Introduction
Interventionalists are especially cautious with carotid artery stenting (CAS) because complications can lead to devastating and permanent neurological sequelae, even death. Preparation for CAS can often seem excessive; however, careful and detailed planning is the key to circumvent unwanted outcomes. CAS should be used for appropriately selected patients. Knowing the fundamentals of the procedure and some tricks to adapt the procedure for the patient’s anatomy and disease are important to avoid complications.
Ironically, some of the initial studies evaluating CAS were performed using stenting to treat intimal flap complications sustained during carotid angioplasty for stenosis. At the time, the bailout seemed an appropriate option given the severity of the stenosis and the instability of the lesion. Unfortunately, in the earliest stages of CAS, stents and delivery systems were faulty, an appropriate antithrombotic regimen was not established, and treating physician technical competence was not ensured. Both procedural difficulties and unwanted complications led to the premature abandonment of CAS. Collaboration among neurologists, cardiologists, vascular surgeons, neurosurgeons, and interventional radiologists is crucial to select appropriate patients. The development of self-expanding stents, embolic protection devices, and a regimen of dual antiplatelet therapy led to the revival of CAS.
CAS has since gone from being the believed replacement for carotid endarterectomy (CEA), to the vascular procedure subject to intense scrutiny with more than 6500 patients studied in six large randomized clinical trials. Appropriate patient selection for surgical intervention and determining proper surgical intervention to treat carotid stenosis are goals of the currently ongoing Carotid Revascularization and Medical Management for Asymptomatic Carotid Stenosis Trial (CREST-2) trial. Today, practitioners offering CAS do so cautiously for a select population with understanding of the complications and risks and benefits profile.
The number and sequelae of the complications associated with CAS have been highlighted with multiple clinical trials but how to avoid and treat these complications has not received as much attention. This chapter looks at the some of the most commonly encountered complications associated with CAS and methods for complication avoidance and management.
Procedural Planning
Simple steps can be taken prior to the procedure to help reduce the complication rate associated with CAS. A thorough history should include a detailed account of any stroke history, in addition to vascular and cardiac history. Prior use of anticoagulation or antiplatelet therapy should be noted, as well as contraindications for such therapy. Patients should have a well-documented neurologic examination performed prior to the procedure. Physical examination should also include a pulse examination of potential access sites. Antiplatelet therapy with clopidogrel should be started 5 days prior to the procedure. Patients should receive a loading dose on the day of the procedure prior to CAS if they are not already on medication. Imaging studies including a bilateral carotid arterial duplex, computed tomography angiography (CTA), or magnetic resonance angiography (MRA) of the chest, neck, and brain should be performed to assess the contralateral internal carotid artery (ICA), vertebral arteries, aortic arch, the Circle of Willis, and other pertinent anatomy. The surgical approach should be established and the appropriate length sheaths, catheters, and wires should be available. Three-dimensional imaging reconstructions can help clarify the appropriate stent, diameter, and length. The interventionalist should ensure that appropriate devices are available for the procedure. The importance of procedural planning cannot be emphasized enough.
Access Difficulties
Access difficulty can present in extremely dilated aortic arches, aortic arches with severe atheroma with unrecognized ostial lesions of the common carotid or brachiocephalic arteries, and in those patients with tortuous vessels. An angled Glide catheter (Terumo, Somerset, New Jersey) and 0.035′′ Glidewire (Terumo, Somerset, New Jersey) are generally the initial choices to cannulate the innominate, right common, or left common carotid arteries. In difficult arch anatomy, particularly bovine arches, a reverse curve catheter such as a JB2 (Terumo Somerset, New Jersey), Vitek (Cook Medical, Bloomington, Indiana), or Simmons-1 (Terumo, Somerset, New Jersey) can be used (or SIM select or SIM2 [Cook Medical]) ( Fig. 44.1 ).
