predicated on the treatment being initiated as expeditiously as possible. Outcome predictors include duration of occlusion being greater than 6 hours, quadriplegia, coma, or a NIH stroke scale on admission greater than 20 (Fig. 7A-C). Failed medical management, however, may necessitate angioplasty or stenting.
Restenosis Fortunately, restenosis has been relatively low with stent placement of the subclavian and other vessels off the aortic arch. As shown in Table 2, restenosis rates have been reduced to 0 to 18% for 2- to 4-year follow-ups. Factors for good rates have probably been due to the relatively large size of the vessel, distal branches outflow, and high flow rates. However, restenosis does occur. We have found an increased rate of subclavian restenosis among our hemodialysis population. When discovered, we will gain access carefully through the lumen of the stent and re-angioplasty the lesion, although, as simple as it sounds, we make sure that we are not through the struts of the stent. If you have excess trouble advancing your balloon catheter, recheck to make sure that you are within the lumen. If unsuccessful with angioplasty, we will place a second stent.
Conclusion Complications Fortunately, complication rates of subclavian artery stenosis are as low as 2%. Again, this is presumably due to the retrograde flow of the vertebral artery at the time of stenting. A serious complication, however, may be dissection and possible extravasation. This can occur in heavily calcified lesions of the ostium in occluded subclavian arteries (Fig. 8A-C). No series exists, but complications of left common carotid arteries are higher due to the more disastrous results of embolic debris into the carotid circulation. It is essential that all interventionalists become familiar with or have immediate access to those professionals who are familiar with neuroanatomy, neurorescue techniques, microcatheters, and thrombolytic therapy.17
With few exceptions, endovascular stenting of the great vessels off the aortic arch is associated with fewer periprocedural complications and more favorable outcomes than conventional surgical reconstruction. Restenosis of these vessels excluding the vertebral has not been an issue with long-term patency being reported as high as 95% at 1 year. Embolic complications are also being further reduced since the introduction of embolic protection devices. Surprisingly, however, even without embolic protection, the embolic event rate was less than 1%. Prophylactic stenting of subclavian stenosis in the asymptomatic patient remains an unanswered issue. It would appear, however, that with the long-term patency of the internal mammary as a conduit graft during coronary artery bypass surgery, preserving the patency of the subclavian artery has become even more significant. Careful patient
Endovascular interventions selection and operator experience are the two most essential fundamentals in minimizing periprocedural events and managing occlusive disease involving the aortic arch vessels.
References 1. Haas WK, Fields WS, North RR, et al: Joint study of extracranial arterial occlusion. II. Arertiography, techniques, sites and complications. JAMA 203:961, 1968 2. Reivich M, Holling H, Roberts B, et al: Reversal of blood flow through vertebral artery and its effect on cerebral circulation. New Eng J Med 265:878-885, 1961 3. Reivich M, Holling H, Roberts B, Toole JF: Editorial: New vascular syndrome: “the subclavian steal.” New Engl J Med 265:912-913, 1961 4. Fields WS, Lemak NA: Joint study of extracranial arterial occlusion VII Subclavian steal: a review of 168 cases. JAMA 222:1139-1143, 1972 5. Perler BA, William GM: Carotid-subclavian bypass: a decade of experience. J Vasc Surg 12:716-723, 1990 6. Ackerman H, Diener HC, Seboldt H, et al: Ultrasonographic follow up of subclavian stenosis and occlusion: natural history and surgical treatment. Stroke 19:431-435, 1988 7. Conors JJ, Wojak JC: Interventional Neuroradiology: Strategies and Practical Techniques. Philadelphia, PA, WB Saunders, 1999, pp 493499 8. Parot JD: The subclavian steal syndrome. Arch Surg 88:661-665, 1969
