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Embolization to the brain is a universal occurrence during carotid artery stenting (CAS) procedures. This has been documented by several well conducted ex vivo studies, by the routine use of transcranial Doppler monitoring, and by analyzing the blood aspirated after the use of distal occlusion balloons. It is also widely agreed upon that the goal of cerebral protection during CAS is to suppress or decrease the number of particles and/or air bubbles reaching the brain during the procedure.
Embolization occurs during every stage of CAS, but embolic protection starts once the cerebral protection device is deployed and finishes when it is retrieved; this means that embolization can still occur during the initial placement of the catheter in the aortic arch or carotid artery and can also be seen after the procedure is completed. Careful technique and limitation of instrumentation is crucial to reduce or suppress embolization during the initial phase of the procedure. Administration of antiplatelet therapy and appropriate use of stents of adequate size and cell configuration will sufficiently address most of the postprocedure embolic events. Crossing the lesion produces significant embolization (40,000 particles on average). In our study of carotid plaques after endarterectomy, we found that 24% of plaques have thrombus lining. In a study performed at Stanford, the incidence was 49%.
Outcomes after CAS are related to multiple factors, including age of the patient, presence of symptoms, plaque morphology, cerebral functional reserve, aortic arch anatomy, experience of the operator, and type of cerebral protection device used, among others. There is no proof yet that microembolic signals or high-intensity transitory signals on transcranial Doppler studies are related to new cerebral lesions using diffusion-weighted (DW) magnetic resonance imaging (MRI) studies. Correlation between new lesions detected by DW-MRI and cognitive function is still ongoing. It is recognized, however, that high-intensity transitory signals are better tolerated in young patients with good cerebral functional reserve than in older patients with low functional reserve. It seems reasonable to say that high-intensity transitory signals cannot do any good to the brain, and their occurrence should be at least a reason for concern. Until we have conclusive evidence about the occurrence of high-intensity transitory signals during CAS and its potential damage to the brain, we would prefer to try to suppress or minimize its occurrence.
Flow reversal appears to be closer to the ideal device when CAS is undertaken. What is already known is that silent cerebral infarcts are relevant because they produce a steeper decline in cognitive function and increase the incidence of dementia. Deleterious effects of iodinated contrast media injected in the cerebral vasculature are well described. Using flow reversal, contrast can be readily aspirated once the injection has delineated the artery or arteries interrogated. Bubbles that are trapped in the delivery system were detected during stent deployment; aspiration will bring those bubbles out of the body using flow reversal.
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