title: Infection with Helicobacter pylori is not a major independent risk factor for stable coronary heart disease: lack of a role of cytotoxin-associated protein A-positive strains and absence of a systemic inflammatory response.
abstract: BACKGROUND
  There is controversy about the association between Helicobacter pylori infection and manifestations of coronary heart disease (CHD), the potential role of the more virulent H pylori strains, and whether or not a positive serostatus is related to increased levels of markers of systemic inflammation.
  
  
  RESULTS
  We assessed the prevalence of an infection with H pylori and in particular the anti-cytotoxin-associated protein A (CagA) antibody response of the more virulent strains expressing CagA in 312 patients with stable CHD and in 479 control subjects. Serological prevalence of H pylori infection (IgG titer) was significantly higher in patients than in control subjects after adjustment for age and sex (44.2% versus 31.3%, P<0.001). After adjustment for various covariates in multiple logistic regression, the odds ratio (OR) for CHD was 1.3 (95% CI, 0.9 to 1.9) given a positive IgG serostatus. The prevalence of CagA-positive strains was 27.9% in patients and 21.7% in control subjects (P=0.076 adjusted for age and sex). The OR for CHD in the fully adjusted model was 1.1 (95% CI, 0.7 to 1.7). None of the inflammatory markers (C-reactive protein, fibrinogen, plasma viscosity, or leukocytes) was significantly different according to serostatus.
  
  
  CONCLUSIONS
  In this large case-control study, the association of H pylori infection with stable CHD was strongly reduced and was no longer statistically significant after controlling for potential confounders. We also found no independent association between the more virulent strains and CHD. In addition, a positive serostatus was not associated with a systemic inflammatory response. Thus, these data do not support the hypothesis that infection with H pylori might be a major risk factor for stable CHD.
authors.affiliation: Department of Internal Medicine II-Cardiology, University of Ulm Medical Center, Ulm, Germany. wolfgang.koenig@medizin.uni-ulm.de
authors.forename: W
authors.initials: W
authors.lastname: Koenig
authors.forename: D
authors.initials: D
authors.lastname: Rothenbacher
authors.forename: A
authors.initials: A
authors.lastname: Hoffmeister
authors.forename: M
authors.initials: M
authors.lastname: Miller
authors.forename: G
authors.initials: G
authors.lastname: Bode
authors.forename: G
authors.initials: G
authors.lastname: Adler
authors.forename: V
authors.initials: V
authors.lastname: Hombach
authors.forename: W
authors.initials: W
authors.lastname: März
authors.forename: M B
authors.initials: MB
authors.lastname: Pepys
authors.forename: H
authors.initials: H
authors.lastname: Brenner
mesh_terms: D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial / Q000032:analysis; D001426:Bacterial Proteins / Q000032:analysis; D015415:Biomarkers; D001944:Breath Tests; D002247:Carbon Isotopes; D016022:Case-Control Studies; D003327:Coronary Disease / Q000453:epidemiology* / Q000382:microbiology*; D005260:Female; D016481:Helicobacter Infections / Q000453:epidemiology* / Q000276:immunology; D016480:Helicobacter pylori / Q000737:chemistry / Q000276:immunology* / Q000472:pathogenicity; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D016036:Seroepidemiologic Studies; D018746:Systemic Inflammatory Response Syndrome / Q000453:epidemiology* / Q000276:immunology; D014508:Urea / Q000032:analysis; D014774:Virulence
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D015415:Biomarkers; D002247:Carbon Isotopes; D007070:Immunoglobulin A; D007074:Immunoglobulin G; C080866:cagA protein, Helicobacter pylori; D014508:Urea