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Spagnoli LG, Mauriello A, Sangiorgi G, et al. Extracranial Thrombotically Active Carotid Plaque as a Risk Factor for Ischemic Stroke. JAMA. 2004;292(15):1845–1852. doi:https://doi.org/10.1001/jama.292.15.1845
Author Affiliations: Anatomic Pathology (Drs
Spagnoli, Mauriello, Fratoni, and Bonanno), Department of Cardiovascular Diseases
(Dr Sangiorgi), Division of Vascular Surgery (Drs Pistolese and Ippoliti),
University of Rome Tor Vergata, Rome, Italy; Minnesota Cardiovascular Research
Institute, Minneapolis (Dr Schwartz); Departments of Neurologic Surgery (Dr
Piepgras) and Internal Medicine and Cardiovascular Diseases (Dr Holmes), Mayo
Clinic and Mayo Foundation, Rochester, Minn.
Context Recent studies suggest that factors other than the degree of carotid
stenosis are involved in ischemic stroke pathogenesis, especially modifications
of plaque composition and related complications.
Objective To examine the role of carotid plaque rupture and thrombosis in ischemic
stroke pathogenesis in patients undergoing carotid endarterectomy, excluding
those with possible cardiac embolization or with severe stenosis of the circle
Design, Setting, and Patients A total of 269 carotid plaques selected from an Interinstitutional Carotid
Tissue Bank were studied by histology after surgical endarterectomy between
January 1995 and December 2002. A total of 96 plaques were from patients with
ipsilateral major stroke, 91 plaques from patients with transient ischemic
attack (TIA), and 82 plaques from patients without symptoms.
Main Outcome Measures Differences in the frequency of thrombosis, cap rupture, cap erosion,
inflammatory infiltrate, and major cardiovascular risk factors between study
Results A thrombotically active carotid plaque associated with high inflammatory
infiltrate was observed in 71 (74.0%) of 96 patients with ipsilateral major
stroke (and in all 32 plaques from patients operated within 2 months of symptom
onset) compared with 32 (35.2%) of 91 patients with TIA (P < .001) or 12 (14.6%) of 82 patients who were without
symptoms (P < .001). In addition, a
fresh thrombus was observed in 53.8% of patients with stroke operated 13 to
24 months after the cerebrovascular event. An acute thrombus was associated
with cap rupture in 64 (90.1%) of 71 thrombosed plaques from patients with
stroke and with cap erosion in the remaining 7 cases (9.9%). Ruptured plaques
of patients affected by stroke were characterized by the presence of a more
severe inflammatory infiltrate, constituted by monocytes, macrophages, and
T lymphocyte cells compared with that observed in the TIA and asymptomatic
groups (P = .001). There was no significant
difference between groups in major cardiovascular risk factors.
Conclusion These results demonstrate a major role of carotid thrombosis and inflammation
in ischemic stroke in patients affected by carotid atherosclerotic disease.
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