Cerebral perfusion and cerebral ischemia in patients with symptomatic carotid artery stenosis

Next to thromboembolism from the atherosclerotic plaque, impaired cerebral perfusion is the main mechanism of cerebral ischemia in patients with symptomatic carotid artery stenosis. There is supporting evidence of a synergistic effect of both embolic and hemodynamic factors. An understanding of both mechanisms in the occurrence of cerebral ischemia is important. This thesis explored the role of cerebral perfusion in patients with symptomatic carotid artery stenosis. Three etiologic questions related to cerebral perfusion were addressed in this thesis. First, is cerebral perfusion related to the presence of a carotid artery stenosis? Second, does cerebral perfusion improve due to the treatment of carotid stenosis by carotid endarterectomy (CEA) or carotid artery stenting (CAS)? Third, is cerebral perfusion related to the occurrence of cerebral ischemia? In chapter 2 describes an inverse relation found between the degree of carotid artery stenosis and the cerebral perfusion in the ipsilateral MCA territory was found. The improvement of cerebral perfusion after CEA and CAS on cerebral perfusion is described in patients with an unilateral carotid artery stenosis in chapter 3. An important new finding in this study is that significantly more improvement in cerebral perfusion was found in the patients treated with CAS than in patients treated with CEA. Pre-operative cerebral perfusion asymmetries were assessed in patients with symptomatic carotid artery stenosis before CEA in chapter 4. The occurrence of the cerebral hyperperfusion syndrome after CEA is related to higher cerebral perfusion asymmetries before treatment. Cerebral perfusion measurements were related to the occurrence of silent ischemia, as in the presence of ischemic lesions on diffusion weighted imaging (DWI), after CAS in chapter 5. The occurrence of new ipsilateral lesions was related to impaired cerebral perfusion before the procedure. This supports the synergistic effect of both embolic and hemodynamic factors. In chapter 6 the difference in the occurrence of silent cerebral ischemia after CEA or CAS were examined by DWI before and after treatment. Approximately three times more patients in the CAS group than in the CEA group had new ischemic lesions on DWI on post-treatment scans. In chapter 7 we used multidetector-row CT angiography to examine the prevalence of in-stent lesions during follow-up after carotid artery stenting. In-stent lesions are present in 20% of the patients treated with CAS. The presence of in-stent lesions was not related to ischemic complications or in-stent restenosis at one year follow-up. In chapter 8 the findings of this thesis are discussed and the three etiologic question posed in the introduction are answered. First, the presence of a carotid artery stenosis in patients with symptomatic carotid artery stenosis results in impaired cerebral perfusion. Second, cerebral perfusion improves after CAS and CEA and may explain the decreased risk of recurrent ischemic events in long-term follow-up. Third, impaired cerebral perfusion in patients with symptomatic carotid artery stenosis is related to the occurrence of their ischemic symptoms. These findings support the presence and role of cerebral perfusion in the occurrence of ischemia in patients with symptomatic carotid artery stenosis