Subclavian steal phenomenon (or syndrome) originates from severe stenosis or occlusion of the proximal subclavian artery resulting in the reversal of blood flow in the ipsilateral vertebral artery (VA) to perfuse the limb. Blood flows retrogradely from the brain (via blood from the contralateral VA or the circle of Willis) to the limb instead of anterogradely from the heart directly to the limb as a result of a hemodynamically significant proximal subclavian stenosis or occlusion. Symptoms of subclavian steal include those associated with vertebrobasilar insufficiency or upper extremity claudication, such as cranial nerve deficits, syncope or unexplained loss of consciousness, gait and balance disturbances, ipsilateral arm pain, or a change in pallor.
Noninvasive imaging modalities are useful in the initial evaluation and establishment of the diagnosis of subclavian steal. Computed tomography (CT) angiography or magnetic resonance (MR) angiography is useful for further anatomical understanding of the location of the lesion, lesion size, the location and orientation of adjacent vessels, and particularly for treatment planning. In addition, both CT-based and MR-based imaging provide information about the character of the lesion. Heavy concentric calcification, which is better seen on CT, or hypointensity on CT indicate a necrotic lipid rich core, which may impact the treatment strategy. On MR imaging, evidence of plaque hemorrhage may suggest potential fragility of the lesion and a higher risk for distal embolization. Ultrasound imaging also provides lesion information that helps treatment planning.
Treatment of symptomatic subclavian steal from subclavian stenosis may be performed via open, endovascular, or a combined/hybrid approach. In this chapter, we focus on endovascular treatment, which involves percutaneous balloon angioplasty and/or subclavian stent placement, the associated complications, and prevention of these complications. Patients with symptoms of subclavian steal syndrome and findings of stenosis on imaging are considered candidates for endovascular revascularization.
Meticulous review of the noninvasive vessel images aids in planning and ultimately implementing a successful procedure. This includes evaluation of the aortic arch type, identification of the stenotic lesion including its location and grade, and identification of the location and orientation of associated proximal and/or distal branching vessels, most importantly the VA.
This preprocedure plan is the key to a successful procedure and avoidance of complications. The considerations include the relationship of the lesion with the VA ostium. This is because angioplasty and stenting may result in plaque rupture, protrusion, and embolization up the VA and into the brain with devastating consequences. Although the lesion may be more proximal to the VA ostium, findings of severe plaque hemorrhage on MR imaging, severe hypoechoicity on ultrasound, or hypointensity on CT suggest high embolic potential. In these cases, a strategy to prevent VA embolization is critical. Arch anatomy also plays a key role. If the access is difficult in a severe type III arch, direct brachial access may be a better solution. Keep in mind that most balloon-mounted stents with diameters of 7 mm or greater require a 7- or 8-French sheath and that size is often too large for radial access. When using embolic protection of the VA, access is best done through a radial approach. In these cases, a second contemporary femoral access site provides a stent delivery route by means of the aorta.
We administer dual antiplatelet agents (aspirin and clopidogrel) 7 days prior to intervention. A platelet assay for clopidogrel and aspirin is obtained and evaluated to ensure efficacy prior to the procedure. If there is an inadequate response, we switch to a more effective antiplatelet agent. As noted previously, a precise strategy based on noninvasive imaging provides rationale for the access site. For this chapter, we will describe a high embolic risk proximal subclavian symptomatic plaque. For the majority of subclavian lesions, vertebral protection is not necessary, because retrograde flow is typically protective for embolization into the cerebral circulation. To achieve distal protection from embolus traveling to the neurovascular circulation, we commonly use dual access through both radial and femoral sites ( Fig. 49.1 ). Dual access allows manipulation of the subclavian artery stenotic lesion through one catheter and protection of the VA by the placement of a balloon through the other catheter ( Tip Box 49.1 ). Placement of the balloon in the VA ostium also allows precise marking and, therefore, avoidance of inadvertent coverage with the subclavian stent.
Dual access is not necessary; however, it can confer increased distal protection to the neurovasculature.
Following arterial access with a micropuncture kit, a sheath (6–9 French) is introduced at the femoral (radial or brachial) access site. Typically, we use a 0.035″ hydrophilic Glidewire (Terumo Interventional Systems, Somerset, New Jersey) navigated to the aortic arch. A diagnostic catheter is then advanced over the Glidewire. For interventional procedures, we routinely administer 70 units/kg of bodyweight of heparin intravenously aimed at a goal of activated clotting time of >250 seconds. In either case, the heparin is administered once access is achieved.
An angiogram of the subclavian artery from the aortic arch is performed that displays the anatomy and the pathological lesion. If needed, a 5-French pigtail catheter can be used for aortic arch angiography using an injector to opacify optimally all arch great vessels. Measurements of the stenotic segment, including the nominal vessel on either end of the stenotic segment, are obtained; and branching vessel points, particularly the VA, are noted and taken into consideration when selecting the endovascular stent or stent-angioplasty balloon endovascular construct.
