Subclavian steal

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  • One of the causes of vertebrobasilar insufficiency; results from stenosis of the subclavian artery proximal to the takeoff of the vertebral artery
    • NOTE: order of subclavian branches from proximal to distal is common carotid, vertebral, thryocervical trunk, costocervical trunk
  • Symptoms: consistent with brachial ischemia (pain or fatigue with use of the arm)
  • Treatment: subclavian to subclavian bypass, axilloaxillary bypass, vertebral artery to common carotid artery end to side anastomosis, endovascular angioplasty

Contents

INTRODUCTION

In 1960, Contorni reported the first angiographic demonstration of retrograde flow in the VA ipsilateral to a proximal subclavian artery stenosis in a neurologically asymptomatic patient.197 In 1961, Fisher explained that subclavian artery stenosis or occlusion could result in reduction of blood flow to the arm, reversal of flow to the ipsilateral VA, and claudication or neurological deficits of the arm when there is inadequate intracranial or extracranial collateral circulation.198 He named this new vascular disease a “subclavian steal syndrome” (SSS). Since the inception of this term, the clinical significance and natural history of subclavian steal have evolved from a disease that is morbid with neurological symptoms including vertigo, syncope, ataxia, paresthesia, and motor or visual deficits to a condition that is often asymptomatic.199-205 Moreover, SSS, which was surgically treated even when the patient was asymptomatic until 1980, is now considered for treatment only in those who have symptoms.

This syndrome is reported to occur in approximately 6% of patients who have an asymptomatic cervical bruit. Over the last 2 decades, noninvasive imaging modalities, such as Doppler ultrasound, MR imaging and angiography, and Xenon-enhanced CT, have complemented angiography as investigative tools.207,208 A variety of surgical treatments and complications have been reported for SSS over the past 4 decades. Since Bachman and Kim reported the first successful angioplasty for SSS in 1980, subclavian angioplasty with or without stenting has been performed as an alternative treatment to surgery.213 In this section, the authors will briefly review the endovascular management of SSS.

INDICATIONS

Contrary to earlier beliefs that most patients with SSS have symptoms, the steal alone is rarely a cause of posterior circulation ischemia.214 The advancement of noninvasive imaging tools has contributed to better understanding of the natural history of a subclavian steal. Bornstein and Norris reported a 2-year follow-up review of 32 patients with asymptomatic subclavian steal with no cerebrovascular event related to the steal.215 Moran et al. studied 55 patients with SSS with Doppler ultrasound imaging over a mean follow-up period of 4.1 years.216 During this period, only 7.2% of patients developed symptoms of vertebrobasilar ischemia. No posterior circulation strokes were reported. However, 18% of the patients developed symptoms of anterior circulation ischemia or stroke. Hennerici et al. reviewed the medical records of 324 patients with subclavian steal detected via on the basis of findings of Doppler ultrasound studies and reported symptoms of vertebrobasilar ischemia in only 5% of these patients.217 The majority of patients (64%) were asymptomatic. The remainder had lateralizing hemispheric symptoms. These studies suggested that SSS might become symptomatic when there is hemodynamic insufficiency in the presence of coexisting severe carotid occlusive disease or inadequate intracranial collateralization. For these reasons, revascularization is not advocated for asymptomatic patients.

Subclavian angioplasty with or without stent placement may be indicated for symptomatic SSS in patients who have medical comorbid conditions that increase the risk of perioperative complications. No prospective, randomized study is available to compare the efficacy of surgical versus endoluminal revascularization for SSS. The advantages of an endovascular approach include the avoidance of general anesthesia and surgical complications. The disadvantages of angioplasty with or without stenting include potential dissection, thrombosis, and embolization. The durability of patency after subclavian angioplasty is difficult to interpret as most series have not performed follow-up angiography and have relied on Doppler studies. However, long-term patency after subclavian angioplasty alone for stenosis (ranging from 54 to 100% at 2 months to 5 years) appears superior to that for occlusion (<50% at 4 to 88 months of follow-up).

