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, regardless of its location.
• 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 associated territory.

Transient Ischemic Attack

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

Total Occlusion

• When the internal carotid artery is totally occluded, it can lead to slow flow or thrombosis. The severity of symptoms depend 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