title: Helicobacter pylori infection, chronic atrophic gastritis and major cardiovascular events: a population-based cohort study.
abstract: OBJECTIVE
  There is debate whether infection with Helicobacter (H.) pylori, the main inducer of chronic atrophic gastritis (CAG), is a risk factor for cardiovascular disease and premature mortality.
  
  
  METHODS
  Serological measurements of H. pylori infection and pepsinogen (PG) I and II were obtained in a population-based German cohort of 9953 older adults (50-74 years). Cox regression was employed to estimate hazard ratios (HR) and 95% confidence intervals (CI) for myocardial infarction, stroke, cardiovascular and all-cause mortality during five-year follow-up.
  
  
  RESULTS
  According to serology, 4977 participants (51.9%) were infected with H. pylori (2604 with cytotoxin-associated gene A (cagA) strains) and 541 (5.7%) had CAG (PGI<70 ng/mL and PGI/PGII<3). During follow-up, 540 participants died (163 from cardiovascular causes), 170 experienced a primary myocardial infarction and 241 had a stroke. Neither cytotoxin-associated gene A (cagA) negative nor cagA positive H. pylori infections were associated with an increased risk for myocardial infarction, stroke or all-cause mortality. Intriguingly, infection with cagA positive H. pylori strains was inversely associated with cardiovascular mortality (HR, 0.62; CI: 0.41-0.94). No statistically significant associations were observed for the small group of participants with CAG, but point estimates of adjusted HRs for myocardial infarction, stroke and cardiovascular mortality were all below 1 (0.71, 0.59 and 0.65, respectively).
  
  
  CONCLUSIONS
  Our results do not support the hypothesis that H. pylori infection or CAG are risk factors for cardiovascular disease or mortality and instead suggest an inverse relationship of cagA positive H. pylori infection with fatal cardiovascular events.
authors.affiliation: Division of Clinical Epidemiology and Aging Research, German Cancer Research Center, Heidelberg, Germany. b.schoettker@dkfz-heidelberg.de
authors.forename: Ben
authors.initials: B
authors.lastname: Schöttker
authors.forename: Mariam A
authors.initials: MA
authors.lastname: Adamu
authors.forename: Melanie N
authors.initials: MN
authors.lastname: Weck
authors.forename: Heiko
authors.initials: H
authors.lastname: Müller
authors.forename: Hermann
authors.initials: H
authors.lastname: Brenner
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000453:epidemiology* / Q000382:microbiology / Q000401:mortality; D002908:Chronic Disease; D005260:Female; D005757:Gastritis, Atrophic / Q000201:enzymology / Q000453:epidemiology* / Q000382:microbiology / Q000401:mortality; D005858:Germany / Q000453:epidemiology; D016481:Helicobacter Infections / Q000453:epidemiology* / Q000382:microbiology / Q000401:mortality; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology; D020116:Pepsinogen A / Q000097:blood; D020115:Pepsinogen C / Q000097:blood; D016016:Proportional Hazards Models; D018570:Risk Assessment; D012307:Risk Factors; D020521:Stroke / Q000453:epidemiology; D013997:Time Factors
chemical_list: D015415:Biomarkers; D020115:Pepsinogen C; D020116:Pepsinogen A