Relevant Anatomy

The paired internal carotid arteries (ICAs) are the major conduits for blood flow to the brain. An understanding of their anatomy, including the origin of the common carotid arteries (CCAs) in the aortic arch, is fundamental in assessing the feasibility of any endovascular intervention.

The most proximal large vessel off the aortic arch is the brachiocephalic (or innominate) artery, which divides into the right CCA and the right subclavian artery. The left CCA is the next major branch off the aortic arch, followed by the left subclavian artery. Both the right and left CCAs bifurcate into internal and external carotid arteries at the level of the mid to upper cervical region. The CCA bifurcation and most proximal cervical ICA segment are the most common sites for carotid stenosis.

A very important consideration is the relative position of the origin of the great vessels (brachiocephalic, left CCA, and left subclavian arteries) and the apex of the aortic arch itself. As people age, the aortic arch becomes elongated, calcified, and less compliant, causing the takeoff of the brachiocephalic artery to be more proximal relative to the apex of the arch itself. A classification system has been developed to describe this relationship ( Fig. 1 ). A so-called type I arch is one in which all 3 great vessels arise from the apex of the arch; A type II arch is one in which the takeoff of the brachiocephalic artery is between the 2 horizontal planes delineated by the apices of the outer and inner curves of the aortic arch, at the level of the arch apex; a type III arch is one in which the origin of the brachiocephalic artery lies below the horizontal plane delineated by the apex of the inner curve of the aortic arch at the level of the arch apex. This aortic arch classification is important because it correlates with increasing difficulty in catheterizing the great vessels and an increase in risk of complications during endovascular interventions. Another important anatomic aspect to keep in mind is the development of progressive great vessel elongation with aging, which leads to increased vessel tortuosity, mostly at the proximal segments of these vessels. This factor creates great difficulty in obtaining stable endovascular access and is also related to increased risk of embolic complications.

Aortic arch classification according to the takeoff of the brachiocephalic artery in relationship to the apex of the arch. Types I, II, and III reflect a progressively more difficult arch to navigate, with type III being most difficult (see text).

( From Eller JL, Siddiqui AH. Stent design choice based on anatomy (chapter 39). In: Gonzalez F, et al, editors. Neurointerventional surgery, tricks of the trade. Thieme, in press.)

Aortic arch anatomic variations are also relevant. One of the most common anatomic variations is the so-called bovine arch, where the left CCA and the brachiocephalic artery share a common origin or the left CCA originates from the brachiocephalic artery itself. The angle created by the left CCA and the aortic arch in these cases makes access difficult for standard endovascular catheters. One has to be aware of such variations to successfully gain vascular access. In these circumstances, as well as in situations whereby there is significant tortuosity, elongation of vessels, and/or other kinds of anatomic variations in the takeoff of great vessels from the arch, the ability to safely and successfully navigate the arch anatomy becomes the greatest challenge to successful completion of an endovascular procedure and may be a contraindication for the procedure altogether.

Pathophysiology and Natural History of Carotid Atherosclerosis

Histopathologically, carotid stenosis is a narrowing of the native carotid lumen, with deposition of plaque material of either soft, atheromatous or hard, calcified consistency. Clinical factors associated with the development of atheromatous plaque in the carotid arteries include hypercholesterolemia, hypertension, diabetes mellitus, obesity, and cigarette smoking. The role of systemic and/or local inflammation has also been described; an inflammatory process may lead to plaque formation, rupture, or hemorrhage.

The natural history of carotid atherosclerosis depends on the presence or absence of symptoms. In asymptomatic patients, the degree of stenosis may worsen over time; this progression correlates with an increased risk of ipsilateral stroke. Two studies have demonstrated that patients with asymptomatic carotid bruits are at an increased risk for neurologic and/or cardiac events; however, these events are not necessarily related to the territory of the affected carotid artery. Another study described a higher incidence of silent infarcts ipsilaterally to high-grade (>75%) carotid stenosis when compared with lower grades of stenosis.

The medical management of carotid stenosis has evolved significantly. The incidence of ipsilateral stroke in patients with stenosis treated medically in the ACAS (where medical management consisted of aspirin alone) was approximately 2.2% annually. In the ACST (where medical management consisted of aspirin plus angiotensin inhibitors and statins), the incidence of ipsilateral ischemic stroke diminished to approximately 1.7% annually. More recent studies show a less than 1% annual incidence of ipsilateral strokes in asymptomatic carotid stenosis treated medically.

The natural history of symptomatic carotid stenosis has also been well described. Previous studies have demonstrated that the risk of stroke following a first-time carotid TIA is close to 5% annually, with more than 50% of such strokes happening in the first year and 21% of them happening in the first month after such an event. The natural history of carotid stenosis is also influenced by plaque morphology; the presence of ulceration or intraplaque hemorrhage may be associated with a higher likelihood of ischemic events. Carotid revascularization has become the standard of care for patients with symptomatic carotid stenosis because of the dramatic stroke risk reduction shown in NASCET and ECAS.

