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Updated: May 26, 2026

Rapid Detection of Fecal Antigen of Helicobacter pylori Infection Based on Double Antibody Sandwich Detection Technology
Published on: May 23, 2025
Helicobacter pylori infection, chronic atrophic gastritis and major cardiovascular events: a population-based cohort
Ben Schöttker1, Mariam A Adamu, Melanie N Weck
1Division of Clinical Epidemiology and Aging Research, German Cancer Research Center, Heidelberg, Germany. b.schoettker@dkfz-heidelberg.de
Insights
Helicobacter pylori infection, including cagA-positive strains, does not increase cardiovascular disease or mortality risk. Interestingly, cagA-positive H. pylori infection shows an inverse association with fatal cardiovascular events.
Area of Science:
- Cardiovascular epidemiology
- Infectious disease research
- Gastroenterology
Background:
- Helicobacter pylori (H. pylori) is a primary cause of chronic atrophic gastritis (CAG).
- The link between H. pylori infection and cardiovascular disease (CVD) risk remains debated.
- CAG is also being investigated for its potential role in systemic diseases.
Purpose of the Study:
- To investigate the association between H. pylori infection and CAG with cardiovascular disease and mortality.
- To determine if H. pylori infection status, particularly with cytotoxin-associated gene A (cagA) strains, impacts risks for myocardial infarction, stroke, and overall mortality.
Main Methods:
- A population-based German cohort of 9953 older adults (50-74 years) was studied.
- Serological tests measured H. pylori infection and pepsinogen (PG) levels.
- Cox regression analysis assessed hazard ratios (HR) for cardiovascular events and mortality over five years.
Main Results:
- Over 50% of participants were infected with H. pylori; 5.7% had CAG.
- No increased risk for myocardial infarction, stroke, or all-cause mortality was linked to H. pylori infection (cagA-negative or cagA-positive).
- A significant inverse association was found between cagA-positive H. pylori infection and cardiovascular mortality (HR: 0.62).
Conclusions:
- H. pylori infection and CAG are not supported as risk factors for cardiovascular disease or mortality.
- An inverse relationship between cagA-positive H. pylori infection and fatal cardiovascular events is suggested.
- Further research may clarify the complex interplay between H. pylori and cardiovascular health.
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.
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