Abstract

Carotid artery disease is one of the main causes of stroke, apart from other cardiac causes or disease of the brain itself. About 80% of all strokes are ischemic and approximately 25-50% of these are caused by an unstable carotid artery plaque.1 The risk factors for carotid stenosis are similar to those for athero- sclerosis and include hypertension, diabetes, cigarette smoking and dyslipidemia. Prevention of stroke caused by carotid bifurcation stenosis can be achieved by accurate identification and evaluation of patients at risk. Pathophysiology of carotid atherosclerosis is similar to that in other vascular beds. However, atherosclerosis in the carotid artery is usually unifocal, and 90% of lesions are located within 2 cm. of the internal carotid artery (ICA) origin. Extracranial internal carotid artery stenosis accounts for 15 to 20% of ischemic strokes, depending on the population studied. The degree of carotid stenosis is associated with the degree of stroke risk. Carotid ath- erosclerosis can produce retinal and cerebral symptoms by way of 1 of 2 major mechanisms. progressive carotid stenosis leading to insitu occlusion and hypoperfusion (less common), or intracranial arterial occlusion resulting from embolization (more common). Embolism from unstable plaque is the major mechanism of stroke in carotid atherosclerosis.2,3 Stroke is more likely to be due to embolism rather than hypoperfusion even in patients with >70% carotid stenosis, and the risk of stroke may be lower in patients with >90% stenosis, due to post-stenotic narrowing in the distal ICA, which reduces flow and risk of embolism. Patients present- ing with carotid distribution cerebral ischemia should be thoroughly evaluated for treatable causes, including sources of emboli from the carotid arteries, heart, and aortic arch. Patients with or without carotid stenosis may also develop symptomatic cerebral hypoperfusion from systemic causes.

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