Next, the stenotic segment is crossed with a 5-French diagnostic catheter, if possible. Sometimes the 0.035″ Glidewire will cross the lesion but the catheter will not. Therefore, we always use a 0.035″ exchange wire to cross and to exchange the diagnostic catheter out for a 0.035″ Quick-Cross catheter (Spectranetics, Colorado Springs, Colorado) to cross the lesion. The nose cone of the Quick-Cross catheter is much smaller than a 5-French diagnostic catheter, and that helps with crossing the lesion. If the lesion is safely crossed with the wire and catheter, especially if the lesion is of high embolic risk, we prefer to use a primary balloon-mounted stent with VA protection. The delivery sheath should be advanced past the lesion to prevent dislodgment of the stent graft in the stenosis and then withdrawn over the stent graft once it is in place. This may require use of a more supportive wire, such as an Amplatz (Cook Medical, Bloomington, Indiana) or an InQwire (Merit Medical, South Jordan, Utah). However, if the lesion is more calcified, predilation with an undersized balloon may be required to cross the lesion with the aforementioned construct. The sheath can then be advanced over the balloon, as it is gradually deflated, to pass the lesion before placing the stent graft.
We have a strong preference for covered balloon-expandable stents for the subclavian artery. This artery is in a nonmobile segment of the body and therefore does not require a self-expanding stent such as would be required for the cervical carotid artery where a balloon-expandable stent will remain deformed once it has been deformed by motion or external deformation. This is because the stent graft covers the plaque and avoids intraprocedural as well as delayed plaque prolapse and distal embolization. Each stent has distinct benefits and disadvantages; however, we prefer the iCast balloon-expandable covered stent (Atrium Medical, Hudson, New Hampshire) or the VIABAHN balloon-expandable covered stent or the VBX (Gore, Newark, Delaware) for subclavian stenting. The key element and frequently the limiting factor are optimal stent size (length) to cover the lesion without obstructing the vertebral ostium or overhanging into the aorta.
Subsequent placement of additional stents may become necessary if the lesion is not covered by the initial stent. The most frequent cause for this is “watermelon-seeding” of the stent from the balloon across a high-grade heavily calcified stenosis. In such cases, it makes sense to protect the vertebral ostium with a balloon and perform predilation of the lesion. If stenosis remains following deployment of the initial stent, the ideal procedure is to bring in a higher atmospheric pressure tolerance balloon for additional angioplasty. If the lesion is longer than the initial stent, it may require tandem stent placement for additional length. However, if we feel the stent has not expanded adequately, we prefer to use high atmosphere rated balloons, which can be inflated to 24 atmospheres. For constructs with proximal overhang in the lumen of the parent vessel, we flare the proximal stent open. This is achieved with a Flash Ostial Dual-Balloon Angioplasty Catheter (Ostial Corp., Santa Clara, California). The dual balloon design of the Flash Ostial System incorporates two diameters: one diameter for dilation within the stent and the larger diameter for dilation within the parent vessel at the proximal end of the stent. Expanding the balloon causes the proximal end of the stent to dilate, or flare, and cover the ostia of the vessel in which the stenotic lesion is located. The biggest advantage of this is that re-access becomes easier because of the flared ends. This system does operate over a 0.014″ wire and therefore requires prior exchange of the 0.035″ wire to a 0.014″ wire in order to flare the end of the flash balloon.
In high-risk lesions distal protection of the VA is best done by a single- or double-lumen balloon occluding the VA ostium. Placing a filter can be problematic because the filter can snag in the subclavian stent, and therefore we do not use distal embolic filters in the VA during subclavian stenting. The balloon system can be delivered through a 5- or 6-French guide catheter through a radial approach over a 0.014″ microwire and inflated manually to assure occlusion of the ostium. This approach allows visualization of the vertebral ostium during deployment of the subclavian stent avoiding potential occlusion of the VA. However, protection of the VA is probably unnecessary in most patients if the lesion is not high risk and there is truly reversal of flow in the VA, because this reversal of flow tends to direct any embolic material to the arm, rather than the brain.
For cases where we are unable to cross the lesion in an anterograde fashion (from the aorta), we have two choices. First, we can establish brachial access and cross the lesion in a retrograde fashion with a wire and then place the stent from the brachial access site. The second option is to snare a wire from below once the lesion is crossed from the arm access site, typically with a 0.035″ wire from the distal (radial artery) access site. We then snare the 0.035″ wire with a 35-mm Amplatz GooseNeck snare (Medtronic, Minneapolis, Minnesota) delivered by way of a transfemoral approach through an appropriately sized delivery sheath, typically 8-French. Once snared, we pull the femoral sheath across the lesion in a “floss” technique ( Fig. 49.2 ). This allows for balloon predilation of the stenotic lesion as well as the advancement of catheters proximal and distal to the lesion. We then deploy a balloon from the radial side into the VA while the stent is deployed from the femoral side. This prevents distal embolic particles from flowing into the cerebrovascular circulation during lesion manipulation and stent deployment. Although the cerebrovascular circulation is protected, the distal upper extremity remains at risk. Embolic complications to the limbs are commonly silent and considered rare. Compared with ischemic emboli in the cerebrovascular circulation that may affect neurological function, the effect of small emboli would go unnoticed in the limbs. Larger emboli may affect distal perfusion of critical (eloquent) vascular territories and result in the need for further treatment via endovascular or open surgical embolectomy.