225 9. Diethrich EB, Garrett Hem, Ameriso J, et al: Occlusive disease of the common carotid and subclavian arteries treated by carotid-subclavian bypass. Analysis of 125 cases. Am J Surg 114(5):800-808, 1967 10. Sandmann W: Curr Ther Vasc Surg 122-125, 1991 11. Motarjeme A, Keider JW, Zuska AJ: Percutaneous transluminal angioplasty of the brachiocephalic of the brachiocephalic arteries. AJR Am J Roentgenol 138:457-462, 1982 12. Dotter ET, Judkins MR: Transluminal treatment of arteriosclerotic obstructions: description of new technique and preliminary report of its application. Circulation 30:654-670, 1964 13. Ringelstein EB: Delayed reversal of vertebral artery blood flow following percutaneous transluminal angioplasty for subclavian steal syndrome. Neuroradiology 26:189-198, 1984 14. Jain D, Shaker SM, Burg M, et al: Effects of mental stress on left ventricular and peripheral vascular performance in patients with coronary artery disease. J Am Coll Cardiol 31(6):1314-1322, 1998 15. Chastain HD, Campbell MS, Iyer S, et al: Extracranial vertebral artery stent placement: in-hospital and follow-up results. J Neurol 91(4):547552, 1999 16. Schumacher HC, Khaw AV, Meyers PM, et al: Intercranial angioplasty and stent placement for cerebral atherosclerosis. J Vasc Interv Radiol 15:S123-S132, 2004 17. Wholey MH, Wholey M, Tan WA, et al: Review and management of neurologic complications related to carotid artery stent placement. J Endovasc Ther 8(4):343-351, 2001
W
ith few exceptions, most of the occlusive disease involving the great vessels off the aortic arch is no longer considered a surgical disease. For example, both the right and the left subclavian arteries, the left common carotid origin, the innominate origin, and the proximal divisions of the right and left vertebral arteries are all quite amenable to endovascular stenting. There are however exceptions and these may occur when either aneurysmal disease, sepsis, trauma, or total occlusions that may not be amendable to recanalization by endovascular techniques are present. The causes of stenotic lesions in these vessels are similar to other vessels, where the majority is caused by atherosclerotic disease, although other causes such as dissection, fibromuscular disease (FMD), and various vasculitidies are not infrequent. The majority of the supraaortic atherosclerotic occlusive lesions involves the left subclavian artery.1 Such disease results in a “subclavian steal,” which was first described in 1961 by Reivich and coworkers.2,3 By occluding the left subclavian artery, arterial flow is provided by the right subclavian artery with flow into the right vertebral artery and then retrograde flow into the left vertebral artery and subsequently into left subclavian artery. Additional collaterals also include the external carotid, the ascending cervical artery, and the thyrocervical trunk. Though present, the number of patients who become symptomatic are relatively uncommon; in a study of 1114 patients with disease involving the innominate and subclavian arteries, only 168 (15%) demonstrated signs and symptoms of subclavian stenosis.4 In Perler and Williams’ study of 6534 patients, only 17% were noted to have stenosis of 30% or more.5 Of these patients, only 24% had clinical and angiographic evidence of subclavian steal.5 The progression of the disease is also limited. Only 17% of 67 patients in Ackerman and coworkers study had progression of disease in 2 years.6 Only 4 of 55 asymptomatic patients developed vertebrobasilar symptoms in 4-year follow-up.6 The diagnosis of subclavian steal is based on having upper *Pittsburgh Vascular Institute, UPMC Presbyterian Shadyside, Pittsburgh, PA. †Department of Cardiovascular Interventional Radiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas. Address reprint requests to Mark H. Wholey, MD, Pittsburgh Vascular Institute, 5230 Centre Avenue, Pittsburgh, PA 15232. E-mail: [email protected].
