title: Quantification of macrophage content in atherosclerotic plaques by optical coherence tomography.
abstract: BACKGROUND
  Macrophage degradation of fibrous cap matrix is an important contributor to atherosclerotic plaque instability. An imaging technology capable of identifying macrophages in patients could provide valuable information for assessing plaque vulnerability. Optical coherence tomography (OCT) is a new intravascular imaging modality that allows cross-sectional imaging of tissue with a resolution of approximately 10 micro m. The aim of this study was to investigate the use of OCT for identifying macrophages in fibrous caps.
  
  
  RESULTS
  OCT images of 26 lipid-rich atherosclerotic arterial segments obtained at autopsy were correlated with histology. Cap macrophage density was quantified morphometrically by immunoperoxidase staining with CD68 and smooth muscle actin and compared with the standard deviation of the OCT signal intensity at corresponding locations. There was a high degree of positive correlation between OCT and histological measurements of fibrous cap macrophage density (r=0.84, P<0.0001) and a negative correlation between OCT and histological measurements of smooth muscle actin density (r=-0.56, P<0.005). A range of OCT signal standard deviation thresholds (6.15% to 6.35%) yielded 100% sensitivity and specificity for identifying caps containing >10% CD68 staining.
  
  
  CONCLUSIONS
  The high contrast and resolution of OCT enables the quantification of macrophages within fibrous caps. The unique capabilities of OCT for fibrous cap characterization suggest that this technology may be well suited for identifying vulnerable plaques in patients.
authors.affiliation: Wellman Laboratories of Photomedicine, Massachusetts General Hospital and Harvard Medical School, Boston, Mass 02114, USA. tearney@helix.mgh.harvard.edu
authors.forename: Guillermo J
authors.initials: GJ
authors.lastname: Tearney
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yabushita
authors.forename: Stuart L
authors.initials: SL
authors.lastname: Houser
authors.forename: H Thomas
authors.initials: HT
authors.lastname: Aretz
authors.forename: Ik-Kyung
authors.initials: IK
authors.lastname: Jang
authors.forename: Kelly H
authors.initials: KH
authors.lastname: Schlendorf
authors.forename: Christopher R
authors.initials: CR
authors.lastname: Kauffman
authors.forename: Milen
authors.initials: M
authors.lastname: Shishkov
authors.forename: Elkan F
authors.initials: EF
authors.lastname: Halpern
authors.forename: Brett E
authors.initials: BE
authors.lastname: Bouma
mesh_terms: D000199:Actins / Q000032:analysis; D000368:Aged; D019412:Anatomy, Cross-Sectional; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001158:Arteries / Q000737:chemistry; D001161:Arteriosclerosis / Q000473:pathology*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000473:pathology; D008027:Light; D008264:Macrophages / Q000166:cytology*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000737:chemistry / Q000166:cytology; D012680:Sensitivity and Specificity; D014054:Tomography / Q000379:methods*; D000097382:CD68 Molecule
chemical_list: D000199:Actins; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; C067980:CD68 antigen, human; D000097382:CD68 Molecule