Carotid artery stenosis pathophysiology
Carotid artery stenosis Microchapters |
Diagnosis |
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Treatment |
ACC/AHA Guideline Recommendations |
Periprocedural Management of Patients Undergoing Carotid Endarterectomy |
Atherosclerotic Risk Factors in Patients With Vertebral Artery Disease |
Occlusive Disease of the Subclavian and Brachiocephalic Arteries |
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Carotid artery stenosis pathophysiology On the Web |
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Risk calculators and risk factors for Carotid artery stenosis pathophysiology |
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