1089-2516/05/$-see front matter © 2005 Elsevier Inc. All rights reserved. doi:10.1053/j.tvir.2005.02.007
extremity ischemia where a pressure gradient of 20 mm Hg is noted and symptoms of arm claudication, paresis, and atheroembolic digital ischemia are seen. Less commonly, there is vertebrobasilar insufficiency, which includes symptoms of ataxia, diploplia, syncope, vertigo, dizziness, nausea, and vomiting. Another syndrome, which has been increasing in frequency, includes coronary steal syndrome in which a stenosis proximal to internal mammary-coronary artery bypass may cause ischemic symptoms. The growing use of the left internal mammary artery (LIMA) for coronary bypass procedures has resulted in greater surveillance and treatment of the left subclavian artery (Fig. 1A-D). Though debatable, highgrade, proximal subclavian arterial stenoses in relatively asymptomatic patients are now considered appropriate therapy to maintain the capacity to use the LIMA. Similarly, there is the increased need to maintain subclavian patency for patients undergoing or expecting possible hemodialysis. Subclavian stenosis is frequently seen as a cause for failed hemodialysis fistulas. Doppler examinations of the brachiocephalic arteries usually confirm the diagnosis of subclavian steal by showing retrograde flow of the ipsilateral vertebral artery. MRA is increasingly being used to diagnose subclavian artery stenoses, although angiography has traditionally been the gold standard. Innominate artery stenosis is relatively uncommon. When the atherosclerotic disease involves the innominate artery, the symptoms may be more severe and include cerebral symptoms. The occlusion in the innominate artery causes retrograde flow from the vertebral and into the right common carotid and the right subclavian artery. Symptoms generally include vertebrobasilar insufficiency with ataxia, diploplia, syncope, vertigo, dizziness, nausea, and/or vomiting. It may also include upper extremity ischemia and atheroembolic digital ischemia. Indications to treat vertebral artery origin lesions include symptoms of vertebrobasilar insufficiency and more related to simple flow related stenoses, as opposed to embolic events.7 Vertebrobasilar symptoms may be related to head or neck position or the more classic patterns related to blood pressure and orthostatic factors.
Treatment The treatment modalities for occlusive disease involving subclavian, left common carotid, or innominate arteries has been 215
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Figure 1 (A) High-grade subclavian stenosis with significant decrease antegrade flow through LIMA. (B) Radionuclide study demonstrating reversible septal ischemia in the stress and resting phase study. (C) Following effective stenting of left subclavian and restoration of antegrade flow through LIMA. (D) Radionuclide stress examination postsubclavian stenting demonstrating no further septal ischemia following restoration of LIMA.
surgery, endovascular treatment, or medical therapy. Surgical options include endarterectomy or more common, bypass procedures. There has been a long history of subclavian bypass procedures; Parot and coworkers introduced carotidsubclavian transposition in 1964.8 Diethrich and coworkers introduced carotid subclavian bypass in 1967 reporting relief of 93% in 125 patients with operative mortality of 4.8%.9 The patency of such surgical procedures has been good with 5-year patency of 90% for surgical bypasses and 96% patency for transpositions.9 However, it is very invasive with its share of surgical morbidity and mortality. Direct carotid to ipsilateral artery bypass and transposition has been reported to have ⬍5% morbidity and ⬍2% mortality.10 Whether surgical or endovascular treatment, patient’s prognosis remains good. Because of the dramatic symptoms of upper extremity ischemia or cerebral ischemia, patients seek medical attention rather quickly. As a result, patients tend to have focal lesions in large vessels relatively early in
disease progression, so long-term results are good. There is generally excellent relief of ischemic symptoms. However, there are poor results (only 20%) of improving dizziness. Today, angioplasty and stent placement in the treatment of proximal arch vessel lesions is considered the treatment of choice by most interventionists.11 Dotter and Judkins have performed endovascular treatment of lesions involving the great vessels off the aortic arch since the original description in 1964.12 Early interventionalists have angioplastied lesions arising from the innominate, right subclavian, left common carotid, and left subclavian arteries. Angioplasty performed before 1989 alone on short stenotic lesions had a good technical success rate, high complication rate, and marginal primary patency. As Table 1 shows, early interventional radiologists had a technical success of 92%, complication rate of 5% with 1% CNS problems, and a restenosis rate of 19% at 2 years.12 With the advent of lower profile balloon catheters (from 7 to 5 French) and improved wire technology, compli-
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Table 1 Early Angioplasty (Prior to 1989) Results of Subclavian Artery Stenoses Author
Patients
Technical Success
Restenosis Rate
Complication Rate
Follow-up
Wholey/Erbstein Wilm’s et al
24 23
88% 91%
16% (4/24) 13% (3/23)
4% (1/24) 4% (1/23)
18-26 mos 25 mos
cation rates improved to 0 to 2%, but still restenosis remained high with rates of 4 to 22%. With the advent of stent technology, occlusive disease and long stenoses could now be treated successfully and the primary patency rates could be improved. The traditional indications for endovascular stent placement included suboptimal angioplasty results, recurrent or ⬎30% residual stenosis, gradient ⬎10 mm Hg, thromboemboli, or late restenosis after angioplasty. Because of superior patency results, however, almost all lesions are stented (refer to Table 2). Restenosis rates have been reduced to 0 to 18% for 2- to 4-year followups. Surprisingly, the neurologic complication rate of subclavian stent placement has been low. This may be due to the retrograde vertebral artery flow. Following angioplasty and stent placement, the vertebral artery retrograde flow does not reverse until 20 seconds to 4 minutes.13 With the advent of embolic protection filters and systems, complications should decrease further. The treatment of innominate artery stenosis is similar to that of subclavian stenoses except that extra attention must be made not to compress the nearby right common carotid artery. The treatment of the left common carotid artery is also similar to the subclavian technique, although great care must be taken to avoid disastrous neurocomplications.
