doi: 10.1161/01.STR.0000013741.41309.67
(Stroke. 2002;33:1214.)
© 2002 American Heart Association, Inc.
Original Contributions |
Bone Formation in Carotid Plaques
A Clinicopathological Study
From the University of Pittsburgh Medical Center, Department of Pathology and Laboratory Medicine (J.L.H.), and University of Pennsylvania School of Medicine, Department of Medicine, Division of Cardiovascular Medicine (T.K., M.W., B.S., E.R.M.) and Department of Surgery, Division of Vascular Surgery (R.F., M.E.M., J.P.C., M.G., D.N., R.M., A.C.), Philadelphia.
Correspondence to Emile R. Mohler, III, MD, University of Pennsylvania School of Medicine, Room 432 PHI Bldg, 39th & Market St, Philadelphia, PA 19104. E-mail mohlere{at}uphs.upenn.edu
Background and Purpose— Bone formation and dystrophic calcification are present in carotid endarterectomy plaques. The clinical significance of these findings is unknown. The purpose of this study was to determine whether bone formation and extensive dystrophic calcification are associated with stable plaques and protective against ischemic vascular events.
Methods— Carotid endarterectomy plaques were collected from 142 patients (94 men) with carotid stenosis. The specimens were evaluated for lamellar bone formation, dystrophic calcifications, inflammatory infiltrates, neovascularization, and histological type or grade of plaque according to a standard AHA grading system. Immunohistochemical staining was performed to identify vascular endothelial cells in neovascularization (factor VIII) and lymphocytes. Clinical data, including history of cerebrovascular and cardiovascular events, were recorded at the time of surgery.
Results— Patients with calcification of carotid plaques had fewer symptoms of stroke and transient ischemic attack (P=0.042) than those without calcification. Stroke and transient ischemic attack occurred less frequently in patients with plaques with large calcific granules (P=0.021). Of the patients, 13% had lamellar bone formation, which directly correlated with the presence of sheetlike calcifications (P=0.0001) and inversely correlated with ulcerated lesions (P=0.048). The presence of bone also correlated with diabetes (P<0.01) and coronary artery disease (P<0.01). Of the 20 patients with bone, 6 had a history of stoke and transient ischemic attack (P=0.5).
Conclusions— The results indicate that bone formation tends to occur in heavily calcified carotid lesions devoid of ulceration and hemorrhage. Patients with extensive calcification of the carotid plaques are less likely to have symptomatic disease.
Key Words: calcification • inflammation • stroke
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