A thorough history should be undertaken to determine symptom status. A full neurologic examination should then be performed by an individual certified in the NIH stroke scale.⁴⁴ A baseline carotid duplex, and ideally a computed tomography (CT) or magnetic resonance imaging (MRI) of the head, should be obtained. Once a severe stenosis is identified, clinical and anatomical features need to be considered and a decision regarding the best approach should be made in conjunction with the patient and family. We prefer premedication with aspirin and clopidogrel (at least 300 mg prior to intervention with sufficient time to achieve efficacy), and prehydration to minimize hypotension.

An arch aortography is performed under digital subtraction in the left anterior oblique (LAO) 30° to 40°. In this image the patient’s head should be turned toward the right and tilted upward. Arch aortography is important in identifying the aortic arch (whether it is type I, II, or III), which will impact endovascular approach and the selection of appropriate catheters in order to engage the carotid arteries (Figure 34.2).⁴⁵ Additionally, the takeoff of carotid and vertebral arteries should be examined. Other factors such as degree of calcification, presence of ostial common carotid disease, and involvement of the external carotid artery may affect the procedural approach and success (Figure 34.3). Subsequently, using appropriate diagnostic catheters such as 5F angled glide or JR4 for type I arch and Vitek, Simmons, or JB2 for more challenging anatomy, selective two-vessel (or four-vessel if indicated) cerebral angiography is performed. When performing selective angiography, the patient’s head should be secured to the table using carotid head gear. Images in the ipsilateral 30°-40° and lateral projections should be considered. Formal measurements must be made of the target lesion using NASCET criteria where distal reference is used beyond the carotid bulb. Intracranial cerebral angiography should be performed at baseline to rule out intracerebral arterial abnormalities and to establish the baseline arterial anatomy (Figure 34.4). Of particular importance are the lesion morphology and the presence of collateral flow, patency of the
circle of Willis, and the dominance of the intracerebral arterial supply (Figure 34.5).⁴⁶

A list of available equipment for carotid angioplasty and stenting is provided in Tables 34.4 and 34.5. The femoral approach is typically used, although the radial approach in selected cases is possible and may be preferred. Almost all devices are 6F compatible, allowing the use of an 80-cm-long nonkinkable sheath (i.e., Cook Shuttle, Destination, Pinnacle, or ArrowFlex sheaths). Unlike a 90-cm sheath, the 80-cm sheaths are compatible with standard bailout equipments that are typically 100 cm long. We typically use a telescoping system for carotid artery intervention. A 5F long diagnostic catheter is placed inside a sheath once the sheath has already been advanced to the mid descending aorta. The carotid artery of interest is engaged using the diagnostic catheter. Subsequently, the glide wire is advanced into the external carotid artery. Occasionally the wire is left in distal common carotid artery under close watch not to accidently touch the lesion with sheath manipulation. The sheath is advanced up to the ostium of the innominate or left carotid artery. The 5F diagnostic catheter is then advanced to the distal common carotid artery holding the wire and sheath in place. The sheath is then advanced over the diagnostic catheter (or slipcath) in the common carotid artery. The process may require several iterations of advancing catheters and removing slack from the system to achieve final positioning. Once a desired location is reached, the glide wire and catheter are slowly removed to prevent air trapping. One should never cross the carotid lesion with a 0.035 inch wire or catheters.