In the case of extremely dilated aortic arches, a sidewinder curved catheter such as a Simmons-3 (Terumo Somerset, New Jersey) can be used to access the brachiocephalic artery ( Fig. 44.2 ). With cannulating the right common carotid artery, the stabilizing introducer sheath should not be too close to the aortic arch because this will decrease the maneuverability of the catheter used to access the right ostium.
Tortuosity in the common carotid artery can be a hindrance to sheath or guide catheter placement. Access should be accomplished by placing a stiff wire, such as an Amplatz (Boston Scientific Marlborough, Massachusetts), in the external carotid artery as far as possible. The tip of the sheath or guide catheter should be secured in the common carotid artery approximately 1 cm below the bifurcation without advancing the introducer into the bifurcation. When the lesion of interest is in the distal common carotid or the external carotid artery is occluded, an Amplatz with a J tip and short (3 cm) floppy segment can be used. Another option would be to use a telescoping guiding sheath over a slip catheter (JB2, Simmons-1, or Vitek) over a stiff Glidewire (Terumo Somerset, New Jersey) to facilitate positioning of the sheath. When maneuvering the introducer sheath over the catheter to the carotid stenosis, if the sheath does not track easily over the catheter, the catheter should be removed and replaced with the sheath’s inner introducer. The catheter can then be replaced once the sheath is moved into the appropriate position. Common carotid artery (CCA) tortuosity or a stenosis difficult to traverse can be crossed with a Glidewire and 5-French catheter. Be cognizant that when placing the introducer sheath in a long tortuous CCA, this might result in bifurcation displacement and kinking of the vessel complicating stenting. Advancement of the guide catheter or sheath should be done under fluoroscopic guidance or roadmap guidance ( Fig. 44.3 ). ICA tortuosity can also be overcome by using a 0.014′′ “buddy” guidewire to assist with straightening out the vessel and the use of a V18 wire to help aid guide catheter sturdiness.
Some anatomic limitations can impede the use of transfemoral access for CAS. Not only can diseased aortic arches and tortuous arch vessels preclude using transfemoral access, aortoiliac and femoral occlusive disease, previous vascular interventions in the groin, and obesity can make CAS with standard transfemoral access impossible. Older individuals (>70 years) have inferior outcomes with transfemoral CAS compared with CEA, probably because of the atheromatous burden leading to embolic events. Careful assessment of the aortic arch is important in the elderly population and may lead to alteration in access site. In such cases, transcervical access might be preferred. In a large meta-analysis of procedures using transcervical access, Sfyroeras et al. showed a technical success rate of 96% for 579 procedures performed. The incidence of transient ischemic attack (TIA), stroke, and death was 2.7%, 1.1%, and 0.41%, respectively. The transcervical approach was analyzed using both flow reversal with an arteriovenous shunt and no flow reversal for stroke incidence, and no difference was noted between the two groups.
The transcervical approach avoids having to navigate through potential atheromatous burden in the iliac arteries, aorta, and arch vessels and dislodging embolizing debris. Flow reversal creates a large arteriovenous shunt between the common carotid artery and ipsilateral jugular vein redirecting blood flow away from the internal carotid artery. The procedure can in most patients be done under local anesthetic. Full details of the transcervical approach with flow reversal are described elsewhere.
Alternatively, transradial approaches can be used to access the carotid artery if the femoral approach is not feasible. From the right side, this negates the need to traverse the aortic arch ( Fig. 44.4 ).
Crossing Preocclusive Stenotic Lesions
Wire selection is of paramount importance when crossing the stenosis for CAS. Wires larger than 0.018′′ should generally be avoided crossing the stenosis to decrease risk of embolization. If a smaller wire is being used to cross the stenosis, once the lesion is crossed, the wire should be exchanged for a 0.018′′ wire to ensure stability and easier advancement of the device required during stenting. Wire exchanges require repeat angiography because the wire stiffness can change the anatomy and presumed stenosis location. It is important to visualize the distal placement of the wire to avoid intracranial location with increased risk of injury to the vessel. The wire needs to be advanced distally enough to allow placement of the filter or protection device.