Technique of Supraaortic Stenting Approach Deciding on which approach to employ is one of the first major decisions. It will dictate which type of sheaths, wires, and stents to be deployed. We generally prefer to come from the common femoral route because of long-term experience and because of the lower risk of hematoma complications that can occur from brachial approaches. Brachial approach is preferred in many subclavian and innominate artery occlusions, especially in those lesions lacking a characteristic nipple in the proximal segment of the artery. We will also use this approach when the takeoff of the subclavian or innominate artery is at such a steep angle to the aorta that traditional femoral access is foreboding (Fig. 2A, B). Also, if severe aor-
toiliac disease is present, we will naturally choose the brachial approach. When selected, we prefer the low brachial approach near the olecranon fossa because of the difficulty in holding pressure to brachial in the upper arm. We almost never use the axillary approach because of the brachial plexus injury that can result from an expanding hematoma. On occasion when there is combined internal carotid artery stenosis and left common carotid stenosis, we may consider endarterectomy followed by retrograde positioning of the common carotid stent.
Technique Left Subclavian Stenoses For subclavian artery lesions, we will select the targeted vessel with a 5-French diagnostic catheter either separately or through a long 6-French vascular sheath, or an 8-French guide catheter. Once arterial access is obtained, we will anticoagulate with either Heparin or initiate bivilarubin (weightrelated dosage). A LAO projection with the pigtail catheter in the aortic arch is first performed. Under roadmapping and under the best image angle, we will cross the lesion carefully. With the guidewire past the lesion, we then advance the guide just proximal to the lesion. We will predilate lesions that are severely diseased and pose a risk of stripping or impeding the passage of our balloon-mounted stents. Predilatation helps to reduce the risk of stent migration as well as allowing for a quick reference as to the vessel size and lesion length. We will recheck the images to see important vessel takeoffs as well as to assess possible dissections. For ostial lesions, we will occasionally use an RAO view to see the origin well. Rarely do we advance the sheath or guide over and past the lesion. If the sheath should go past the lesion, we will let the sheath backbleed before advancement of the balloonmounted stent. We will then advance the balloon-mounted stent to the lesion, being certain that important vessels such as the internal mammary and the vertebral arteries are not compromised. If the vertebral is at risk, we will leave a 0.014” guidewire as a safety wire in the vertebral artery during subclavian stenting. We then hold the balloon carefully because
Table 2 Endovascular Subclavian Stent Results Author
Patients
Tech Success
Restenosis Rate
Cx
Follow-up
Henry ’99 Sullivan ’98 Sueoka ’96 Kumar ’95
46 66 7 27
91% 94% 100% 100%
16% 15% 0 0
3% 17% 0 11%‡
4 years* 36 mos† 12 mos
*J Endovasc. Surg 1999, 6:33-41. †J Vasc Surg. 1998;28(6):1059-65. ‡Two brachial art. injury, one stent displacement.
