Stenting of the Great Vessels
Endovascular treatment of pathologies of the great vessels leading to the cerebrovasculature is becoming increasingly common. This is achieved by use of stents to reinforce an injured vessel lumen or expand the lumen in stenotic segments. Here we discuss the indication for stenting, types of stents available, and associated complications from these procedures and their management.
KeywordsCarotid artery stenting Vertebral artery stenting Subclavian artery stenting
Carotid artery stenting
Common carotid artery
Computed tomographic angiogram or angiography
Digital subtraction angiography
External carotid artery
Internal carotid artery
National Institutes of Health Stroke Scale
Checklist: Stenting of the Great Vessels
• Balloons (4, 6 mm diameter)
• Additional rotating hemostatic adapter and tubing
• Dyna-CT protocol
• Additional heparinized saline bag for line flush
• Staff pager numbers
– Anesthesia attending
• Pressure monitoring equipment for mean arterial pressure
• Endotracheal tube (if not under minimum alveolar concentration)
• Choice of balloons
• Choice of multiple stents
• Distal protection device
• Proximal protection device
• Recognized occlusion and inability to pass wire across lesion
• Recognized migration of stent
• Device failure
• Recognized vessel dissection
Initiate and Engage
• Determine if alternative access needed
• Anesthesia: vital signs
• Anesthesia: additional assistance
• Nurses and technologists to page for additional assistance
• Technicians to open additional stents, wires as requested
• Angioplasty stenotic segment
• Calcium channel blockers for vasospasm
• Stent deployment over dissection
• Additional imaging as needed
Complication Avoidance Flowchart
Check activated coagulation time is 2–3× baseline prior to lesion manipulation
Nontherapeautic antiplatelet agents is adequate
IV Gp IIb/IIIa inhibitors
Re-bolus antiplatelet medications
Preprocedure aspirin and Plavix effect assays, re-dose if needed
Distal protection device
Prolonged heparin, antiplatelet therapy
Hydrophilic guidewire for vessel selection. Judicious advancement of microcatheter
Groin closure failure
Closure device, dilation of entry tract, prolonged compression, checking the ACT prior to closure
Balloon occlusion, possible stenting, consider heparin reversal
Careful wire or catheter manipulation
The great vessels leading to the cerebrovascular circulation include the vertebral and carotid arteries, as well as their parent vessels, the subclavian and innominate arteries. Pathologies involving these vessels and requiring treatment may include atherosclerotic disease, spontaneous dissection, radiation injury, trauma, or iatrogenic injury from another procedure (surgical or endovascular).
Before delving into the nuances of great vessel stenting, interventionists should recognize that despite the “gold standard” role of digital subtraction angiography (DSA) in obtaining a diagnosis, the treatment of vascular disease does not come without risk. Therefore, an understanding of vascular anatomy and anatomical variants is paramount prior to any stenting of the great vessels. Complication avoidance must be advanced to the forefront of procedural planning because vessel perforation, iatrogenic stroke, and dissection are potential adverse outcomes any time the vasculature is accessed endovascularly. The reported rate of extracranial artery dissection from diagnostic DSA ranges from 0.07 to 0.3% and is higher for the vertebral artery than for the carotid artery [1, 2]. The mechanism of dissection is most commonly subintimal injection of contrast media. Most angiographically significant dissections remain clinically asymptomatic and resolve spontaneously with a 48 h course of anticoagulation therapy. Further treatment is with prolonged antiplatelet therapy or, in some instances, stenting of the dissection.
Carotid artery stenting (CAS) for atherosclerotic disease has been demonstrated to have long-term morbidity and mortality equivalent to that for carotid endarterectomy (CEA). The rate of perioperative stroke from cerebral embolism is reported to be higher with CAS than CEA [3, 4, 5, 6]. Associated procedural risk factors for CAS include carotid tortuosity, distal landing zone, concentric calcification, pseudo-occlusion, National Institutes of Health Stroke Scale (NIHSS) score > 10, femoral artery access difficulty, and renal disease.
