Introduction
The Carotid Wallstent (Boston Scientific, Marlborough, MA) is one of the most used stents in the endovascular treatment of carotid stenosis, particularly because of its design, which allows excellent plaque coverage. For that reason, it seems adequate for the treatment not only of stable uncomplicated plaques but also of dishomogenous stenosis. Although the advantages given in terms of plaque coverage are significant, as shown by the diminished rate of postprocedural events compared with open cell stents, the conformability is reduced, with a higher rate of malapposition of the struts. Moreover, the rigidity of the device and the interaction between the metallic struts lead to other possible problems, which are, however, extremely limited in terms of frequency and overall clinical impact as we will see in this chapter.
Endoluminal stent coverage
Because the main purpose of a carotid stent is the prevention from cerebral embolism, the endoluminal coverage of the device is crucial. De Donato et al. analyzed the interaction between carotid plaques and stents by optical coherence tomography and found that plaque prolapse was significantly lower compared with open and hybrid cell stents (23.3% versus 68.6% and 30.8% respectively; P<0.01).
Moreover, as shown in previous work from our group, the carotid Wallstent surface is covered by a new pseudo-intimal layer shortly after implantation. The completeness of this new layer is dependent on adequate coverage of the plaque at the proximal end of the stent where an intact intima is present ( Fig. 47.1 ).
Although the degree of neointimal coverage does not seem to be related to the number of microemboli detected by transcranial Doppler, a complete stent coverage is a potential adjunctive barrier to plaque prolapse and endoluminal fragmentation.
Classification of carotid stent complication
Nicosia et al. divided the carotid stent complications according to their anatomical distribution in cervical and intracranial complication. Those directly related to the stent pertain to the cervical group and, although of different types, are rarely device specific. As a matter of fact, only plaque prolapse is strictly correlated with the stent design. Acute stent thrombosis, residual stenosis, and incorrect stent deployment, which are the other possible stent complications, are primarily the consequences of operator-dependent technical details, such as indication to revascularization, stent positioning and deployment, and medical management. Plaque prolapse has been defined by Clark et al. as a >0.5-mm protrusion of plaque components through the stent cells and it is considered “significant” when determining a visible lumen stenosis. In addition to these morphological features, plaque prolapse is clinically relevant because it may lead to stent thrombosis or cerebral embolization, and although it may be evident at completion angiography at the end of the carotid artery stenting procedure, a precise angiographic definition is lacking. Intravascular ultrasound and optical coherence tomography are the most reliable methods to identify plaque prolapse, showing that the closed cell design of the Wallstent allows the greatest protection from this phenomenon.
Incorrect stent deployment can be defined as an operator-dependent defect; however, the characteristics of the stent may play an important role in this complication. As a matter of fact, the closed cell design causes a greater degree of stiffness in the device, leading to increased risk of misalignment during deployment. This was shown by de Donato et al., who found that closed-cell design was significantly associated with a higher rate of malapposed struts compared with open cell or hybrid cell (34% versus 15% and 16%, respectively; P<0.01).
The use of the Wallstent in tortuous vessels should be carefully considered, because of its rigidity. It may be considered an inappropriate stent choice in these patients, rather than a complication of the stent itself. If the misplacement is minimal, within a few millimeters from the desired position, no consequences are to be expected. However, in case of very tight stenosis or excessive tortuosity of the vessel, the radial forces of the stent struts may cause a watermelon effect on the stent with the stent being displaced either proximally or distally to the target zone. As shown in Fig. 47.2 , a stent may be deployed incorrectly because of the forces exerted by the struts toward a rigid calcified plaque, leading to the necessity of deploying a second more proximal stent in order to achieve complete plaque coverage. These forces may also lead to a late misplacement. Shortening may be also aggravated by the straightening of the vessel, which is relevant when a closed-cell stent is inserted and deployed into a tortuous or stiff vessel. Part of the problem may be related to the diameter mismatch between the stent, the proximal common carotid, and the internal carotid artery. As a matter of fact, since the metal tends to distribute the force uniformly across its surface, the external energy of the widening proximal end may be transmitted as a contrary internal force at the distal end, where the lumen diameter is smaller. This is particularly evident in the case of stenting of post-endarterectomy stenosis, because the decreased compliance of the artery may worsen the diameter mismatch between the stent and the artery.
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