Potential link between Helicobacter pylori and ischemic heart disease: does the bacterium elicit thrombosis?
S Fagoonee1, C De Angelis, C Elia
1Department of Biology, Biochemistry and Genetics and Molecular Biotechnology Center, University of Turin, Turin, Italy.
Insights
Helicobacter pylori infection may contribute to early acute coronary syndrome events by promoting platelet aggregation and thrombosis. Research shows H. pylori strains interact with platelets, potentially increasing ischemic heart disease risk.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Hematology
Background:
- Numerous observations link Helicobacter pylori (H. pylori) infection to ischemic heart disease (IHD).
- The potential role of H. pylori in acute coronary syndrome (ACS) pathogenesis remains controversial.
- This study investigates H. pylori's pathogenic mechanisms related to IHD, focusing on platelet aggregation and thrombosis.
Purpose of the Study:
- To explore the potential pathogenic mechanisms linking H. pylori infection to ischemic heart disease.
- To investigate the role of H. pylori in platelet aggregation and thrombosis, key factors in acute coronary syndrome.
Main Methods:
- A MEDLINE search was conducted for English-language publications from 1965 to 2009.
- Reviewed studies investigating the link between H. pylori and cardiovascular events, specifically focusing on platelet function and thrombosis.
- Examined findings from human and animal models regarding H. pylori's interaction with platelets and leukocytes.
Main Results:
- Some H. pylori strains bind von Willebrand factor and interact with glycoprotein Ib, inducing platelet aggregation in humans.
- Animal models showed H. pylori infection promoted platelet-leukocyte aggregate formation in gastric venules.
- Antibodies against L- and P-selectin abrogated this aggregate formation, suggesting a role for these adhesion molecules.
Conclusions:
- H. pylori infection may play a role in the early stages of acute coronary syndrome through mechanisms involving platelet aggregation.
- The interaction of H. pylori with von Willebrand factor and glycoprotein Ib is a key finding.
- Further research is needed to elucidate these mechanisms and translate findings into clinical practice for managing ischemic heart disease.
Abstract:
Over the past fifteen years, numerous observations have linked Helicobacter pylori (H. pylori) infection to ischemic heart disease (IHD). Despite the controversial literature data, it has been postulated that if a role is plausible, it will be in the early events of the acute coronary syndrome. According to this model, we focused on the potential pathogenic mechanisms relating H. pylori to IHD like platelet aggregation and thrombosis. To identify all publications in this field, a MEDLINE search of studies published in English from 1965 to 2009 was conducted. Although very few investigations were found, these showed data of paramount importance. In particular, it has been demonstrated that some strains of H. pylori bind von Willebrand factor and interact with glycoprotein Ib to induce platelet aggregation in humans. In experiments from animal models, such infection promoted the formation of platelet aggregates by both a marked increase in the flux of rolling leukocytes and the appearance of platelet and leukocyte-platelet aggregates in gastric venules. This aggregate formation was abrogated by antibodies against specific adhesion molecules (L- and P-selectin). The future challenge is to gain more knowledge in this field and to translate these information into clinical practice.
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