Certain safety precautions are necessary for CAS procedures: 1) catheters should always be bled back to avoid any air or cholesterol embolization. 2) anticoagulation and anti-platelet therapy should commence prior to advancing any catheters into the carotid system. 3) less time in the carotid system is better. Although one should be cautious and deliberate in the performance of these procedures, the number of complications increases with additional intraarterial time. 4) catheter advancement should always be over a wire, and larger catheters should be transitioned in a stepwise, coaxial fashion over smaller catheters. 5) only atraumatic guidewires should be advanced into the internal carotid artery to minimize the risk of spasm or dissection. 6) predilatation is recommended to confirm the ability to adequately dilate the stenosis. 7) the use of self-expanding (SE) stents is preferred for the carotid bifurcation and other compressible sites.⁴⁷,⁴⁸ Balloon-expandable (BE) stents should be used only for aorto-ostial carotid lesions and distal (e.g., intracranial) internal carotid artery lesions. Eighth, when encountering resistance during advancement of balloons or stent delivery systems, removal and redilation with lower profile devices is appropriate. If an SE stent will not easily cross a predilated lesion, it should not be forced. Ninth, careful periprocedural hemodynamic monitoring is essential. Manipulation within the area of the carotid sinus can cause both acute and prolonged hypotension and bradycardia,⁴⁹ requiring fluid resuscitation, atropine or α-adrenergic agents. Pacing is rarely needed but should be readily available.⁵⁰ Postprocedure hypertension must also be avoided, so as to minimize the chances of hyperperfusion syndrome, a potentially devastating entity that is occasionally seen following revascularization, particularly in elderly patients with previous near-occlusion and underperfused cerebral circulation. Tenth, postdilation should be performed to relatively low or nominal pressure. It is not necessary to eliminate completely the stenosis to achieve an excellent result.⁵¹ Indeed, attempts to reduce the stenosis to 0% relative to the reference segment may lead to distal embolization, dissection, or resistant hypotension relating to carotid body stimulation or compression.⁵¹

If not all, the majority of stents used for carotid disease are nitinol SE stents; however, in rare cases we have used covered stents. Whether open or closed-cell design will have an important clinical significance is not well known. Newer hybrid stents, where the middle of stent is closed cell but ends are open are being developed.⁵²,⁵³ In general, the closed-cell design stents are more rigid (Table 34.5).

The combination of carotid stenting with distal protection has revolutionized carotid intervention (Table 34.4). The first randomized trial demonstrating outstanding results of carotid stenting with distal protection was the SAPPHIRE³¹ trial and this was quickly followed by several registries like ARCHeR⁵⁴ and SECuRITY.⁵⁵ In general, the available cerebral protection devices function either by filtering atheromatous debris out of the flowing blood distal to the lesion or by occluding antegrade flow proximal or distal to the lesion to allow removal of atheromatous debris. Each design has relative merits and potential disadvantages. The filtering devices allow for continuous visualization for precise stent placement and allow cerebral perfusion as antegrade blood flow is unobstructed. The current filter pore size ranges from 80 to 150 microns, raising the question of what diameter of atheromatous debris is required to cause neurologic sequelae. The occluding devices, by design, limit visualization and, in the absence of adequate collateral circulation, may result in prolonged cerebral ischemia. Retrograde embolization to the aortic arch may occur if aggressive injection is performed. However, occluding devices offer the theoretical advantage of protecting against a wider range of particulate sizes. The optimal protection device or combination of protection device and stent remains unclear and is a source of intense clinical investigation. However, early data indicate that proximal protection may have some advantage over distal embolic devices.⁵⁶

Similar to carotid and vertebral disease as described above, a full history and physical exam is the critical component of great vessel intervention. Understanding the patient’s symptoms and whether they relate to great vessel stenosis or occlusion are important to prevent inappropriate intervention. The presence of bruits on physical exam is important, but their lack does not negate the likelihood of great vessel disease. In our clinic the first test to confirm great vessel stenosis or occlusion is a noninvasive duplex ultrasound evaluation, with determination of the direction of flow in the vertebral arteries (antegrade or retrograde, the latter indicating the presence of a steal phenomenon) and documentation of associated carotid disease. If there is a clinical suggestion of vasculitis, an erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) should be measured. Frequently, computed tomography angiography (CTA) of the arch and great vessels is performed to help with the interventional approach. Once a decision regarding intervention has been made, premedication with aspirin is standard, with optional addition of clopidogrel.⁶⁹ There are currently no data regarding duration of clopidogrel therapy in this setting but in general, we treat all individuals with dual antiplatelet therapy for at least 1 month followed by life-long aspirin.