title: Increased risk of atherosclerosis is confined to CagA-positive Helicobacter pylori strains: prospective results from the Bruneck study.
abstract: OBJECTIVE
  Accumulating evidence indicates that a variety of infections contribute to the pathogenesis of atherosclerosis, but there is controversy concerning the impact of Helicobacter pylori infections in atherosclerosis.
  
  
  METHODS
  We evaluated seropositivity to H pylori and to its cytotoxin-associated gene A (CagA) product in a large, prospective, population-based study (n=684). Intima-media thickness and atherosclerosis of carotid arteries were thoroughly assessed by high-resolution duplex scanning.
  
  
  RESULTS
  In our study population, H pylori infections defined by seropositivity have no relationship with levels of classic cardiovascular risk factors or markers of systemic inflammation, except for elevated levels of immune reactions to mycobacterial heat shock protein 65. The latter showed a trend toward highest levels in those harboring virulent H pylori strains (P=0.08). Common carotid artery intima-media thickness-both absolute values and changes between 1995 and 2000-were significantly enhanced in subjects seropositive to CagA but not in those infected with CagA-negative H pylori strains. There was a clear dose-response relation between anti-CagA antibodies and both intima-media thickness and atherosclerosis risk. Notably, the risk of atherosclerosis associated with CagA seropositivity was amplified by elevated C-reactive protein levels.
  
  
  CONCLUSIONS
  Infections with virulent CagA-bearing H pylori strains may contribute to the pathogenesis of early atherosclerosis by aggravating immune-inflammatory reactions.
authors.affiliation: Institute for Biomedical Aging Research, Austrian Academy of Sciences, Innsbruck, Austria.
authors.forename: Manuel
authors.initials: M
authors.lastname: Mayr
authors.forename: Stefan
authors.initials: S
authors.lastname: Kiechl
authors.forename: Michael A
authors.initials: MA
authors.lastname: Mendall
authors.forename: Johann
authors.initials: J
authors.lastname: Willeit
authors.forename: Georg
authors.initials: G
authors.lastname: Wick
authors.forename: Qingbo
authors.initials: Q
authors.lastname: Xu
mesh_terms: D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial; D001161:Arteriosclerosis / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000382:microbiology*; D001426:Bacterial Proteins / Q000235:genetics* / Q000276:immunology; D015415:Biomarkers / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D015897:Comorbidity; D003710:Demography; D005260:Female; D016481:Helicobacter Infections / Q000453:epidemiology / Q000235:genetics* / Q000276:immunology; D016480:Helicobacter pylori / Q000235:genetics* / Q000276:immunology / Q000302:isolation & purification; D006801:Humans; D007558:Italy / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011446:Prospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D016036:Seroepidemiologic Studies; D017539:Tunica Intima / Q000000981:diagnostic imaging; D017540:Tunica Media / Q000000981:diagnostic imaging; D014463:Ultrasonography; D014774:Virulence / Q000235:genetics
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D015415:Biomarkers; C080866:cagA protein, Helicobacter pylori; D002097:C-Reactive Protein