title: Antibodies to common infectious agents in coronary artery disease patients with and without rheumatic conditions.
abstract: OBJECTIVE
  The mechanism linking inflammation to atherosclerosis is unknown. We have previously demonstrated a high occurrence of inflammation in the aortic adventitia of patients with coronary artery disease (CAD), which was more pronounced in patients with inflammatory rheumatic diseases (IRDs), and which might be involved in the pathogenesis of cardiovascular disease. In theory, infections might play a role in the pathogenesis of vascular inflammation or atherosclerosis, or both. This study compared seropositivity and the burden of several common infections in patients with CAD, both with and without IRD, and in healthy controls (HCs). Moreover, we looked for relationships between the examined antibodies and inflammatory infiltrates in the aortic adventitia.
  
  
  METHODS
  We examined sera for Chlamydophila pneumoniae, Mycoplasma pneumoniae, Helicobacter pylori, CMV, Streptococcus pyogenes, parvovirus B19, HBV and HCV with commercially available serological tests in 67 patients with IRD, 52 patients without IRD and 30 HCs.
  
  
  RESULTS
  We observed neither any statistically significant differences in the examined antibodies between the groups nor a difference in the burden of infection. Except for a protective effect of mycoplasma immunoglobulin A (IgA), we did not find any other associations between the examined antibodies and the occurrence of aortic adventitial mononuclear cell infiltrates.
  
  
  CONCLUSIONS
  Our study does not support the notion that chronic infections or infectious burden contribute to accelerated occurrence of CAD in IRD. Mycoplasma IgA was related to a lower occurrence of aortic adventitial inflammation.
authors.affiliation: Department of Medical Microbiology, Hospital Innlandet Trust, Lillehammer NO 2609, Norway. carolagrub@hotmail.com
authors.forename: Carola
authors.initials: C
authors.lastname: Grub
authors.forename: Cathrine
authors.initials: C
authors.lastname: Brunborg
authors.forename: Viggo
authors.initials: V
authors.lastname: Hasseltvedt
authors.forename: Pål
authors.initials: P
authors.lastname: Aukrust
authors.forename: Oystein
authors.initials: O
authors.lastname: Førre
authors.forename: Sven Martin
authors.initials: SM
authors.lastname: Almdahl
authors.forename: Ivana
authors.initials: I
authors.lastname: Hollan
mesh_terms: D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D000914:Antibodies, Viral / Q000097:blood; D001011:Aorta / Q000473:pathology; D001424:Bacterial Infections / Q000150:complications* / Q000276:immunology; D016022:Case-Control Studies; D003238:Connective Tissue / Q000473:pathology; D003324:Coronary Artery Disease / Q000382:microbiology* / Q000473:pathology; D005260:Female; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D008297:Male; D008875:Middle Aged; D011019:Pneumonia, Mycoplasma / Q000276:immunology; D012216:Rheumatic Diseases / Q000150:complications*; D014777:Virus Diseases / Q000150:complications* / Q000276:immunology
chemical_list: D000907:Antibodies, Bacterial; D000914:Antibodies, Viral; D007070:Immunoglobulin A