title: Diffuse and active inflammation occurs in both vulnerable and stable plaques of the entire coronary tree: a histopathologic study of patients dying of acute myocardial infarction.
abstract: OBJECTIVE
  This study was undertaken to define and compare geographic coronary artery inflammation in patients who were dying of acute myocardial infarction (AMI), chronic stable angina (SA), and noncardiac causes (CTRL).
  
  
  BACKGROUND
  Biochemical markers and flow cytometry provide indirect evidence of diffuse coronary inflammation in patients dying of acute coronary syndromes. Yet no histopathologic studies have corroborated these findings. A key unanswered question is whether the inflammatory burden involves the entire coronary tree or is limited to a few plaques.
  
  
  METHODS
  We examined 544 coronary artery segments from 16 patients with AMI, 109 segments from 5 patients with SA, and 304 coronary segments from 9 patients with CTRL.
  
  
  RESULTS
  An average of 6.8 +/- 0.5 vulnerable segments per patient were found in the AMI group (in addition to culprit lesions) compared with an average of 0.8 +/- 0.3 and 1.4 +/- 0.3 vulnerable lesions/patient in the SA and CTRL groups, respectively. The AMI group, independent of the type of plaque observed, showed significantly more inflammatory infiltrates compared with the SA and CTRL groups (121.6 +/- 12.4 cell x mm2 vs. 37.3 +/- 11.9 cell x mm2 vs. 26.6 +/- 6.8 cell x mm2, p = 0.0001). In AMI patients, active inflammation was not only evident within the culprit lesion and vulnerable plaques but also involved stable plaques. These showed a three- to four-fold higher inflammation than vulnerable and stable plaques from the SA and CTRL groups, respectively.
  
  
  CONCLUSIONS
  This histopathologic study found that both vulnerable and stable coronary plaques of patients dying of AMI are diffusely infiltrated by inflammatory cells.
authors.affiliation: Department of Pathology, University of Rome Tor Vergata, Rome, Italy.
authors.forename: Alessandro
authors.initials: A
authors.lastname: Mauriello
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Sangiorgi
authors.forename: Stefano
authors.initials: S
authors.lastname: Fratoni
authors.forename: Giampiero
authors.initials: G
authors.lastname: Palmieri
authors.forename: Elena
authors.initials: E
authors.lastname: Bonanno
authors.forename: Lucia
authors.initials: L
authors.lastname: Anemona
authors.forename: Robert S
authors.initials: RS
authors.lastname: Schwartz
authors.forename: Luigi Giusto
authors.initials: LG
authors.lastname: Spagnoli
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000787:Angina Pectoris / Q000473:pathology*; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001167:Arteritis / Q000473:pathology*; D017252:CD3 Complex / Q000032:analysis; D002423:Cause of Death; D002908:Chronic Disease; D003324:Coronary Artery Disease / Q000473:pathology*; D003327:Coronary Disease / Q000473:pathology*; D023921:Coronary Stenosis / Q000473:pathology; D003328:Coronary Thrombosis / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology; D005260:Female; D005434:Flow Cytometry; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D007124:Immunoenzyme Techniques; D018836:Inflammation Mediators / Q000032:analysis; D007962:Leukocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000473:pathology*; D013601:T-Lymphocytes / Q000473:pathology; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D017252:CD3 Complex; D006684:HLA-DR Antigens; D018836:Inflammation Mediators; C067980:CD68 antigen, human; D000097382:CD68 Molecule