Technical improvements in carotid revascularization based on the mechanism of procedural stroke.

The benefit of carotid revascularization in patients with severe carotid artery stenosis is hampered by the risk of stroke due to the intervention itself. The risk of periprocedural strokes is higher for carotid artery stenting (CAS) as compared to carotid endarterectomy (CEA). Over the past years, the pathophysiological mechanism responsible for periprocedural stroke seems to unfold step by step. Initially, all procedural strokes were thought to be the result of technical errors during surgical repair: cerebral ischemia due to clamping time of the carotid artery, cerebral embolization of atherosclerotic debris due to manipulation of the atheroma or thrombosis of the artery. Following improvements in surgical techniques, technical skills, new intraoperative monitoring technologies such as angioscopy, and the results of the first large clinical randomized controlled trials (RCT) it was believed that most periprocedural strokes were of thromboembolic nature, while a large part of these caused by technical error. Nowadays, analyses of underlying pathophysiological mechanisms of procedural stroke make a clinically relevant distinction between intra-procedural and postprocedural strokes. Intra-procedural stroke is defined as hypoperfusion due to clamping (CEA) or dilatation (CAS) and embolization from the carotid plaque (both CEA and CAS). Postprocedural stroke can be caused by thrombo-embolisation but seems to have a primarily hemodynamic origin. Besides thrombotic occlusion of the carotid artery, cerebral hyperperfusion syndrome (CHS) due to extensively increased cerebral revascularization is the most reported pathophysiological mechanism of postprocedural stroke. Multiple technical improvements have attempted to lower the risk of periprocedural stroke. The introduction of antiplatelet therapy (APT) has significantly reduced the risk of thromboembolic events in patients with carotid stenosis. Over the years, recommendations regarding APT changed. While for a long time APT was discontinued prior to surgery because of a fear of increased bleeding risk, nowadays continuation of APT during carotid intervention (aspirin monotherapy or even dual APT including clopidogrel) is found to be safe and effective. In CAS patients, dual APT up to three months' postprocedural is considered best. Stent design and cerebral protection devices (CPD) for CAS procedure are continuously under development. Trials have suggested a benefit of closed-cell stent design over open-cell stent design in order to reduce procedural stroke, while the benefit of CPD during stenting is still a matter of debate. Although CPD reduce the risk of procedural stroke, a higher number of new ischemic brain lesions detected on diffusion weighted imaging was found in patients treated with CPD. In patients undergoing CEA under general anesthesia, adequate use of cerebral monitoring (EEG and transcranial Doppler [TCD]) has reduced the number of intraoperative stroke by detecting embolization and thereby guiding the surgeon to adjust his technique or to selectively shunt the carotid artery. In addition, TCD is able to adequately identify and exclude patients at risk for CHS. For CAS, the additional value of periprocedural cerebral monitoring to prevent strokes needs urgent attention. In conclusion, this review provides an overview of the pathophysiological mechanism of stroke following carotid revascularization (both CAS and CEA) and of the technical improvements that have contributed to reducing this stroke risk.