title: Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: the remodeling paradox.
abstract: OBJECTIVE
  To relate local arterial geometry with markers that are thought to be related to plaque rupture.
  
  
  BACKGROUND
  Plaque rupture often occurs at sites with minor luminal stenosis and has retrospectively been characterized by colocalization of inflammatory cells. Recent studies have demonstrated that luminal narrowing is related with the mode of atherosclerotic arterial remodeling.
  
  
  METHODS
  We obtained 1,521 cross section slices at regular intervals from 50 atherosclerotic femoral arteries. Per artery, the slices with the largest and smallest lumen area, vessel area and plaque area were selected for staining on the presence of macrophages (CD68), T-lymphocytes (CD45RO), smooth muscle cells (alpha-actin) and collagen.
  
  
  RESULTS
  Inflammation of the cap or shoulder of the plaque was observed in 33% of all cross sections. Significantly more CD68 and CD45RO positive cells, more atheroma, less collagen and less alpha-actin positive staining was observed in cross sections with the largest plaque area and largest vessel area vs. cross sections with the smallest plaque area and smallest vessel area, respectively. No difference in the number of inflammatory cells was observed between cross sections with the largest and smallest lumen area.
  
  
  CONCLUSIONS
  Intraindividually, pathohistologic markers previously reported to be related to plaque vulnerability were associated with a larger plaque area and vessel area. In addition, inflammation of the cap and shoulder of the plaque was a common finding in the atherosclerotic femoral artery.
authors.affiliation: Department of Cardiology, Utrecht University Hospital, Interuniversity Cardiology Institute of The Netherlands. g.pasterkamp@hli.azu.nl
authors.forename: G
authors.initials: G
authors.lastname: Pasterkamp
authors.forename: A H
authors.initials: AH
authors.lastname: Schoneveld
authors.forename: A C
authors.initials: AC
authors.lastname: van der Wal
authors.forename: C C
authors.initials: CC
authors.lastname: Haudenschild
authors.forename: R J
authors.initials: RJ
authors.lastname: Clarijs
authors.forename: A E
authors.initials: AE
authors.lastname: Becker
authors.forename: B
authors.initials: B
authors.lastname: Hillen
authors.forename: C
authors.initials: C
authors.lastname: Borst
mesh_terms: D000199:Actins / Q000378:metabolism*; D000368:Aged; D000369:Aged, 80 and over; D001161:Arteriosclerosis / Q000276:immunology / Q000473:pathology*; D001167:Arteritis / Q000276:immunology / Q000473:pathology*; D003094:Collagen / Q000378:metabolism*; D005260:Female; D005263:Femoral Artery / Q000276:immunology / Q000473:pathology*; D006801:Humans; D007091:Image Processing, Computer-Assisted; D007124:Immunoenzyme Techniques; D008264:Macrophages / Q000276:immunology / Q000473:pathology*; D008297:Male; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology*; D014654:Vascular Patency / Q000502:physiology
chemical_list: D000199:Actins; D003094:Collagen