Comparatively, a series of 87 brachiocephalic angioplasty and stent procedures included postprocedural complications consisting of brachial hematoma in 3.4% of cases, arteriovenous fistula requiring operative repair in 1.1%, brachial pseudoaneurysm requiring operative repair in 1.1%, femoral hematoma requiring operative repair in 1.1%, embolism to the brachial and left internal mammillary arteries each in 1.1%, congestive heart failure in 1.1%, renal failure in 1.1%, stent covering the left vertebral ostia in 2.3%, common carotid artery (CCA) dissection in 3.4%, and stroke in 2.3% .
Meanwhile, a series of 110 subclavian artery angioplasty and stenting procedures included eight failures due to atherosclerosis . In this series, seven patients had complications including three with groin hematoma, two with peripheral emboli, and two with amaurosis fugax.
Another center reported 48 consecutive stenting procedures for occlusive lesions of the subclavian and innominate arteries . They reported four complications: two cases of entry site hematomas, one of distal hand ischemia, and one cerebral ischemic event.
Patients with head and neck cancers who undergo surgical tumor resection and radiation to the neck are at risk for post-irradiated carotid blowout syndrome [10, 11]. In such patients, carotid pathology can be categorized based on risk of bleeding (threatened, impending, or active extravasation) or vessel irregularity on imaging (1, no disruption; 2, focal irregularity; 3, pseudoaneurysm; or 4, active extravasation) [10, 12]. Vessel reconstruction with stent placement or embolization is necessary to prevent extravasation in those at risk or to achieve hemostasis in those with active extravasation. Technical success of quelling active hemorrhage was achieved in all patients in both stenting and embolization groups. Complication rates of acute infarction for stenting and embolization are reported as 11.1% and 10.5%, respectively .
Trauma presents a unique challenge for great vessel stenting, both immediately with vessel integrity and on a delayed basis with the possibility of pseudoaneurysm development. A review of studies in the literature from 1995 to 2007 found reports of endovascular graft repair of the following great vessel injuries: 179 carotid artery, 13 vertebral artery, 7 innominate (brachiocephalic) artery or trunk, and 91 subclavian artery . Blunt carotid injury, at 137 cases, was by far the most common reported injury followed by penetrating 39 and iatrogenic 7. Blunt injury is often easy to overlook because of distracting injury (traumatic brain injury, spinal cord injury, or torso injury) or patient intoxication. A grading scale has been developed to classify blunt trauma: I, luminal irregularity or dissection of the vessel with <25% to 50% narrowing; II, luminal irregularity or dissection with >50% narrowing; III, pseudoaneurysm; IV, occlusion; and V, extravasation . Management involves a stepped treatment with anticoagulation as the basis for grade I injury, stenting for grades II and V, and coil embolization with stenting of grade III [13, 15, 16].
Patients with vertebral artery injuries most commonly present with tinnitus and pain, and the management involves conservative management with anticoagulation or intervention with vessel sacrifice via embolization. Dissection, although uncommon, may involve the basilar circulation and necessitate treatment via stenting or vessel sacrifice.
Subclavian and innominate injuries are also often quiescent in their presentation, though if symptomatic, upper extremity claudication is the most common finding. Again, conservative management is undertaken with antiplatelet agents or anticoagulants. However, there is debate concerning lesions that require treatment in the trauma population. The patients tend to be younger and more prone to being lost to follow-up. Thus, the choice between a bare-metal stent, requiring a longer course of anticoagulation, and a covered stent, which endothelializes more rapidly, is uncertain.
Great vessel stenting is fraught with potential perilous pitfalls at various stages throughout the intervention. Careful study of the preprocedural noninvasive vessel imaging (CTA/MRA) is paramount for success. An understanding of the arch type, location, and grade of vessel pathology and anomalous anatomy helps the intervention proceed without complication.
First, the creation of a vascular access site is required for endovascular angioplasty and stenting. At our institution, most interventional procedures are performed under conscious sedation. Femoral artery access is obtained >90% of the time. However, utilization of the smaller-caliber radial artery or brachial artery may be necessary for patients with poor femoral access or unfavorable aortic arch anatomy. Furthermore, in the cardiac literature, these approaches have been shown to have lower risk of access site bleeding and major complication [17, 18]. Also, upper limb approaches allow for direct access to subclavian or innominate pathology and may incur less risk of infection . We will refer to these approaches as retrograde throughout this chapter.
