title: Focal and multi-focal plaque macrophage distributions in patients with acute and stable presentations of coronary artery disease.
abstract: OBJECTIVE
  This study was designed to utilize optical coherence tomography (OCT) images of coronary atherosclerotic plaque macrophages to investigate the relationship between macrophage distributions and clinical syndrome.
  
  
  BACKGROUND
  The relative significance of focal macrophage infiltration and generalized coronary inflammation for predicting acute coronary events is a currently a source of considerable controversy in cardiology. Lack of a high-resolution cross-sectional imaging modality has limited macrophage evaluation in vivo.
  
  
  METHODS
  Intracoronary OCT imaging was performed at culprit and non-culprit plaques in patients presenting with stable angina pectoris, unstable angina pectoris,and ST-segment elevation myocardial infarction. Macrophage densities were quantified from these images and analyzed with respect to the clinical presentations of the patients under investigation.
  
  
  RESULTS
  A significantly greater macrophage density was found in unstable patients, both for fibrous and lipid-rich plaques (p = 0.025 and p = 0.002, respectively). Within each patient, the macrophage densities at culprit and non-culprit lesions correlated significantly (r = 0.66, y = 0.88x + 0.43, p = 0.01). Sites of plaque rupture demonstrated a greater macrophage density than non-ruptured sites (6.95 +/- 1.60%, 5.29 +/- 1.17%; p = 0.002). Surface macrophage infiltration was a stronger predictor of unstable clinical presentation than subsurface infiltration for culprit lesions (p = 0.035) but not for remote lesions (p = 0.80).
  
  
  CONCLUSIONS
  Our results demonstrate that increases in both multi-focal and focal macrophage densities are highly correlated with symptom severity. By providing a means of detecting increases in plaque macrophage content before an acute event, this technique may aid in determining prognosis and guiding preventive therapy.
authors.affiliation: Cardiology Division, Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Briain D
authors.initials: BD
authors.lastname: MacNeill
authors.forename: Ik-Kyung
authors.initials: IK
authors.lastname: Jang
authors.forename: Brett E
authors.initials: BE
authors.lastname: Bouma
authors.forename: Nicusor
authors.initials: N
authors.lastname: Iftimia
authors.forename: Masamichi
authors.initials: M
authors.lastname: Takano
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yabushita
authors.forename: Milen
authors.initials: M
authors.lastname: Shishkov
authors.forename: Christopher R
authors.initials: CR
authors.lastname: Kauffman
authors.forename: Stuart L
authors.initials: SL
authors.lastname: Houser
authors.forename: H Thomas
authors.initials: HT
authors.lastname: Aretz
authors.forename: Denise
authors.initials: D
authors.lastname: DeJoseph
authors.forename: Elkan F
authors.initials: EF
authors.lastname: Halpern
authors.forename: Guillermo J
authors.initials: GJ
authors.lastname: Tearney
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease / Q000473:pathology / Q000503:physiopathology; D003327:Coronary Disease / Q000473:pathology* / Q000503:physiopathology; D003331:Coronary Vessels / Q000473:pathology*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology; D008264:Macrophages / Q000473:pathology* / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000473:pathology* / Q000503:physiopathology; D041623:Tomography, Optical Coherence