title: Asymptomatic carotid plaque rupture with unexpected thrombosis over a non-canonical vulnerable lesion.
abstract: OBJECTIVE
  Several studies have demonstrated that carotid plaque rupture and thrombosis represent the most important factors correlated with the onset of acute cerebrovascular symptoms. Nevertheless, ruptured thrombotic plaques have been described also in asymptomatic patients. What still needs to be clarified is why a plaque rupture leads either to an acute ischemic syndrome or, in a minor group of patients, remains asymptomatic. The purpose of this study was to systematically compare the histologic features of thrombotic plaques both in asymptomatic and symptomatic patients in order to identify specific findings that could explain the peculiar clinical behavior that characterizes each of the clinical settings.
  
  
  METHODS
  A total of 157 thrombotic plaques from 60 asymptomatic patients and 97 with major stroke who consecutively underwent CEA were serially sectioned and studied by histology.
  
  
  RESULTS
  A minute cap disruption very frequently characterizes thrombotic plaques of asymptomatic patients and it was always smaller than large ulcers observed in thrombotic symptomatic plaques (651 ± 687μm vs. 4150 ± 3526, p=0.001). In asymptomatics this typical feature was associated with fewer inflammatory cells (20.1 ± 8.8 vs. 33.9 ± 26.1 cells × hpf, p=0.001), smaller lipidic-necrotic core (33.9%± 2.9% vs. 42.0% ± 2.4%; p=0.04) and larger calcification (16.2 ± 12.8% vs. 8.1 ± 12.2%, p=0.02). Symptomatic patients with thrombotic plaques showed higher incidence of metabolic syndrome (p=0.002) and moderate-high Framingham risk scores (p=0.001) comparing to asymptomatic individuals.
  
  
  CONCLUSIONS
  The transformation from a stable to a vulnerable plaque is a gradual process in the natural history of the disease and plaque rupture is an event not necessarily occurring at a late phase but also at earlier one. In this case, the rupture will be most likely smaller and clinically asymptomatic.
authors.affiliation: Anatomic Pathology, University of Rome Tor Vergata, Italy. alessandro.mauriello@uniroma2.it
authors.forename: Alessandro
authors.initials: A
authors.lastname: Mauriello
authors.forename: Francesca
authors.initials: F
authors.lastname: Servadei
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Sangiorgi
authors.forename: Lucia
authors.initials: L
authors.lastname: Anemona
authors.forename: Erica
authors.initials: E
authors.lastname: Giacobbi
authors.forename: Doriana
authors.initials: D
authors.lastname: Liotti
authors.forename: Luigi Giusto
authors.initials: LG
authors.lastname: Spagnoli
mesh_terms: D000208:Acute Disease; D000368:Aged; D050197:Atherosclerosis; D002339:Carotid Arteries / Q000473:pathology*; D018450:Disease Progression; D016894:Endarterectomy, Carotid / Q000379:methods; D005260:Female; D006801:Humans; D007249:Inflammation; D007511:Ischemia / Q000473:pathology; D008055:Lipids / Q000737:chemistry; D008297:Male; D024821:Metabolic Syndrome / Q000473:pathology; D008875:Middle Aged; D009336:Necrosis; D058226:Plaque, Atherosclerotic / Q000473:pathology*; D012307:Risk Factors; D013927:Thrombosis / Q000473:pathology*
chemical_list: D008055:Lipids