Difficulty placing embolic protection devices distal to the stenosis is more commonly encountered with filter devices as opposed to balloon embolic protection devices. The crossing profiles for filter devices with U.S. Food and Drug Administration (FDA) approval for use in CAS are 3.4–3.9 French as opposed to balloon devices, which are closer to 3 French. Filter embolic protection devices also have an abrupt change in stiffness between the filter and wire, which can limit trackability. Such difficulties are usually circumvented with predilation of the stenosis. In a study assessing technical difficulties crossing stenotic lesions, Powell et al. reported inability to cross the lesion in 29% of CAS cases using filter embolic protection devices. In 5% of those CAS cases, predilation still did not facilitate filter embolic protection devices to cross the stenosis. In all of these cases, CAS was successfully performed with balloon embolic protection devices. None of the CAS stenoses originally treated with balloon embolic protection devices was unable to be crossed or required predilation. This suggests that a tight lesion might be better treated with a balloon embolic protection as opposed to a filter device for distal protection, especially if the stenosis is narrower than 3.4 French. The MoMa device (Medtronic, Minneapolis, Minnesota) and balloon guide can allow flow reversal state instead of filter protection.
Predilation of stenoses should be performed selectively given the increased risk of periprocedural neurologic events. Nominal pressure should be used unless the lesion is heavily calcified and expected to recoil. Predilation time should be limited to a few seconds if the balloon attains its full shape quickly. Predilation time should only be prolonged (<120 seconds) if the balloon attains its full shape slowly. Preocclusive lesions might require serial predilation with a 1.5-mm or 2-mm balloon, followed by a 4-mm balloon. If the stent to be used does not pass easily through the stenosis after predilation with a 4-mm balloon, a 5-mm balloon should be used for additional predilation. Each additional predilation should be followed with an arteriogram. Only heavily calcified lesions should be postdilated and only if residual stenosis is detected by angiography or intravascular ultrasound (IVUS).
In tight lesions or severe tortuosity, embolic protection devices that are not attached to a wire and advanced independently over a wire might be preferable. Balloon embolic protection devices that advance independently over a wire, such as the GuardWire (Medtronic Minneapolis, Minnesota), have increased flexibility through highly stenotic lesion and tortuous anatomy.
Problems Associated with Embolic Protection
It is important to evaluate distal ICA anatomy because deployment of embolic protection devices cannot be done within torturous segments (see Chapter 45 ). Filter embolic protection devices must be deployed in straight portions of the distal ICA so that there is adequate apposition to the vessel wall. There also needs to be adequate distance between the lesion and the embolic protection device to allow stent deployment. Balloon embolic protection devices are longer and require a greater distance from the lesion and do not allow protection after balloon deflation. If this distance is inadequate, another form of embolic protection should be used. The position of the embolic protection device must also be carefully monitored at all times. Any prolapse of the guide can allow the filter to cross the lesion while deployed.
If there is an excessive amount of embolic debris caught by the filter, a stagnant column of blood proximal to the filter can result on completion angiography. Filter clogging is an uncommon complication but should be identified with a completion angiogram, especially if poststenting balloon dilation is to be performed. Aspiration can be performed via a catheter with side port, such as an Export AP aspiration catheter (Medtronic, Minneapolis, Minnesota) (or expressway aspiration catheter), placed proximally to the stent. Nitroglycerin can also be given after aspiration in such cases to help restore flow.
Inability to remove the filter embolic protection device is also an infrequent complication that most commonly occurs because of the inability of the capture catheter to cross the stent. This can occur especially if the stent final position is angled or if the embolic protection device wire is too close to the stent. Both can hinder the advancement of the retrieval catheter. Techniques to enable filter capture include repositioning the patient’s head to straighten out the stent, external neck compression with swallowing, and advancing the stabilizing sheath into the proximal stent.
