The carotid bifurcation plaque: pathologic findings associated with cerebral ischemia.

Embolization from or decreased flow through cervical carotid and vertebral arteries causes ischemic stroke syndromes. Specific pathologic findings were studied in 50 symptomatic patients who underwent 69 carotid endarterectomies. Detailed analyses of their carotid plaques included correlations between photographs of gross specimens, microscopic findings, angiograms, preoperative symptoms and long-term postoperative follow up. Carotid plaques were primarily fibrous with significant (greater than 70%) stenoses encountered in 70% of the arteries. Stenoses were due to simple fibrous thickening in only 20%; the remainder due to intraplaque hemorrhage, atheromatous debris and, least often, luminal thrombus with or without ulceration. Intramural hemorrhage was frequent in plaques associated with focal neurologic symptoms and may have preceded localized collections of atheromatous debris. Ulceration occurred in 1/3 of all plaques, symptomatic or not. It is concluded that the carotid plaques start as fibrointimal thickening evolving to symptomatic stages by the occurrence of one or more of a number of pathologic changes, intraplaque hemorrhage being prominent. A single rational therapeutic regimen seems impossible until patients can be classified according to their pathologic changes diagnosed non-invasively.