Atherosclerotic plaque rupture in symptomatic carotid artery stenosis

Plaque rupture is often the precipitating event in acute coronary syndromes. We hypothesized that a similar process occurs in stenotic carotid plaques in association with ischemic neurologic symptoms. Our purpose was to examine several morphologic features of stenotic carotid plaques and to determine which characteristics are more commonly associated with plaques obtained from patients with symptomatic carotid artery disease than with those from patients with asymptomatic carotid artery disease.

Forty-four carotid endarterectomy specimens (from 25 asymptomatic and 19 symptomatic patients) were analyzed with pentachrome staining and light microscopy. The asymptomatic patients and symptomatic patients had similar mean percent stenosis (77% vs 74%). Other risk factors, including hypertension, diabetes mellitus, coronary artery disease, smoking history, serum cholesterol, and triglyceride levels, were similar between groups.

Patients with symptomatic carotid artery disease were found to have more frequent plaque rupture, fibrous cap thinning, and fibrous cap foam-cell infiltration when compared with the asymptomatic group. Plaque rupture was seen in 74% of symptomatic plaques and in only 32% of plaques from asymptomatic patients (p = 0.004). Fibrous cap thinning was noted in 95% of symptomatic plaques and in 48% of asymptomatic plaques (p = 0.003). Infiltration of the fibrous cap with foam cells was also significantly more common in the symptomatic plaques (84% vs 44% of asymptomatic plaques; p = 0.006). In addition, intraplaque fibrin was more common in symptomatic plaques than in asymptomatic (100% vs 68%; p = 0.008). No significant differences were found between the two groups with respect to plaque hemorrhage, the presence of a necrotic core, luminal thrombus, smooth muscle cell infiltration, eccentric shape, and plaque type (fibrous, necrotic, or calcified).

As in the coronary artery system, rupture of the atherosclerotic plaque may play an important role in the pathogenesis of ischemic stroke caused by carotid artery stenosis. The process of inflammation, involving foam-cell infiltration of the fibrous cap, may contribute to rupture of the atherosclerotic plaque.