Transient Intraoperative Neurologic Compromise
Transient intraoperative neurologic compromise is a dreaded complication that can be monitored by performing the procedure with the patient awake. The patient can be asked to perform tasks, such as squeezing a squeaky toy upon command. In this way, neurologic compromise can be immediately recognized. Powell et al. reported transient neurologic compromise in 10% of CAS patients treated with balloon embolic protection occurring within several minutes of balloon inflation. Neurologic symptoms were described as global. Eight of 10 patients with neurologic symptoms were successfully treated with stenting after the mean arterial pressure was increased by 20–25 mmHg for balloon insufflation for embolic protection, suggesting that the issue was one of global hypoperfusion rather than an embolic event. The remaining two patients did not tolerate balloon inflation and either required the use of a filter embolic protection device or carotid endarterectomy. Being prepared with alternative modes of embolic protection might be beneficial if the patient cannot tolerate temporary occlusion of flow.
If balloon occlusion with a balloon embolic protection device results in transient neurologic intolerance, it can often be overcome with ischemic preconditioning. If there is immediate intolerance to balloon inflation, the balloon is rapidly deflated when symptoms occur. Once neurologic function returns to normal, the balloon embolic protection is re-inflated and CAS is completed. In the experience of Chaer et al. using balloon occlusion preconditioning, symptoms completely resolved in 4–20 minutes and successful CAS was performed. Balloon deflation for neurologic intolerance and hemodynamic instability should be preceded by aspiration of embolic material.
Intraoperative Hemodynamic Instability
A common physiologic response to balloon angioplasty of the carotid artery is bradycardia occurring in 27%–37% of CAS cases. Hypotension is also common with the reported incidence in CAS ranging from 14% to 28%. In the carotid sinus, adventitial baroreceptors are triggered with expansion leading to hemodynamic lability. Multiple researchers found that stenosis localized to the carotid bulb was an independent risk factor of procedural hemodynamic instability and required drug intervention. Moreover, the aggressiveness of dilation measured as the change in stenosis severity before and after CAS has been attributed to procedural hypotension and bradycardia.
Prolonged hypotension is also not uncommon. Defined by Gökçal et al. as a blood pressure of less than 90 mmHg for greater than 1 hour, prolonged hypotension occurred in 16.8% of patients undergoing carotid artery stenting. More than 70% of those patients were reported to have a contralateral stenosis. Interestingly, prolonged intraoperative hypotension was recognized more frequently in patients who did not have a diagnosis of diabetes mellitus. The diagnosis of diabetes mellitus and history of long-term smoking were found to be protective. Both comorbid conditions are believed to be protective because they impair the carotid baroreceptor response, augmenting sympathetic tone resulting in increased heart rate and blood pressure.
Hemodynamic instability during the peri-operative period in CAS patients was also evaluated by Ulley et al. They defined significant hemodynamic instability as a systolic blood pressure greater than 160 mmHg or less than 90 mmHg, or heart rate less than 60 bpm lasting more than 1 h. Significant hemodynamic instability occurred in 63% of the CAS procedures performed. A predictor of hemodynamic instability during the procedure was a history of recent stroke (odds ration [OR] 5.24, 95% confidence interval [CI] 1.28–21.51, P=0.02). The proposed mechanism by which recent stroke results in hemodynamic instability is impaired parasympathetic and sympathetic cardiovascular regulation that cannot make the autonomic adjustments in heart rate and vascular tone for compensation. Moreover, patients with CAS hemodynamic instability were more likely to experience a periprocedural stroke compared with other patients undergoing carotid stenting (8% versus 1%, P=0.03). Prolonged hypotension following CAS was associated with an increased risk of periprocedural morbidity, including minor strokes (16% versus 3%, P=0.003). The detrimental effects of intraoperative hypotension were also noted with higher rates of mortality at follow-up at 30 days and 6 months (4% versus 1%, P=0.05 and 20% versus 4.3%, P=0.02, respectively).
