Ulceration and carotid artery disease.

The association between carotid artery disease and stroke has been recognized for more than a century, but the pathophysiology of ischemic events ipsilateral to carotid plaques remains uncertain. Artery-to-artery embolism is one of several mechanisms causing either transient ischemic attacks (TIAs) or stroke ipsilateral to atherosclerotic plaques. Thrombus at the site of arterial occlusion, atherosclerotic debris, and vertebral artery stenosis or occlusion are well-documented sources of emboli. Ulceration is a frequent finding in carotid plaques/ but the role of ulceration as a source of artery-to-artery embolism is unclear. Controversy exists because of the difficulty in establishing a uniform definition of ulceration and because of the limited diagnostic accuracy of radiological techniques. Little is known about the nature of embolic material released from ulcerated plaques. Grumous material is occasionally observed in carotid plaques, leading to speculation that it may enter the carotid circulation and occlude cerebral vessels. Cholesterol emboli appear in retinal vessels and usually signify ipsilateral carotid artery atherosclerosis. These emboli characteristically do not obstruct flow and are frequently observed without visual symptoms. Cholesterol emboli may also enter the cerebral circulation and cause TIAs. Fibrinplatelet thrombus forms in carotid plaques with severe stenosis. Thrombus also occurs in cavities within plaques and overlying intimal disruptions. Thrombi can be large enough to occlude intracerebral vessels and cause ischemic symptoms. In 1968 Moore and Hall reported complete relief of TIAs in nine patients with ulcerated "nonstenotic" carotid artery plaques following endarterectomy. Since then, many operations have been performed because of the possible embolic potential of ulcerated plaques independent of the severity of stenosis. To justify this approach one must establish a relationship between ulcerated plaques and ischemic symptoms and demonstrate that the natural history of these lesions is sufficiently adverse to warrant the risk of endarterectomy.