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Cerebrovascular accident (CVA) is the third leading cause of death in North America and Europe, accounting for approximately 10–12% of all deaths.w1 CVA may have several aetiologies but is generally characterised as being either thrombotic or haemorrhagic in origin. The thrombotic causes of CVA are multiple and can be divided into large vessel occlusion, small vessel occlusion, and embolisation. Large vessel occlusion from atherothrombosis of the carotid system is responsible for approximately 25% of those afflicted by a CVA. The treatment of carotid atherothrombosis is evolving and involves risk factor management and in selected patients may warrant either surgical carotid endarterectomy or percutaneous carotid stenting. This is a review of the current understanding of carotid atherothrombosis and data regarding percutaneous approaches for those with this condition.
Atherosclerosis is the most common pathologic process affecting the carotid system leading to a CVA. This complex inflammatory process is mediated by both environmental and genetic factors and is extensively reviewed elsewhere.1 In brief, atherosclerotic plaque develops in the intimal layer of the carotid system and has a predilection for the carotid bifurcation and regions near this area. Indeed, even those with increased intimal–medial thickness are at increased risk for a future cardiovascular event.2 Once present, the initial lesion in the carotid arterial system may grow due to lipid laden macrophage expansion in the setting of chronic inflammatory signals. Although the pathophysiology of carotid disease leading to a CVA is not completely understood, the unstable (or ulcerated plaque) may develop due to several types of mechanisms:
Plaque rupture—constituents of the plaque are exuded into the circulation, expressing tissue factor, resulting in thrombus formation in that region.
Erosion—A thrombus can occur on a de-endothelialised (ulcerated), but otherwise intact, plaque. This may lead to vessel occlusion and haemodynamic compromise due to …