Carotid artery revascularization. Surgical and endovascular developments. Stroke is among the most disabling chronic diseases and the third major cause of death in the Western world. In the Netherlands around 12 per 1000 inhabitants suffers a stroke, and in 2005 over 10.000 people died as a result of stroke representing 7.6% of all deaths. In 10-20% of patients stroke is heralded by transient cerebral deficit. These harbingers of stroke allow a certain amount of time to search for the cause of the symptoms and, when stenosis of the corresponding carotid artery is demonstrated, to perform carotid endarterectomy (CEA) as the best treatment in patients with ≥ 70 % diameter artery reduction. Although being one of the most scrutinised areas of medicine, the management of carotid artery disease maintains an unparalleled and enduringly reputation for controversy. The paradox remains that the very operation undertaken to prevent stroke (in the long-term) is associated with a small, but important risk of stroke in the peri-operative period (3-7%). It therefore remains essential that the benefits of surgery in stroke prevention are weighed against the immediate risk of death or stroke, and the incidence of restenosis. The fate of the treated carotid artery is the central theme connecting the chapters in this thesis, focusing both on postprocedural outcome as well as on durability and the incidence of restenosis. Elucidating the underlying mechanism of perioperative stroke and the role of intraoperative monitoring, it appeared that strokes from CEA (3.3%) mainly developed in the postoperative phase after a symptom free interval. Thromboembolism with occlusion of the operated artery showed most important in the pathogenesis. Patients destined to suffer an early postoperative stroke have a 1- to 2- hour period of increasing embolization before cerebral deficit becomes apparent. We studied the effect of 3 different antiplatelet regimens on the rate of postoperative embolization following CEA, but we did not find a significant relationship. For post-endarterectomy restenosis both repeat CEA and carotid angioplasty and stenting (CAS) could be performed with a low incidence of periprocedural complications with durable stroke protection. However, following CAS the rate of in-stent restenosis was high. An additional disadvantage of CAS might be the covering of the external carotid artery (ECA) orifice. Significant progression of ≥ 50% stenosis in the ipsilateral ECA occurred after CAS. Progression of ECA disease however did not lead to occlusion during follow up. Our experience with the surgical managment of in-stent restenosis was described in 4 consecutive patients who underwent successful standard CEA with removal of the stent. The optimal treatment of in-stent restenosis remains to be defined, but CEA with stent removal appears to be feasible. An animal experiment was conducted to evaluate carotid diameter and velocity changes due to stent placement. Alterations were stent type dependent, and did not justify a general approach to new velocity criteria indiscriminately applied to all stents. The final chapter summarizes the knowledge about the quality of the current revascularization techniques and debates how outcomes can be optimised in the future
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