Vascular access is achieved either through surgical cutdown or percutaneous exposure and dilation. The latter confers easier closure via a closure device. Either access site may be closed with suture and adequate hemostasis. Following the introduction of a sheath (6–9 French [Fr]) into the access site, a vessel run (angiogram) is obtained to verify arterial placement and the absence of access site dissection. A total of 70 units/kg bodyweight of heparin is administered intravenously for systemic heparinization.
Then, the guidewire is advanced to the aortic arch, and a diagnostic catheter is advanced. We use a 0.035-inch hydrophilic glidewire over which we advance the diagnostic catheter to climb the arch. A diagnostic angiogram is obtained to better characterize the vessel, lesion pathology. Three-dimensional reconstructions of the angiogram may be utilized for a better understanding of anatomical considerations, such as branching arteries, true lumen, and pseudolumen. Reconstructions from these noninvasive imaging studies are compared with the physiological live view provided by the DSA, and any variations are taken into account.
Stenotic segments are often predilated with balloon angioplasty before deployment of the stent. This helps prevent poststent placement stenosis or premature separation of the balloon from the stent. Stent placement is undertaken with a balloon-expandable stent device or, alternatively, by a self-deploying/self-expanding stent.
After the CCA has been engaged with the guide catheter, we focus on crossing the lesion with a distal embolic protection filter. Several filters are available on the market; our preferences are the NAV6 (Abbott) and the EZ Filter (Boston Scientific). Once the filter is deployed, usually anterior to the C1 arch, close attention is given to the amount of time the filter is engaged in the distal ICA (filter time). Prestent deployment plasty versus poststent deployment plasty is a decision made by the surgeon. Selection of the stent is determined by the degree of vessel stenosis, length of the stenotic segment, consistency of the plaque, and the size of the vessel.
Additional stents may be necessary if the initial stent does not cover the entire length of the lesion, if there is persistent stenosis, or if persistent intraluminal thrombus is apparent on intravascular ultrasound (IVUS) imaging obtained after stent placement. If the proximal stent overhangs into the lumen of the parent vessel, we flare the stent open with a Flash Ostial Dual Balloon Angioplasty (Ostial Corp.) [20, 21]. Angiographic success is determined by visualization of brisk flow through the stenotic segment, with no evidence of thrombosis, endoleak, or dissection.
Pre-and posttreatment measurements of the blood pressure across the lesion demonstrate the physiological success of the treatment. A value of <5 mmHg for the pressure gradient across the stent is considered physiologically successful.
We routinely use IVUS imaging following stent placement. Unlike the two-dimensional perspective of DSA, IVUS allows for intra-arterial imaging of vessel anatomy. The IVUS findings can be compared to the luminal diameter of the CTA and the arterial wall pathology identified immediately. This proves especially useful for plaque thrombus and intraluminal thrombus that may cheese grate through a porous stent and require removal by aspiration or pinning against the vessel wall by the placement of a second stent.
Complications associated with stenting of the great vessels are uncommon. The most frequently encountered complications include access site hematoma, distal peripheral vascular embolism, central nervous system embolism, vessel intima dissection, and in-stent thrombosis .
The advent of percutaneous access site closure systems has significantly reduced both the time required for access site closure and the risk of an associated access site hematoma. These devices typically integrate suturing the vessel wall closed or placement of a hemostatic sealant over the access site. We utilize the Angio-Seal Vascular Closure Device (St. Jude Medical), in which a sealant is delivered into the extravascular space. If oozing of blood is noted after delivery of the sealant, pressure is held manually until hemostasis is achieved. The patient lays flat with a leg immobilizer for 6 h after the procedure. Dilation of the subcutaneous tissues above the vessel, after the initial skin incision is made at the beginning of the procedure, allows for efflux of hemorrhage out of the skin, rather than trapping it in the subcutaneous space.
