UNLABELLED: Backgrounds and Purpose- Restenosis is an important complication after carotid endarterectomy, but little is known about plaque composition in early versus late restenosis and which plaque characteristics are associated with symptomatic clinical presentation of restenotic lesions. METHODS: Endarterectomy specimens of 822 consecutive patients undergoing carotid endarterectomy (33 restenotic; 789 primary) were subjected to histological examination for the presence of macrophages, smooth muscle cells, collagen, calcifications, luminal thrombus, intraplaque bleeding and lipid core size. RESULTS: Early restenotic plaques showed marked accumulation of smooth muscle cells and fibrous tissue, whereas late restenotic plaques demonstrated increased macrophage infiltration, calcification and lipid core (P trend <0.05), resembling primary plaques. Patients with symptomatic restenosis had plaques with higher macrophage infiltration (P=0.01) and a larger lipid core (P=0.02) than asymptomatic patients, independent of recurrence interval. CONCLUSIONS: Restenosis occurring >5 years after primary carotid endarterectomy resembles primary plaques. Symptomatic presentation of restenotic lesions is independently associated with an unstable plaque phenotype.
UNLABELLED: Backgrounds and Purpose- Restenosis is an important complication after carotid endarterectomy, but little is known about plaque composition in early versus late restenosis and which plaque characteristics are associated with symptomatic clinical presentation of restenotic lesions. METHODS: Endarterectomy specimens of 822 consecutive patients undergoing carotid endarterectomy (33 restenotic; 789 primary) were subjected to histological examination for the presence of macrophages, smooth muscle cells, collagen, calcifications, luminal thrombus, intraplaque bleeding and lipid core size. RESULTS: Early restenotic plaques showed marked accumulation of smooth muscle cells and fibrous tissue, whereas late restenotic plaques demonstrated increased macrophage infiltration, calcification and lipid core (P trend <0.05), resembling primary plaques. Patients with symptomatic restenosis had plaques with higher macrophage infiltration (P=0.01) and a larger lipid core (P=0.02) than asymptomatic patients, independent of recurrence interval. CONCLUSIONS:Restenosis occurring >5 years after primary carotid endarterectomy resembles primary plaques. Symptomatic presentation of restenotic lesions is independently associated with an unstable plaque phenotype.
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