title: Angiogenesis and the atherosclerotic carotid plaque: an association between symptomatology and plaque morphology.
abstract: OBJECTIVE
  Symptomatic carotid disease resulting from generation of thromboemboli has been associated with plaque instability and intraplaque hemorrhage. These features of the lesion could be influenced by the fragility and position of neovessels within the plaque. The purpose of this study was to determine whether any association exists between neovessel density, position, morphology, and thromboembolic sequelae.
  
  
  METHODS
  Carotid endarterectomy samples were collected from 15 asymptomatic patients with greater than 80% stenoses and from 13 highly symptomatic patients who had suffered ipsilateral carotid stenotic events within 1 month of surgery. Both groups were matched for gender, age, risk factors, degree of carotid artery stenosis, and plaque size. Samples were stained with hematoxylin/eosin and van Geison. Immunohistochemistry was performed by using an endothelial specific antibody to CD31. Plaques were assessed for histologic characteristics, and neovessels were counted and characterized by size, site, and shape.
  
  
  RESULTS
  There were significantly more neovessels in plaques (P <.00001) and fibrous caps (P <.0001) in symptomatic compared with asymptomatic plaques. Neovessels in symptomatic plaques were larger (P <.004) and more irregular. There was a significant increase in plaque necrosis and rupture in symptomatic plaques. Plaque hemorrhage and rupture were associated with more neovessels within the plaque (P <.017, P <.001) and within the fibrous cap (P <.046, P <.004). Patients with preoperative and intraoperative embolization had significantly more plaque and fibrous cap neovessels (P <.025, P <.001).
  
  
  CONCLUSIONS
  Symptomatic carotid disease is associated with increased neovascularization within the atherosclerotic plaque and fibrous cap. These vessels are larger and more irregular and may contribute to plaque instability and the onset of thromboembolic sequelae.
authors.affiliation: Department of Surgery, University of Leicester, United Kingdom.
authors.forename: M J
authors.initials: MJ
authors.lastname: McCarthy
authors.forename: I M
authors.initials: IM
authors.lastname: Loftus
authors.forename: M M
authors.initials: MM
authors.lastname: Thompson
authors.forename: L
authors.initials: L
authors.lastname: Jones
authors.forename: N J
authors.initials: NJ
authors.lastname: London
authors.forename: P R
authors.initials: PR
authors.lastname: Bell
authors.forename: A R
authors.initials: AR
authors.lastname: Naylor
authors.forename: N P
authors.initials: NP
authors.lastname: Brindle
mesh_terms: D001161:Arteriosclerosis / Q000473:pathology* / Q000503:physiopathology / Q000601:surgery; D002339:Carotid Arteries / Q000473:pathology*; D016893:Carotid Stenosis / Q000473:pathology* / Q000503:physiopathology / Q000601:surgery; D003925:Diabetic Angiopathies; D016894:Endarterectomy, Carotid; D006470:Hemorrhage / Q000473:pathology; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications; D006973:Hypertension / Q000150:complications; D008833:Microcirculation / Q000473:pathology; D017202:Myocardial Ischemia / Q000150:complications; D009336:Necrosis; D009389:Neovascularization, Pathologic / Q000473:pathology* / Q000503:physiopathology; D012307:Risk Factors; D012422:Rupture, Spontaneous / Q000473:pathology; D012907:Smoking; D018709:Statistics, Nonparametric; D013923:Thromboembolism / Q000473:pathology / Q000503:physiopathology