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M.H. Wholey and M.H. Wholey protection device. At the present time the only available distal embolic protection devices available are the PercuSurge balloon (guidewire), the Boston Scientific EPI Filter wire (Natick, MA), and the Guidant Accunet. All are off-label indications for those applications. Left Subclavian Occlusions Gaining access through left subclavian total occlusions is somewhat more difficult and may require both a femoral and a brachial approach to get access. We will generally start from the femoral route and with manipulations of a diagnostic catheter, such as a headhunter or vertebral-shaped catheter, and with a torquable guidewire (regular or stiff Glidewire or Wholey 0.035” guidewire), we will get through most lesions (Fig. 4A-C). Attention must be made, especially with the stiff glide wire, not to dissect or perforate the subclavian artery. Also, care must be made with the wire crossing the subclavian artery ostium, to be gentle with wire manipulations for fear that the wire will dissect across the ostium with manipulations. Once across the lesion, predilation and balloon-mounted
Figure 2 (A, B) Total occlusion of the innominate artery. Recanalization with balloon-expandable stent resulting in no residual stenosis and improvement in antegrade flow through the right common carotid as well as the right subclavian and right vertebral.
of the aortic arch pulsations and deploy the stent quickly to approximately 8 atm. We will then perform a poststenting angiogram and assess the stent apposition to the vessel diameter. The origin of the subclavian artery maybe fragile, so we are cautious not to overdilate for fear of dissection. When dissection occurs during stent deployment, it may require an additional overlapping stent. If possible, it is best not to cover either the vertebral or the internal mammary artery. If this is necessary, it is fortunate that the stent cell size allows adequate flow and rarely results in junctional occlusion (Fig. 3A, B). Frequently with a high-grade lesion in the subclavian artery, we will protect the vertebral artery with an embolic
Figure 3 (A) Subclavian stenosis with stenting in a diabetic patient that resulted in edge dissection just proximal to the origin of the internal mammary. (B) Precise positioning of a stent at the dissection site resulted in improved flow with correction of the dissection. Note the internal mammary is preserved along with the left vertebral artery.
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Figure 4 (A) Total occlusion of the left subclavian artery with visible retrograde flow from the left vertebral to reconstitute the subclavian. (B) Dynamic study showing the shunt reversal from the right vertebral to the left vertebral. (C) Reestablishment of antegrade flow in the vertebral and the subclavian following effective stenting of the totally occluded segment.
stent placement proceeds similar to stenotic lesions. Caution, however, is also recommended in the initial dilation of those patients with total occlusion. Frequently the rigid dystrophic calcification results in excessive dissection and occasionally a false aneurysm. For these reasons in total occlusions, it is best to initially underdilate after establishing a minimal lumen and subsequently positioning a balloon expandable stent. In
the event a false aneurysm does develop, it may then be necessary to position a covered stent at that site. Distal Subclavian/Axillary Lesions We are encountering more patients, especially those on hemodialysis, who present with mid and distal subclavian stenosis. We frequently discuss these cases with our vascular
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surgery colleagues for possible surgical options on a case-bycase basis. When we intervene, we will generally prefer to angioplasty alone those lesions at crucial areas such as between the first rib and clavicle as well as at the subclavian/ axillary junction where there is bending and compression. When the lesion does not respond to angioplasty, we will use self-expanding stents such as Wallstents and the nitinol stents. We will oversize the stent 1 to 2 mm greater than the vessel diameter. Through a long 8-French guide, we will deliver and deploy the stent. During deployment, care must be taken to watch the proximal end of the stent, which has a tendency to jump or shrink further distally than planned. Maintain gentle posterior pressure when deploying self-expanding stents. Left Common Carotid Stenoses For left common carotid artery lesions, we will use guiding catheters (usually 8 French) for positioning at the vessel ostium. We will use 0.035” wires with torquability and support to cross the lesion. If the vessel comes off the aorta at a steep angle or is a bovine arch, you may need to take the guidewire farther up into the common carotid or even the external carotid for needed support. We have on occasion used embolic protection devices for these lesions for preventing embolic complications. Like subclavian lesions, we will predilate severe lesions to allow for easy advancement of the balloon-mounted stent. When ready and properly visualized, we will deploy the stent. Again, aortic arch pulsations could lead to errors in placement. Ideally, we like to have the edge of the stent extend approximately 1 mm into the aorta for ostial lesions. Innominate Artery Lesions For innominate artery lesions, technique is similar to that of stenting the left subclavian and the left common carotid artery. Attention must be given to the bifurcation of the right common carotid and the right subclavian arteries. Even if the subclavian is mildly stenotic, the stent in the right common carotid could result in a significant lesion of the unaffected subclavian (Fig. 5A, B). Kissing stents may then be required. Innominate and right subclavian lesions are frequently managed from the brachial approach.
