Abstract
Carotid Endartectomy (CEA) has been proven to benefit patients with carotid bifurcation stenosis. For patients unfit for this therapy an alternative has been developed, namely Carotid Angioplasty and Stenting (CAS). No anesthesia or neck dissection is necessary in this procedure. In this thesis several aspects of CAS are investigated, stemming
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from a prospective database of 1000+ procedures from our tertiary referral center for vascular diseases. We routinely perform Trans Cranial Doppler (TCD) during CAS, to establish embolic load. In Chapter 2A we compared pre and post-procedural cerebral MRI scans. In 15% of cases new MRI lesions were found, the majority asymptomatic. In Chapter 2B pre and post-procedural retinal exams also revealed a 15% rate of emboli, none symptomatic. In both studies no correlation between TCD detected microemboli and cerebral or retinal emboli was found. In Chapter 2C Cerebral Protection Devices (CPD’s) were investigated. These devices were designed to minimize the embolic risk during CAS. Paradoxically an increase in TCD detected microembolic load was established when CPD’s were used. In Chapter 3A the effect of stent implantation on carotid mobility was investigated. Although highly flexible ex-vivo, the dedicated carotid stents tested proved to be rigid after head movements, leading to an increased angulation at the distal end of the stent, when the head was bent forward. To evaluate if this configurational change lead to impeded volumetric flow rate (VFR) a further study was performed, which is presented in Chapter 3 B. Patients after CAS were compared to patients post CEA. The increased angulation found in the previous study, in CAS patients was confirmed, and did not occur in CEA patients. There was however, no difference in VFR. During many CAS procedures the origin of the External Carotid Artery (ECA) is overstented. Chapter 3C describes the fate of the ECA, during CAS and at extended follow-up. The ECA on the stented side shows an increased rate of stenosis formation, compared to the contralateral side. This finding is more pronounced in cases of ECA overstenting. During follow up no ECA occlusions occurred. In Chapter 4A CAS for post-CEA restenosis was compared to CAS for primary atherosclerotic lesions. Clinical results were better for restenoses, with no strokes or deaths occurring in this group. There was no difference in TCD detected microembolic load. Chapter 4B describes extended follow up of CAS for post CEA restenosis. Results show that CAS post CEA provides adequate protection against stroke. However the rate of re-restenosis, 19% in 5 years, is considerable. Chapter 4C describes patients undergoing CAS for post-irradiation stenosis. Clinical results of CAS are also good in this group. During 3.3 years of follow up an adequate, but not perfect, protection against ipsilateral stroke was found. In the opinion of the author, CAS should not be considered to be a competitor for CEA, but rather a useful complementary treatment modality for patients with carotid bifurcation stenosis, for whom CEA is a less appealing option. Further improvements in stent and protection device design are expected and eagerly awaited.
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