Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke

Luigi Giusto Spagnoli, Alessandro Mauriello, Giuseppe Sangiorgi, Stefano Fratoni, Elena Bonanno, Robert S. Schwartz, David G. Piepgras, Raimondo Pistolese, Arnaldo Ippoliti, David Holmes

Research output: Contribution to journalArticle

319 Citations (Scopus)

Abstract

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 of Willis. 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 groups. 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.

Original languageEnglish (US)
Pages (from-to)1845-1852
Number of pages8
JournalJournal of the American Medical Association
Volume292
Issue number15
DOIs
StatePublished - Oct 20 2004

Fingerprint

Stroke
Thrombosis
Transient Ischemic Attack
Rupture
Carotid Artery Thrombosis
Tissue Banks
Circle of Willis
Endarterectomy
Carotid Artery Diseases
Carotid Endarterectomy
Carotid Stenosis
Monocytes
Histology
Pathologic Constriction
Macrophages
Outcome Assessment (Health Care)
Inflammation
T-Lymphocytes

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke. / Spagnoli, Luigi Giusto; Mauriello, Alessandro; Sangiorgi, Giuseppe; Fratoni, Stefano; Bonanno, Elena; Schwartz, Robert S.; Piepgras, David G.; Pistolese, Raimondo; Ippoliti, Arnaldo; Holmes, David.

In: Journal of the American Medical Association, Vol. 292, No. 15, 20.10.2004, p. 1845-1852.

Research output: Contribution to journalArticle

Spagnoli, LG, Mauriello, A, Sangiorgi, G, Fratoni, S, Bonanno, E, Schwartz, RS, Piepgras, DG, Pistolese, R, Ippoliti, A & Holmes, D 2004, 'Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke', Journal of the American Medical Association, vol. 292, no. 15, pp. 1845-1852. https://doi.org/10.1001/jama.292.15.1845
Spagnoli LG, Mauriello A, Sangiorgi G, Fratoni S, Bonanno E, Schwartz RS et al. Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke. Journal of the American Medical Association. 2004 Oct 20;292(15):1845-1852. https://doi.org/10.1001/jama.292.15.1845
Spagnoli, Luigi Giusto ; Mauriello, Alessandro ; Sangiorgi, Giuseppe ; Fratoni, Stefano ; Bonanno, Elena ; Schwartz, Robert S. ; Piepgras, David G. ; Pistolese, Raimondo ; Ippoliti, Arnaldo ; Holmes, David. / Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke. In: Journal of the American Medical Association. 2004 ; Vol. 292, No. 15. pp. 1845-1852.
@article{e78992edba7e4f469d4925a6c32d30e4,
title = "Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke",
abstract = "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 of Willis. 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 groups. 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.",
author = "Spagnoli, {Luigi Giusto} and Alessandro Mauriello and Giuseppe Sangiorgi and Stefano Fratoni and Elena Bonanno and Schwartz, {Robert S.} and Piepgras, {David G.} and Raimondo Pistolese and Arnaldo Ippoliti and David Holmes",
year = "2004",
month = "10",
day = "20",
doi = "10.1001/jama.292.15.1845",
language = "English (US)",
volume = "292",
pages = "1845--1852",
journal = "JAMA - Journal of the American Medical Association",
issn = "0002-9955",
publisher = "American Medical Association",
number = "15",

}

TY - JOUR

T1 - Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke

AU - Spagnoli, Luigi Giusto

AU - Mauriello, Alessandro

AU - Sangiorgi, Giuseppe

AU - Fratoni, Stefano

AU - Bonanno, Elena

AU - Schwartz, Robert S.

AU - Piepgras, David G.

AU - Pistolese, Raimondo

AU - Ippoliti, Arnaldo

AU - Holmes, David

PY - 2004/10/20

Y1 - 2004/10/20

N2 - 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 of Willis. 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 groups. 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.

AB - 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 of Willis. 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 groups. 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.

UR - http://www.scopus.com/inward/record.url?scp=5444243895&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=5444243895&partnerID=8YFLogxK

U2 - 10.1001/jama.292.15.1845

DO - 10.1001/jama.292.15.1845

M3 - Article

VL - 292

SP - 1845

EP - 1852

JO - JAMA - Journal of the American Medical Association

JF - JAMA - Journal of the American Medical Association

SN - 0002-9955

IS - 15

ER -