title: Atheromatous plaque cap thickness can be determined by quantitative color analysis during angioscopy: implications for identifying the vulnerable plaque.
abstract: BACKGROUND
  Coronary angioscopy in acute myocardial infarction has frequently revealed disrupted yellow lesions. Furthermore, postmortem studies have demonstrated that these lesions have thin collagenous caps with underlying lipid-rich cores.
  
  
  OBJECTIVE
  We hypothesized that the yellow color is due to visualization of reflected light from the lipid-rich yellow core through a thin fibrous cap. Thus, quantification of yellow color saturation may estimate plaque cap thickness and identify vulnerable plaques.
  
  
  METHODS
  To test this hypothesis, the feasibility of detecting cap thickness was tested using both a model of lipid-rich plaque and human atherosclerotic plaque. The model was constructed by injecting a yellow beta-carotene-lipid emulsion subendothelially into normal bovine aorta. Human plaque was obtained from cadaver aorta. Digitized images were obtained by angioscopy, and percent yellow saturation was analyzed using a custom computer program. Plaque cap thickness was measured by planimetry of digitized images on stained tissue sections. Percent yellow saturation was then correlated with plaque cap thickness.
  
  
  RESULTS
  In the bovine model, plaque cap thickness and percent yellow saturation correlated inversely (r2 = 0.91; p = 0.0001). In human plaques, yellow saturation was significantly greater in atheromatous than in white plaques (p < 0.0004). Also, there was a high correlation between plaque cap thickness and yellow saturation at various angles of view between 40 degrees and 90 degrees, the greatest between 50 degrees and 80 degrees (r2 = 0.75 to 0.88).
  
  
  CONCLUSIONS
  Plaque cap thickness is a determinant of plaque color, and this can be assessed by quantitative colorimetry. Thus, plaque color by angioscopy may be useful for detecting vulnerable plaques.
authors.affiliation: Institute for Prevention of Cardiovascular Disease, Cardiovascular Division, Department of Medicine, Deaconess Hospital, Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Akira
authors.initials: A
authors.lastname: Miyamoto
authors.forename: Alejandro R
authors.initials: AR
authors.lastname: Prieto
authors.forename: Stephan E
authors.initials: SE
authors.lastname: Friedl
authors.forename: Freeman C
authors.initials: FC
authors.lastname: Lin
authors.forename: James E
authors.initials: JE
authors.lastname: Muller
authors.forename: Richard W
authors.initials: RW
authors.lastname: Nesto
authors.forename: George S
authors.initials: GS
authors.lastname: Abela
mesh_terms: D017546:Angioscopy; D000818:Animals; D002417:Cattle; D003124:Colorimetry; D003324:Coronary Artery Disease / Q000473:pathology*; D003331:Coronary Vessels / Q000473:pathology*; D005240:Feasibility Studies; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008055:Lipids / Q000032:analysis; D008954:Models, Biological
chemical_list: D008055:Lipids