In an attempt to improve upon the results of angioplasty, subclavian angioplasty-assisted stenting has become popularized for symptomatic subclavian steal and occlusive disease. Case series have reported minimal rates of complications and high rates of technical success.223-226 However, functional outcome measures have not been consistently reported. Further studies are needed to evaluate the efficacy and long-term patency of angioplasty with stent placement for symptomatic subclavian steal.

TECHNIQUE

Innovative techniques such as balloon insertion into the ipsilateral VA with temporary occlusion of flow and the adjunctive use of thrombolytic agents before subclavian angioplasty and stent placement have been performed since the 1980s. However, the authors will describe a basic technique of subclavian angioplasty and stent placement. The selection of the periprocedural anticoagulation regimen, anesthesia, vascular access approach, wires, guide catheters, balloons, and stents will depend on the patient, the vascular pathology, and the endovascular surgeon. The authors routinely place patients on 325 mg of aspirin and 75 mg of clopidogrel once daily for 3 days before the procedure.

Approach

A brachial or a femoral artery approach or a combination of both approaches may be used to perform subclavian angioplasty and/or stent placement. Typically, a 6- to 8-French sheath (Cook guide sheath, Cook Inc.) is introduced at the femoral or brachial artery access site. Heparin is administered intravenously as a bolus to achieve an activated coagulation time above 250-300 seconds. Fluoroscopic guidance and road-mapping technique are used throughout the procedure. A 0.035-inch, angled hydrophilic guidewire (Glidewire, MediTech Boston Scientific, Watertown, MA) is inserted into a 5-French angled diagnostic catheter (MediTech Boston Scientific). The guidewire-catheter complex is coaxially advanced into the sheath. The stenotic or occluded segment of the subclavian artery is crossed with the guidewire.

Angioplasty

In the case of balloon angioplasty alone, the angled catheter is removed; and a balloon catheter diameter ranging from 6 to 10 mm, length ranging from 3 to 10 cm) is advanced over the guidewire, and angioplasty is performed. The pre-inflation diameter of the balloon should be 1 to 2 mm less than the diameter of the subclavian artery distal to the stenosis or occlusion. Such under-dilation may minimize significant arterial dissection or rupture. If significant (>30%) residual stenosis or occlusion is observed, a second angioplasty may be performed with a slightly larger balloon. Subclavian stenting can be performed if significant stenosis remains after the first or second angioplasty attempts at the same sitting, as long as the residual lumen is large enough to accommodate the stent . In the case of subclavian occlusion, the lesion is crossed with the 0.035-inch guidewire and then the angled catheter; and the guidewire is exchanged for a 0.014- to 0.018-inch wire. Balloon angioplasty and/or stenting can then be performed over the exchange guidewire.

For subclavian artery stenosis or occlusion near the origin of the VA, controversy exists as to how close to the VA origin an angioplasty can be safely performed. Vitek reported no complications with subclavian angioplasty across the VA origin in 50% of 35 subclavian artery angioplasties but cautioned that angioplasty might be unsafe in cases where the lesion involves the VA origin.

Stents

A variety of balloon-expandable and self-expanding stents are available for subclavian stenting. The selection of the stent depends on the size of the adjacent normal artery and the characteristics (length, calcification) and location of the lesion. A self-expanding stent, such as the Wallstent, may be used for a non-calcified long lesion. However, there are limitations with the Wallstent. The maximal diameter of this stent is 10 mm, which would not be suitable for a subclavian artery with a normal diameter of more than 10 mm. In addition, the length of a fully deployed Wallstent cannot always be accurately predicted. Accuracy is important, especially in the ostial lesions off the aortic arch, as a malpositioned stent may protrude into the aortic arch or completely bypass the ostial lesion. Thus, an ostial lesion may be better treated with a balloon-expandable stent, such as a Palmaz stent, or a self-expanding stent that has more predictable length when deployed, such as the Smart stent (Cordis Neurovascular). Post-stent angioplasty may be performed within the stent if significant residual stenosis remains. Angiography is performed after each angioplasty and stent placement. Following the procedure, patients are prescribed 75 mg of clopidogrel daily for 1 month and 325 mg of aspirin for an indefinite period.

