title: Features of unstable carotid plaque during and after the hyperacute period following TIA/stroke.
abstract: BACKGROUND
  The aim was to test the hypothesis that histologically unstable carotid plaque features were more prevalent in patients undergoing carotid endarterectomy (CEA) in the acute period after onset of symptoms and that the plaque would assume more stable histological characteristics as the delay from the most recent event increased.
  
  
  METHODS
  Seven histological features of plaque instability (haemorrhage, large lipid core, chronic plaque inflammation, chronic cap inflammation, marked vascularity, cap rupture and many foam cells) were independently quantified and then correlated with recency of symptoms in patients undergoing CEA.
  
  
  RESULTS
  In patients undergoing CEA ≤14 days of their last event, 87/119 (73%) exhibited ≥5/7 unstable histological plaque features, compared with 22/40 (55%) of patients undergoing delayed surgery (P = 0.048). As expected, there was a sustained decline in the prevalence of unstable plaque features in 61 patients undergoing surgery between days 7-28. However, there was then a marked increase in the prevalence of plaque haemorrhage (59% up to 65%), large lipid core (41% up to 78%), chronic plaque inflammation (71% up to 91%), cap rupture (35% up to 39%), many foam cells (24% up to 43%) and marked vascularity (71% up to 91%) in 23 patients undergoing CEA after 29 days had elapsed.
  
  
  CONCLUSIONS
  Patients undergoing surgery ≤14 days had a significantly higher overall burden of high risk plaque features compared with those undergoing delayed CEA. However, the secondary upsurge across a range of unstable plaque features in patients undergoing CEA after ≥29 days had elapsed suggests that the relationship between recency of symptoms and plaque histology is more complex than had been anticipated in previous studies.
authors.affiliation: Vascular Surgery Group, Department of Cardiovascular Sciences, University of Leicester, LE2 7LX, UK. ms447@le.ac.uk
authors.forename: M K
authors.initials: MK
authors.lastname: Salem
authors.forename: R D
authors.initials: RD
authors.lastname: Sayers
authors.forename: M J
authors.initials: MJ
authors.lastname: Bown
authors.forename: K
authors.initials: K
authors.lastname: West
authors.forename: D
authors.initials: D
authors.lastname: Moore
authors.forename: T G
authors.initials: TG
authors.lastname: Robinson
authors.forename: A R
authors.initials: AR
authors.lastname: Naylor
mesh_terms: D000368:Aged; D002339:Carotid Arteries / Q000737:chemistry / Q000473:pathology* / Q000601:surgery; D016893:Carotid Stenosis / Q000150:complications / Q000175:diagnosis* / Q000378:metabolism / Q000601:surgery; D016009:Chi-Square Distribution; D016894:Endarterectomy, Carotid; D005260:Female; D005487:Foam Cells / Q000473:pathology; D006470:Hemorrhage / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000473:pathology; D002546:Ischemic Attack, Transient / Q000209:etiology*; D008055:Lipids / Q000032:analysis; D008297:Male; D016017:Odds Ratio; D058226:Plaque, Atherosclerotic; D012422:Rupture, Spontaneous; D020521:Stroke / Q000209:etiology*; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D008055:Lipids