Decision of Which Stent For lesions involving the proximal segments of the left subclavian, left common carotid, and especially the innominate artery, we use a balloon-mounted stent. The chance for compression and deformation of the stent is low. Self-expandable stents are not chosen because of the inability to be exactly precise in a region where millimeters count. Furthermore, there is the possibility of stent migration with the self-expandable stents. We will use self-expandable stents for lesions in the mid subclavian in or near the region of the clavicle and first rib or where the stent is externally exposed to compression. We measure the lesion and a normal arterial segment to determine stent length and diameter. We will use QCA from the angiographic images to determine vessel size and lesion length. The predilatation balloon catheter provides a quick reference point in terms of lesion length and also vessel diameter. Never place a balloon-mounted stent
Figure 5 (A) Total occlusion of the innominate with no visible antegrade flow in either the carotid or the right subclavian artery. (B) Six-months post follow-up examination demonstrating the innominate to be widely patent with excellent flow in the subclavian and vertebral as well as the right common carotid. Note the intimal hyperplasia that exists in the 6-month follow-up but does not compromise innominate artery dimensions.
larger than the normal vessel diameter. As a matter of fact, in total occlusions we will purposely slightly undersize.
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Figure 6 (A) High-grade stenotic lesion of the proximal right vertebral. (B) Balloon-expandable stent positioned just at the ostium at the target lesion site and restoring the right vertebral to basically normal dimensions. Note distal protection device in the right vertebral.
Decision of Which Guidewire Guidewire selection depends on the approach, lesion characteristics, and type of stent chosen and availability of equipment. For most proximal subclavian stenoses, coming from the femoral route, a 0.035” torquable guidewire is sufficient. A Glidewire (Terumo, Boston Scientific) may also be used for crossing. Five-French-long balloon catheters can course through most 6-French-long vascular sheaths or 8-French guiding catheters. For more diseased subclavian arteries and for those requiring a brachial approach, we may generally use 0.014” guidewires and 6-French sheaths.
Decision of Guiding Catheter versus Sheath Whether you chose a guiding catheter or sheath, it is important never to compromise your ability to inject contrast to visualize the lesion in relation to the balloon catheter. Likewise, it is essential to obtain the best angle to see the takeoff of the vessel in relation to the aorta. It is also crucial to have the best angle to visualize the takeoff of key vessels (vertebral, common carotid, or internal mammary arteries). Because of respiration, roadmap images are not often helpful. Another feature to be aware of is dramatic aortic pulsations
when deploying a stent. If there is a large gap in diastolic and systolic blood pressures, there can be an excess of pulsations of the vessels. These pulsations can cause large motions (1 cm or more) in the position of the lesion relative to the balloon catheter or self-expanding stent when trying to deploy. Blood pressure control is essential in these patients as well as the need for slightly longer stents. For subclavian and innominate artery lesions, we prefer to use a long 8-French guide or 6-French sheath. For left common carotid lesions, where support against the aortic wall is important, we prefer guiding catheters. When coming from a brachial approach, we use as small a sheath as possible; we generally use a long 6-French sheath. Sheath and guide catheter sizes are also dependent on stent selection. Generally, we will use a stent mounted on a 7- to 8-mm balloon catheter, which can be advanced through an 8-French guide. Larger stent sizes, those mounted on 9- to 10-mm balloon catheters, may require larger sheaths.