Background and Historical Perspectives

The stroke risk reduction attributed to CEA in the classic landmark trials of surgical versus medical management of carotid stenosis is achieved only under the condition of surgical complication rates kept below a very specific threshold. As mentioned earlier, in the NASCET, the 17% absolute stroke risk reduction in patients with 70% or greater stenosis treated surgically was obtained assuming a 30-day rate of perioperative complication (nonfatal strokes, myocardial infarction [MI], or death) of 6% or less. For patients with asymptomatic carotid stenosis enrolled in the ACAS, the benefit of surgery assumed a perioperative complication rate of 3% or less. In addition, the very strict inclusion criteria in both the NASCET and ACAS limited the benefit of CEA to patients considered low risk for surgical intervention.

The search for a minimally invasive endovascular approach for the treatment of carotid stenosis began as early as the 1980s. Interventional neuroradiologists began using balloons in the treatment of several intracranial vascular diseases following the pioneering work of Serbinenko in the late 1960s and early 1970s. Working independently, Mathias and colleagues, Kerber and colleagues, and Theron, were the first to consider balloon angioplasty of the extracranial carotid artery. Theron and colleagues published the first series of 38 carotid balloon angioplasties in 1987, with an 8% embolic complication rate and a 5% carotid dissection rate. This high rate of distal embolic complications prompted the search for ways to protect the brain during these procedures.

Theron developed a triple coaxial catheter system with an occlusive balloon at the tip to be used for embolic protection. This balloon was attached to a microcatheter and inflated within the distal cervical ICA during angioplasty of the stenotic carotid segment. The embolic particles obtained during angioplasty were subsequently aspirated through the guiding catheter before deflating the distal occlusive balloon. This technique led to a reduction in the rate of distal embolic complications to 0% in a series of 43 patients treated by carotid angioplasty and distal balloon protection.

The next major step in the evolution of the endovascular management of carotid stenosis was the introduction of stents. The cardiology literature demonstrated that better clinical and angiographic outcomes were obtained in patients who received a coronary stent than those treated by coronary angioplasty alone, with lower rates of restenosis in those receiving stents. Several researchers began applying this technique in the management of extracranial carotid stenosis in the mid-1990s, with similar improved outcomes, including lower rates of restenosis and avoidance of disastrous carotid dissections.

Stents and embolic protection devices were undoubtedly the 2 major milestones that made CAS a promising and viable alternative to CEA for the treatment of extracranial carotid stenosis. In the following paragraphs, the authors discuss the historical evolution and technical aspects of current embolic protection devices and stents in greater detail, culminating with a description of modern endovascular technique for CAS.

Evolution of Embolic Protection

The first embolic protection device was the aforementioned balloon catheter system developed by Theron and colleagues to occlude the distal cervical ICA during angioplasty procedures. A direct evolution of the original Theron device is the PercuSurge GuideWire (Medtronic, Sunnyvale, CA, USA). This distal embolic protection device consists of a 0.014-in shapeable wire attached to a polyurethane occlusion balloon with a low crossing profile (0.036 in when deflated). Once the wire and balloon are advanced beyond the proximal ICA lesion, the balloon is inflated, occluding flow through the ICA. The stenotic segment is then treated by stenting and angioplasty as deemed necessary. After the stenting procedure is finished, an aspiration catheter is introduced over the wire up to the level of the distal occlusion balloon and used to aspirate the column of blood and debris proximal to the balloon. The aspiration catheter is subsequently removed and the balloon is deflated, thus restoring flow. The main disadvantages of distal balloon occlusion as an embolic protection device include the complete interruption of blood flow to the brain, which is occasionally not tolerated by patients with an inadequate circle of Willis, and the inability to obtain angiographic assessment of the lesion (and the stenting procedure itself) until the balloon is deflated.

To overcome the drawbacks of balloon occlusion devices, filter devices were subsequently developed as a suitable alternative. Filter devices function as an umbrella or windsock deployed between the stenotic carotid lesion and the brain to capture debris released during the stenting procedure, while allowing uninterrupted blood flow and continuous radiographic assessment during the entire procedure. The filter is subsequently recaptured and removed at the end of the procedure. There are different kinds of filter devices; but they all essentially consist of an expandable nitinol frame covered with a porous polyurethane membrane, with the pore size ranging from 36 to 140 μm. They can be divided in 2 main groups: filters built into a microwire, so that they can be moved either proximally or distally by moving the microwire, like the FilterWire EZ filter (Boston Scientific, Mountainview, CA, USA), or filters placed on the microwire but able to move proximally or distally independently of the microwire movements, such as the Emboshield NAV-6 (Abbott Vascular, Santa Clara, CA, USA) ( Fig. 2 ). Once the filter is deployed in the distal ICA beyond the stenotic segment, the filter wire is then used as a delivery wire for stents and angioplasty balloons as needed. Finally, at the end of the procedure, a retrieval catheter recaptures the filter and any trapped debris. The debris can also be aspirated through an aspiration catheter immediately before filter recapture, as is done with distal occlusion balloons, particularly if the debris burden is large and has occluded the filter. The pore size of the filter is related to the risk of filter thrombosis. Smaller pore sizes increase the risk of filter thrombosis as a result of trapping too many particles; conversely, the larger the pore size, the higher the risk of microembolization, even with the filter. As a result of this dilemma, most filters have pore sizes ranging from 100 to 150 μm; although in one study of embolic particles recovered during 75 CAS procedures performed with the PercuSurge device, 50% of the particles were less than 100 μm.

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