title: Impact of intimal pathogen burden in acute coronary syndromes--correlation with inflammation, thrombosis, and autoimmunity.
abstract: BACKGROUND
  Increasing evidence supports a link between serological evidence of pathogen burden (PB) and the risk for future cardiovascular events. Our study evaluates the intimal presence of 4 pathogens in atheroma, clinically associated with acute coronary syndromes (ACS) and stable angina (SA), and the effect on the expression of intimal C-reactive protein (CRP), tissue factor (TF) and human heat-shock protein 60 (hHSP60).
  
  
  METHODS
  Coronary atherectomy specimens retrieved from 60 primary lesions of patients with ACS (n=35) or SA (n=25) were assessed immunohistochemically for the presence of Chlamydia pneumoniae (Cpn), Helicobacter pylori (HP), Cytomegalovirus (CMV) and Epstein–Barr Virus (EBV) and for the expression of CRP, TF, and hHSP60.
  
  
  RESULTS
  Analysis revealed eight lesions without, 22 lesions with one, 19 lesions with two, seven lesions with three, and four lesions with four pathogens. Cpn was present in 73%, HP in 31%, CMV in 16%, and EBV in 40%. Mean value of PB in ACS-lesions was significantly increased. Expressions of CRP, TF, and hHSP60 were significantly higher in ACS lesions. The number of infectious pathogens correlated significant with the expressions of CRP, TF, and hHSP60.
  
  
  CONCLUSIONS
  Our data demonstrate the impact of PB in plaque instability and suggest local proinflammatory, prothrombotic, and proimmunogenic effects.
authors.affiliation: Department of Internal Medicine II/Cardiology, University of Bonn, Bonn, Germany. rene.andrie@ukb.uni-bonn.de
authors.forename: René P
authors.initials: RP
authors.lastname: Andrié
authors.forename: Gerhard
authors.initials: G
authors.lastname: Bauriedel
authors.forename: Izabela
authors.initials: I
authors.lastname: Tuleta
authors.forename: Peter
authors.initials: P
authors.lastname: Braun
authors.forename: Georg
authors.initials: G
authors.lastname: Nickenig
authors.forename: Dirk
authors.initials: D
authors.lastname: Skowasch
mesh_terms: D054058:Acute Coronary Syndrome / Q000276:immunology / Q000382:microbiology / Q000601:surgery / Q000821:virology; D000368:Aged; D000787:Angina Pectoris / Q000276:immunology / Q000382:microbiology / Q000601:surgery / Q000821:virology; D017225:Atherectomy, Coronary; D015551:Autoimmunity; D002097:C-Reactive Protein / Q000032:analysis; D018834:Chaperonin 60 / Q000032:analysis; D016009:Chi-Square Distribution; D016993:Chlamydophila pneumoniae / Q000472:pathogenicity*; D003331:Coronary Vessels / Q000276:immunology / Q000382:microbiology / Q000821:virology; D003587:Cytomegalovirus / Q000472:pathogenicity*; D005260:Female; D016480:Helicobacter pylori / Q000472:pathogenicity*; D004854:Herpesvirus 4, Human / Q000472:pathogenicity*; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000382:microbiology / Q000821:virology; D008297:Male; D008875:Middle Aged; D013925:Thromboplastin / Q000032:analysis; D013927:Thrombosis / Q000276:immunology / Q000382:microbiology / Q000821:virology
chemical_list: D018834:Chaperonin 60; D002097:C-Reactive Protein; D013925:Thromboplastin