title: Clinically stable angina pectoris is not necessarily associated with histologically stable atherosclerotic plaques.
abstract: OBJECTIVE
  To investigate the extent of plaque inflammation in culprit lesions of patients with chronic stable angina.
  
  
  METHODS
  Retrospective study.
  
  
  METHODS
  Amsterdam reference centre.
  
  
  METHODS
  89 consecutive patients who underwent directional coronary atherectomy, 58 of whom met the following inclusion criteria: chronic stable angina (Canadian Cardiovascular Society classification 1-3 (group 1, n = 28)); unstable angina (Braunwald class II (group 2, n = 18)); unstable angina (Braunwald class III (group 3, n = 12)).
  
  
  METHODS
  Directional atherectomy in patients with angina pectoris.
  
  
  METHODS
  Tissue areas of culprit lesions occupied by inflammatory cells and smooth muscle cells related to clinically defined ischaemic syndrome.
  
  
  RESULTS
  Areas (% of total surface area (mean (SEM)) rich in smooth muscle cells were larger in patients with chronic stable angina (group 1, 51.2 (20.9)) than in those with unstable angina (group 2, 42.1 (20.5); group 3, 29.5 (19.4)) (1 v 2 and 2 v 3, NS; 1 v 3, P < 0.004). Macrophage rich areas were significantly smaller in patients with stable angina (group 1, 21.8 (11.9)) than in those with unstable angina (group 2, 31.5 (14.6); group 3, 46.4 (16.7)) (1 v 2, P < 0.02; 2 v 3, P < 0.02; 1 v 3, P < 0.001). Mean numbers of T cells per mm2 were as follows: group 1, 17 (9.4); group 2, 25 (15.9); group 3, 41 (30.6) (1 v 2, P 0.04; 2 v 3, P 0.07; 1 v 3, P < 0.001). Areas with HLA-DR positive cells showed the same pattern as macrophages and T cells and were smaller in stable (29.9 (12.4)) than in unstable angina (group 2, 40.4 (17.6); group 3, 52.4 (12.0)) (1 v 2, P < 0.02; 2 v 3, P < 0.05; 1 v 3, P < 0.001).
  
  
  CONCLUSIONS
  The inverse relation between the extent of inflammatory activity in plaque tissues of culprit lesions and the clinical stability of the ischaemic syndrome supports the concept that reduction of inflammation favours plaque stabilisation. At the same time, the considerable overlap between groups indicates that patients with clinically stable angina do not all have histologically stable plaques.
authors.affiliation: Department of Cardiovascular Pathology, University of Amsterdam, Netherlands.
authors.forename: A C
authors.initials: AC
authors.lastname: van der Wal
authors.forename: A E
authors.initials: AE
authors.lastname: Becker
authors.forename: K T
authors.initials: KT
authors.lastname: Koch
authors.forename: J J
authors.initials: JJ
authors.lastname: Piek
authors.forename: P
authors.initials: P
authors.lastname: Teeling
authors.forename: C M
authors.initials: CM
authors.lastname: van der Loos
authors.forename: G K
authors.initials: GK
authors.lastname: David
mesh_terms: D000787:Angina Pectoris / Q000276:immunology / Q000473:pathology* / Q000601:surgery; D000789:Angina, Unstable / Q000276:immunology / Q000473:pathology / Q000601:surgery; D017225:Atherectomy, Coronary; D003331:Coronary Vessels / Q000276:immunology / Q000473:pathology*; D006684:HLA-DR Antigens / Q000378:metabolism; D006801:Humans; D007090:Image Interpretation, Computer-Assisted; D007150:Immunohistochemistry; D008264:Macrophages / Q000473:pathology; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D011446:Prospective Studies; D013601:T-Lymphocytes / Q000473:pathology
chemical_list: D006684:HLA-DR Antigens