Proximal Vertebral Artery Stent Placement The proximal vertebral vessels are also considered a part of the brachial cephalic group and in fact the anomalous origin of the left vertebral from the aortic arch occurs in 5 to 10% of
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Figure 7 (A) High-grade stenosis in the proximal basilar artery in a patient with symptomatic basilar artery insufficiency being managed medically. (B) Total occlusion of the basilar artery at its origin with failed anticoagulation therapy. Note patency of the posterior inferior cerebella artery. (C) 3.5 mm over 014 wire at the target lesion site in the basilar artery. (D) Postdilation demonstrates normal dimensions of the basilar artery at the target lesion site with restoration of flow in both posterior cerebrals and in the left superior cerebellar. The right superior cerebella remains occluded. (E) Tenmonth follow-up examination demonstrating patency of the basilar artery with satisfactory posterior inferior cerebellar and superior cerebellar flow but with 50% restenosis that did not warrant additional adjunctive angioplasty considering the patient was essentially asymptomatic.
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Figure 8 (A) Total occlusion of the left subclavian artery. (B) Recanalization of the total occlusion following 4-mm balloon angioplasty. Progressive expansion resulted in focal extravasation at the target lesion site.
the patient population. In the vertebral multicenter registry reported by Jain and coworkers,14 54 patients were evaluated with a technical success of 98% and a restenosis at 1 year of 5.5%. The predominant stent utilized in those patients was the balloon-expandable Palmaz stent (Fig. 6A, B). Chastain and coworkers15 reported in the Journal of Neurosurgery in 50 patients 98% technical success in 55 vertebral arteries with no procedural-related complications. A 25-month follow-up did demonstrate two patients with recurrence of vertebrobasilar artery insufficiency and a 6-month angio-restenosis rate of 10%. Schumacher and coworkers16 reported a 1% incidence of vertebroembolic events with 5% overall compli-
cations and a 13% restenosis rate at 2 years when angioplasty alone was utilized. At the present time most vertebral artery stenotic lesions are being managed with balloon-expandable stents considering that the stent does eliminate the potential for dissection in addition to eliminating the elastic recoil that frequently follows the angioplasty procedure. In those patients being evaluated for vertebrobasilar insufficiency, an MRA study to include both extra- and intracranial circulation is a satisfactory screening procedure. When endovascular intervention is necessary, however, that procedure is preceded by a detailed selective vertebral arteriogram to evaluate the entire vasculature in the posterior fossa. Occasionally in
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Figure 8 continued (C) Extravasation resulted in extraplural hematoma that required evacuation and positioning a PTFE covered stent at the target lesion site that controlled further extravasation.
those patients with multivessel occlusive disease, one can clearly demonstrate the segmental atherosclerotic change also present in the cerebellar circulation. Selective examination of the vertebral artery may demonstrate basilar artery stenotic lesions. Unfortunately endovascular management of the basilar artery is attendant with a relatively high complication rate, which can be as variable as 15 to 20%. The medical management of these patients with symptomatic disease also has its limitations considering that recurrent stroke will occur in 14% and the mortality at 15 months as been described as high as 21%.16 Basilar artery complications that might occur during vertebral interventions are predicated on the treatment being initiated as expeditiously as possible. Outcome predictors include duration of occlusion being greater than 6 hours, quadriplegia, coma, or a NIH stroke scale on admission greater than 20 (Fig. 7A-C). Failed medical management, however, may necessitate angioplasty or stenting.
Restenosis Fortunately, restenosis has been relatively low with stent placement of the subclavian and other vessels off the aortic arch. As shown in Table 2, restenosis rates have been reduced to 0 to 18% for 2- to 4-year follow-ups. Factors for good rates have probably been due to the relatively large size of the vessel, distal branches outflow, and high flow rates. However, restenosis does occur. We have found an increased rate of subclavian restenosis among our hemodialysis population. When discovered, we will gain access carefully through the lumen of the stent and re-angioplasty the lesion, although, as simple as it sounds, we make sure that we are not through the struts of the stent. If you have excess trouble advancing your balloon catheter, recheck to make sure that you are within the lumen. If unsuccessful with angioplasty, we will place a second stent.
