Helicobacter pylori and ischemic heart disease
E Vizzardi1, I Bonadei, B Piovanelli
1Department of Cardiology, University of Brescia, Brescia, Italy. enrico.vizzardi@tin.it
Insights
Helicobacter pylori infection may influence cardiovascular diseases, including ischemic heart disease. However, research on the link between H. pylori and coronary artery disease shows conflicting results, necessitating further investigation.
Area of Science:
- Cardiovascular Science
- Infectious Disease Epidemiology
Background:
- Atherosclerotic diseases, such as stroke and ischemic heart disease (IHD), are significant health concerns.
- Helicobacter pylori (H. pylori) infection has been investigated for its potential role in vascular wall damage and atheromatous plaque formation.
Purpose of the Study:
- To explore the relationship between H. pylori infection and the development of coronary artery disease (CAD).
- To investigate potential mechanisms by which H. pylori might influence IHD, including endothelial colonization, lipid profile changes, coagulation, and systemic inflammation.
Main Methods:
- Review of numerous studies examining the association between H. pylori infection and CAD.
- Analysis of proposed pathways linking H. pylori to cardiovascular pathogenesis.
Main Results:
- Studies investigating the role of H. pylori in CAD pathogenesis have yielded conflicting results.
- Some trials found no significant relationship between H. pylori infection and increased CAD risk.
Conclusions:
- The current evidence regarding H. pylori's role in CAD is contradictory.
- Further research is required to clarify the association and explore potential therapeutic strategies, such as H. pylori eradication.
Abstract:
In the last years, a considerable number of studies have been performed on the relationship between infection from Helicobacter Pylori and atherosclerotic diseases, like stroke and ischemic heart disease. In particular, some infections could have a role on the genesis and development of damage to the vascular wall and of atheromatous plaque. It has been suggested that HP could influence the development of IHD through different pathways, such as endothelial cells colonization, changes in the lipid profiles, increased coagulation and platelet aggregation levels, induction of molecular mimicry mechanisms and the promotion of a low-grade systemic inflammation. Based on this hypothesis, it has been performed a considerable number of studies in order to investigate the role of HP in the development and pathogenesis of CAD. Most of this trials gave conflicting results, some denying the presence of a possible relationship between HP infection and increased risk of CAD. Despite of that, results from these studies have raised new interesting perspectives on coronary heart disease, especially regarding the possibility of modifying the clinical history of the disease through eradication of these microorganisms. The results are contradictory and require further investigation.
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