Carotid artery stenosis pathophysiology

Carotid artery stenosis Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]

Overview

Embolism of atherosclerotic lesions in the carotid is the most common mechanism of stroke in patients with carotid artery disease. Thrombosis of the cerebral arteries is also a possible, less common cause of stroke.

Pathophysiology

• Atherosclerotic lesions are commonly located within 2 cm from the bifurcation of the common carotid artery, usually on the posterior wall of the artery. These plaques can extend caudally into the common carotid artery.
• The presence of atherosclerotic plaque is a risk for developing a stroke.
• In addition to compromising the flow to the brain, the plaque can rupture and a superimposed thrombus can develop on the atheroma further exacerbating the stenosis.
• The emboli then travels upstream until it lodges into a cerebral artery compromising blood supply to the territory.

Transient ischemic attack

• Low flow: brief, repetitive attacks
• Embolic: single, more prolonged episodes

Total occlusion

• When the internal carotid artery gets totally occluded, it can lead to slow flow or thrombosis. The severity of the symptoms depends on the adequacy of the collateral circulation.

Delayed stroke

• Occurs many months after carotid occlusion
• From propagation of the thrombus or embolization of the clot upstream.