Embolism to distal arteries of the peripheral or central nervous system can cause significant morbidity and even mortality. Careful selection of a stent of an open- or closed-cell design for the pathology being treated can minimize procedural embolic risk. Likewise, in-stent thrombosis can shower emboli or cause ischemic injury in distal vessels. To minimize embolic risk, we ensure the effectiveness of preprocedural antiplatelet therapy by checking an aspirin effect (platelet function) assay as well as a Plavix (Bristol-Myers Squibb/Sanofi Pharmaceuticals) effect (CYP2C19) assay. Further, for all interventional procedures, we administer a bolus of heparin intravenously and ensure that the activated coagulation time is 2 × −3× the baseline value. Finally, for carotid vessel disease, we utilize the aforementioned embolic protection techniques, either with a filter or with balloon occlusion of the ICA and aspiration of vessel debris (thrombus or particulate matter) following stent deployment . More recently and if the vessel pathology is favorable, we utilize both proximal and distal protection with the Mo.Ma proximal protection device, which allows for complete flow arrest. For use of the Mo.Ma device, a stiff wire is placed in the guidewire, which is then placed in the ECA, after which the device is advanced. Flow arrest is achieved by inflating the ECA occlusion balloon, followed by the proximal CCA balloon. The microguidewire and stent delivery system are then navigated across the stenotic segment of the vessel, and angioplasty and stenting are performed. The delivery system is removed and the ICA is aspirated to remove any embolic debris. The distal balloon and then the proximal balloon are deflated and circulation is resumed.
Access Site Hematoma
Hematoma at the access site can occur from inadequate hemostasis during access site closure. Management is with additional manual pressure to the vessel puncture site to ensure hemostasis. Placement of a 10 lb sandbag on the leg following hemostasis can prevent further swelling. We also perform frequent neurovascular checks of distal pulses during the next 24 h. Although an access site hematoma is typically self-limiting, an expanding hematoma may require surgical exploration and repair. The brachial artery access site has been reported as having a higher incidence of bleeding than the femoral artery access site, necessitating surgical repair . Radial artery access has been associated with a decreased risk of complications compared with femoral artery access .
Anterograde Access Difficulty
Following advancement of the guidewire and microcatheter to the aortic arch, the vessel with the lesion of interest is selected. Inability to advance the guidewire across the lesion may be encountered. If the guidewire cannot be advanced after several attempts have been made, retrograde access may be necessary. For carotid vessel disease, surgical exposure of the carotid artery distal to the lesion allows for retrograde passage of the guidewire. The brachial artery in the ipsilateral arm can be used for access in cases of subclavian or innominate vessel disease. The distance from the retrograde entry approach to the lesion is closer than that from the standard femoral artery access site, lessening the bending action through the wire when attempting to cross severely stenotic lesions.
Dissection seen during the procedure or detected on postprocedural imaging is managed conservatively. Continuation of anticoagulation for 24–48 h after the procedure and use of antiplatelet agents prevents asymptomatic lesions from showering emboli. For symptomatic or delayed symptomatic lesions, an increase in the antiplatelet agent or the addition of another antiplatelet or anticoagulant can prevent further progression. Likewise, the placement of a stent across the dissection prevents further embolic events. The “no-touch” technique, or avoidance of contact of the guidewire with the lesion, has been reported to decrease the risk of embolic complication . Complete occlusion of the subclavian artery or the inability to successfully advance a stent across that artery may warrant surgical transposition of the artery onto the carotid artery .
Distal vessel embolism is often undetected during the vessel stenting procedure. In the initial perioperative period, signs of peripheral ischemic changes include change in skin pallor, cold extremities, and loss of pulses if a larger, more proximal vessel is involved. Intracerebral artery embolus may go undetected or manifest as neurological changes such as amaurosis fugax, vision changes, visual field deficit, sensory changes, or motor weakness. Confirmatory diagnostic imaging via ultrasound imaging or CTA for peripheral vessels and CTA or magnetic resonance imaging with diffusion-weighted imaging or fluid-attenuation inversion recovery for cerebral vessels is necessary. Continuation of anticoagulation and antiplatelet agents prevents further propagation of embolic lesions. The administration of intravenous or intra-arterial tissue plasminogen activator for small vessel embolus or embolectomy for large-vessel occlusion allows for reperfusion.
In-stent thrombosis following a procedure can be a source of embolic events or ischemic perfusion injury. Prevention is undertaken via dual antiplatelet therapy. If thrombosis is detected clinically, diagnostic imaging is obtained via CTA or, preferably, DSA. The latter confers the ability to intervene immediately by revascularization with mechanical embolectomy. Conversion to surgical thromboendarterectomy may also be required. When diagnosis and treatment via thrombectomy or endarterectomy are performed in a timely fashion, clinical sequelae may be minimized.
Stenting of the great vessels is an increasingly common procedure for myriad indications. Careful procedural technique and use of preventative care allow for a diminished risk of complication.
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