Journal
EUROPEAN JOURNAL OF VASCULAR AND ENDOVASCULAR SURGERY
Volume 50, Issue 3, Pages 281-288Publisher
W B SAUNDERS CO LTD
DOI: 10.1016/j.ejvs.2015.05.017
Keywords
Carotid artery stenting; Carotid endarterectomy; Carotid stenosis; Procedural stroke; Stroke mechanism
Categories
Funding
- UK Medical Research Council (MRC) [G0300411]
- Stroke Association [TSA 2005/01, TSA 2007/12]
- Sanofi-Synthelabo
- European Union
- Reta Lila Weston Trust for Medical Research
- Medical Research Council
- UK Department of Health's National Institute for Health Research Biomedical Research Centres funding scheme
- MRC [G0300411] Funding Source: UKRI
- Medical Research Council [G0300411] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0507-10339] Funding Source: researchfish
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WHAT THIS PAPER ADDS Stroke is a complication of carotid revascularisation that limits the benefit of the procedure in overall stroke prevention. To decrease the risk of revascularisation it is important to understand the mechanism of stroke. In a recent randomised trial in which patients were treated with carotid artery stenting (CAS) or carotid endarterectomy (CEA), one-third of the procedural strokes were caused by periprocedural haemodynannic disturbances. This suggests that careful attention to blood pressure control could lower the incidence of procedural stroke. Objective: To decrease the procedural risk of carotid revascularisation it is crucial to understand the mechanisms of procedural stroke. This study analysed the features of procedural strokes associated with carotid artery stenting (CAS) and carotid endarterectomy (CEA) within the International Carotid Stenting Study (ICSS) to identify the underlying pathophysiological mechanism. Materials and methods: Patients with recently symptomatic carotid stenosis (1,713) were randomly allocated to CAS or CEA. Procedural strokes were classified by type (ischaemic or haemorrhagic), time of onset (intraprocedural or after the procedure), side (ipsilateral or contralateral), severity (disabling or non-disabling), and patency of the treated artery. Only patients in whom the allocated treatment was initiated were included. The most likely pathophysiological mechanism was determined using the following classification system: (1) carotid-embolic, (2) haemodynamic, (3) thrombosis or occlusion of the revascularised carotid artery, (4) hyperperfusion, (5) cardio-embolic, (6) multiple, and (7) undetermined. Results: Procedural stroke occurred within 30 days of revascularisation in 85 patients (CAS 58 out of 791 and CEA 27 out of 819). Strokes were predominately ischaemic (77; 56 CAS and 21 CEA), after the procedure (57; 37 CAS and 20 CEA), ipsilateral to the treated artery (77; 52 CAS and 25 CEA), and non-disabling (47; 36 CAS and 11 CEA). Mechanisms of stroke were carotid-embolic (14; 10 CAS and 4 CEA), haemodynamic (20; 15 CAS and 5 CEA), thrombosis or occlusion of the carotid artery (15; 11 CAS and 4 CEA), hyperperfusion (9; 3 CAS and 6 CEA), cardio-embolic (5; 2 CAS and 3 CEA) and multiple causes (3; 3 CAS). In 19 patients (14 CAS and 5 CEA) the cause of stroke remained undetermined. Conclusion: Although the mechanism of procedural stroke in both CAS and CEA is diverse, haemodynamic disturbance is an important mechanism. Careful attention to blood pressure control could lower the incidence of procedural stroke. (C) 2015 The Authors. Published by Elsevier Ltd on behalf of European Society for Vascular Surgery. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
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