PROCEDURAL COMPLICATIONS

The main procedural complications associated with subclavian angioplasty and stenting include hematoma, pseudoaneurysm, and thrombosis at the access site; distal arterial emboli; and arterial dissection. The incidence of these complications ranges from 0 to 11.4%.218-226 Failure to recanalize an occluded subclavian artery is frequently observed with angioplasty alone; early re-occlusion rates as high as 13% have been reported.228 As a result, subclavian artery stenting for the treatment of occlusions has been evaluated at several institutions. Although many series have reported small numbers of cases, initial success rates as high as 100% and asymptomatic and symptomatic restenosis (>50%) rates of 7% and 3%, respectively, at 1 year have been reported.218-226

MORBIDITY AND MORTALITY

Rodriguez-Lopez et al. reported a 3% incidence of postprocedural TIA in 37 patients after treatment with percutaneous balloon angioplasty and stenting of subclavian artery stenosis.225 In the occlusion group (15 of 37 patients), no postprocedural cerebrovascular events or deaths occurred. Ringelstein and Zeumer reported that a delay in the reversal of VA blood flow after percutaneous balloon angioplasty may account for such low incidence of neurological complications.229 Follow-up Doppler study of these patients at 9 months showed no restenosis in the occlusion group. Additional studies are needed to determine the long-term morbidity and mortality of subclavian artery stenting for SSS.

SSS is often associated with extracranial atherosclerotic disease. The subclavian steal becomes symptomatic when there is inadequate intracranial collateralization via the circle of Willis. Subclavian angioplasty or stenting is an alternative treatment option for patients with SSS who are at increased risk for surgery because of their medical comorbidities. In cases of subclavian stenosis, percutaneous angioplasty with or without stent placement appears to be safe and feasible. However, for cases of subclavian occlusion or stenosis that are refractory to angioplasty, stenting appears to be a promising method. Further study is needed to evaluate the durability of these procedures.

References

  1. Smith JM, Koury HI, Hafner CD, Welling RE. Subclavian steal syndrome. A review of 59 consecutive cases. J Cardiovasc Surg (Torino). 1994;35:11-14.
  2. Thomassen L, Aarli JA. Subclavian steal phenomenon. Clinical and hemodynamic aspects. Acta Neurol Scand. 1994;90:241-244.
  3. Walker PM, Paley D, Harris KA, Thompson A, Johnston KW. What determines the symptoms associated with subclavian artery occlusive disease? J Vasc Surg. 1985;2:154-157.
  4. Webster MW, Downs L, Yonas H, Makaroun MS, Steed DL. The effect of arm exercise on regional cerebral blood flow in the subclavian steal syndrome. Am J Surg. 1994;168:91-3.
  5. Fields WS, Lemak NA. Joint Study of extracranial arterial occlusion. VII. Subclavian steal-- a review of 168 cases. JAMA. 1972;222:1139-1143.
  6. Ackermann H, Diener HC, Seboldt H, Huth C. Ultrasonographic follow-up of subclavian stenosis and occlusion: natural history and surgical treatment. Stroke. 1988;19:431-435.
  7. Drutman J, Gyorke A, Davis WL, Turski PA. Evaluation of subclavian steal with two-dimensional phase-contrast and two-dimensional time-of-flight MR angiography. AJNR Am J Neuroradiol. 1994;15:1642-1645.
  8. AbuRahma AF, Robinson PA, Jennings TG. Carotid-subclavian bypass grafting with polytetrafluoroethylene grafts for symptomatic subclavian artery stenosis or occlusion: a 20-year experience. J Vasc Surg. 2000;32:411-419.

Permission

Reprinted with permission from Mohr JP, Choi DW, Grotta JC, Weir B, Wolf PA (eds): STROKE: PATHOPHYSIOLOGY, DIAGNOSIS, AND MANAGEMENT (4th edition), pp. 1475-1520 (chapter 78), Copyright Elsevier 2004. Permission has been granted to reproduce this material in online electronic format for non-exclusive world English rights.

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