Interventionalists and treating anesthesiologists should be prepared to treat CAS bradycardia and hypotension. Prophylactic intravenous administration of atropine (0.5–1.0 mg) or glycopyrrolate (0.4 mg) approximately 1 min prior to balloon inflation in the carotid artery is recommended for most adults undergoing CAS to mitigate the vagal response with carotid baroreceptor stretching. Pacemaker capability should be immediately available. Patients with prior ipsilateral CEA undergoing CAS are unlikely to develop the same bradycardic response, and therefore do not require prophylactic atropine. Additional intravenous atropine can be administered to patients with bradycardia or asystole despite prophylactic dosing.
Initial treatment of hypotension should involve volume resuscitation with 500 mL increments up to 2000 mL. Asking the awake patient to cough forcefully can increase systolic pressures by providing autocardiac compression. Dopamine 3 µg/kg/min titrated to a maximum of 10 µg/kg/min can be used to treat hypotension refractory to volume resuscitation. In the absence of bradycardia, hypotension can also be treated with phenylephrine at 50–300 µg/min. Persistent hypertension can be treated with nicardipine 5–15 mg/h. The treatment goal should be a mean arterial pressure of 75–85 mmHg with systolic blood pressure 90–150 mmHg.
Carotid Artery Spasm
The ICA is very sensitive to intraluminal instrumentation and manipulation. A gentle approach with insertion of the wire into the carotid bifurcation and the use of soft-tipped filter wires can, in some cases, help avoid carotid artery spasm. When a carotid artery spasm occurs in the presence of a contralateral ICA occlusion or an incomplete Circle of Willis, the results can be disastrous. Carotid artery spasm has been reported to occur in 4.0%–26.3% of CAS procedures. The vasospasm in the setting of CAS most frequently occurs in the distal ICA and normally resolves with wire and filter removal.
Most of our understanding of vasospasm relates to the compensatory mechanism encountered in the setting of subarachnoid hemorrhage. The proposed mechanism of carotid artery spasm in the setting of distal protection devices suggests that the outward radial force causes endothelial irritation and possibly injury as it shifts during the procedure. First generation embolic protection devices were more likely to cause vasospasm in comparison with newer devices. The frequency of vasospasm has been reported to be more common when using embolic protection filters as opposed to embolic protection balloons (12% versus 2%, P=0.002).
In a retrospective review of a single center 12-year experience with carotid artery stenting, Fanelli et al. reported ICA vasospasm in 19.4% (123 of 635) of filter-protected CAS procedures. Angiograms performed prior to filter removal in 33 (27%) patients with carotid artery spasm revealed no flow in the vessel distal to the spasm. A total of two minor strokes and six TIAs occurred in the group with carotid artery spasm for a 6.5% neurologic event rate. The neurologic event rate in the population of patients with carotid artery spasm compared with those patients without was similar (P=0.08). The vasospasm was described as self-limiting in 41 (33%) patients, resolving on its own in approximately 15 minutes with filter removal. The rest of the patients required intra-arterial injection of nitroglycerin for carotid artery spasm resolution. The researchers attributed the vasospasm to a specific stiffer embolic protection device.
If the spasm is not resolved with removal of the wire and filter, 100–400 µg of nitroglycerin in 100-µg aliquots can be infused at the carotid artery bifurcation to help with spasm resolution. Papaverine and calcium channel blockers can also be used as alternative agents. Papaverine should not be diluted in heparinized solution because precipitation can occur. A total of 300 mg papaverine (100 mL of 0.3% solution) can be administered to the affected vascular territory at a rate of 3 mL/min to relieve vasospasm. An intra-arterial bolus of 1–2 mg of verapamil can also relieve vasospasm within 5–10 minutes with little to no effect on the patient’s hemodynamics ( Fig. 44.5 ).
