title: Association between complex coronary artery stenosis and unstable angina and the extent of plaque inflammation.
abstract: OBJECTIVE
  Patients with unstable coronary syndromes often have complex morphology of coronary stenoses at angiography. We evaluated the association between qualitative assessment of coronary stenoses and plaque inflammation determined by immunohistochemistry.
  
  
  METHODS
  A total of 79 patients with unstable (n = 46) or stable angina (n = 33) underwent directional coronary atherectomy for culprit lesions. Qualitative analysis of coronary angiograms was performed using a modified Ambrose classification. Coronary lesions were categorized as either simple (concentric and eccentric type I, n = 29) or complex (eccentric type II and multiple irregularities, n = 50). Cryostat sections of retrieved atherosclerotic specimens were stained immunohistochemically with monoclonal antibodies, alpha-actin (smooth muscle cells), CD68 (macrophages), and CD3 (T lymphocytes). The extent of atherosclerotic inflammation within each coronary lesion was determined by the percentage of immunopositive macrophages per total tissue area (including smooth muscle cells) and the number of T lymphocytes per mm(2).
  
  
  RESULTS
  The mean (+/- SD) percentage of macrophages in atherectomy specimens from patients with unstable angina was greater than in specimens from patients with stable angina (21% +/- 14% vs. 13% +/- 10%, P = 0.01); similar results were seen when complex coronary lesions were compared with simple lesions (23% +/- 13% vs. 9% +/- 8%, P <0.001). In multivariate linear regression models, the combination of unstable angina and lesion complexity was strongly associated with the percentage of plaque macrophages.
  
  
  CONCLUSIONS
  The extent of atherosclerotic plaque inflammation is associated with angiographic grading of coronary lesion complexity and unstable angina.
authors.affiliation: Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. m.meuwissen@amc.uva.nl
authors.forename: Martijn
authors.initials: M
authors.lastname: Meuwissen
authors.forename: Allard C
authors.initials: AC
authors.lastname: van der Wal
authors.forename: Karel T
authors.initials: KT
authors.lastname: Koch
authors.forename: Chris M
authors.initials: CM
authors.lastname: van der Loos
authors.forename: Steven A J
authors.initials: SA
authors.lastname: Chamuleau
authors.forename: Peter
authors.initials: P
authors.lastname: Teeling
authors.forename: Robbert J
authors.initials: RJ
authors.lastname: de Winter
authors.forename: Jan G P
authors.initials: JG
authors.lastname: Tijssen
authors.forename: Anton E
authors.initials: AE
authors.lastname: Becker
authors.forename: Jan J
authors.initials: JJ
authors.lastname: Piek
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000150:complications* / Q000175:diagnosis / Q000276:immunology*; D017225:Atherectomy, Coronary; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000150:complications* / Q000175:diagnosis / Q000276:immunology*; D023921:Coronary Stenosis / Q000150:complications* / Q000175:diagnosis / Q000276:immunology*; D005260:Female; D006801:Humans; D008264:Macrophages / Q000276:immunology; D008297:Male; D008875:Middle Aged; D032389:Myocytes, Smooth Muscle / Q000276:immunology; D012720:Severity of Illness Index; D013601:T-Lymphocytes / Q000276:immunology