Conclusion Complications Fortunately, complication rates of subclavian artery stenosis are as low as 2%. Again, this is presumably due to the retrograde flow of the vertebral artery at the time of stenting. A serious complication, however, may be dissection and possible extravasation. This can occur in heavily calcified lesions of the ostium in occluded subclavian arteries (Fig. 8A-C). No series exists, but complications of left common carotid arteries are higher due to the more disastrous results of embolic debris into the carotid circulation. It is essential that all interventionalists become familiar with or have immediate access to those professionals who are familiar with neuroanatomy, neurorescue techniques, microcatheters, and thrombolytic therapy.17
With few exceptions, endovascular stenting of the great vessels off the aortic arch is associated with fewer periprocedural complications and more favorable outcomes than conventional surgical reconstruction. Restenosis of these vessels excluding the vertebral has not been an issue with long-term patency being reported as high as 95% at 1 year. Embolic complications are also being further reduced since the introduction of embolic protection devices. Surprisingly, however, even without embolic protection, the embolic event rate was less than 1%. Prophylactic stenting of subclavian stenosis in the asymptomatic patient remains an unanswered issue. It would appear, however, that with the long-term patency of the internal mammary as a conduit graft during coronary artery bypass surgery, preserving the patency of the subclavian artery has become even more significant. Careful patient
Endovascular interventions selection and operator experience are the two most essential fundamentals in minimizing periprocedural events and managing occlusive disease involving the aortic arch vessels.
References 1. Haas WK, Fields WS, North RR, et al: Joint study of extracranial arterial occlusion. II. Arertiography, techniques, sites and complications. JAMA 203:961, 1968 2. Reivich M, Holling H, Roberts B, et al: Reversal of blood flow through vertebral artery and its effect on cerebral circulation. New Eng J Med 265:878-885, 1961 3. Reivich M, Holling H, Roberts B, Toole JF: Editorial: New vascular syndrome: “the subclavian steal.” New Engl J Med 265:912-913, 1961 4. Fields WS, Lemak NA: Joint study of extracranial arterial occlusion VII Subclavian steal: a review of 168 cases. JAMA 222:1139-1143, 1972 5. Perler BA, William GM: Carotid-subclavian bypass: a decade of experience. J Vasc Surg 12:716-723, 1990 6. Ackerman H, Diener HC, Seboldt H, et al: Ultrasonographic follow up of subclavian stenosis and occlusion: natural history and surgical treatment. Stroke 19:431-435, 1988 7. Conors JJ, Wojak JC: Interventional Neuroradiology: Strategies and Practical Techniques. Philadelphia, PA, WB Saunders, 1999, pp 493499 8. Parot JD: The subclavian steal syndrome. Arch Surg 88:661-665, 1969
225 9. Diethrich EB, Garrett Hem, Ameriso J, et al: Occlusive disease of the common carotid and subclavian arteries treated by carotid-subclavian bypass. Analysis of 125 cases. Am J Surg 114(5):800-808, 1967 10. Sandmann W: Curr Ther Vasc Surg 122-125, 1991 11. Motarjeme A, Keider JW, Zuska AJ: Percutaneous transluminal angioplasty of the brachiocephalic of the brachiocephalic arteries. AJR Am J Roentgenol 138:457-462, 1982 12. Dotter ET, Judkins MR: Transluminal treatment of arteriosclerotic obstructions: description of new technique and preliminary report of its application. Circulation 30:654-670, 1964 13. Ringelstein EB: Delayed reversal of vertebral artery blood flow following percutaneous transluminal angioplasty for subclavian steal syndrome. Neuroradiology 26:189-198, 1984 14. Jain D, Shaker SM, Burg M, et al: Effects of mental stress on left ventricular and peripheral vascular performance in patients with coronary artery disease. J Am Coll Cardiol 31(6):1314-1322, 1998 15. Chastain HD, Campbell MS, Iyer S, et al: Extracranial vertebral artery stent placement: in-hospital and follow-up results. J Neurol 91(4):547552, 1999 16. Schumacher HC, Khaw AV, Meyers PM, et al: Intercranial angioplasty and stent placement for cerebral atherosclerosis. J Vasc Interv Radiol 15:S123-S132, 2004 17. Wholey MH, Wholey M, Tan WA, et al: Review and management of neurologic complications related to carotid artery stent placement. J Endovasc Ther 8(4):343-351, 2001