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[Helicobacter pylori and coronary heart diseases--hypotheses and facts]
1Medizinische Klinik II (Gastroenterologie, Stoffwechsel- und Infektionskrankheiten), Klinikum Remscheid GmbH, Remscheid.
Insights
Helicobacter pylori (HP) infection is not definitively linked to coronary heart disease (CHD). Despite numerous studies, evidence for a correlation between HP seropositivity and CHD remains weak and requires further investigation.
Area of Science:
- Cardiology
- Infectious Diseases
- Gastroenterology
Background:
- The hypothesis suggests Helicobacter pylori (HP) infection may correlate with coronary heart disease (CHD) via chronic inflammation.
- This proposes gastric HP colonization as a potential additional risk factor for CHD.
Purpose of the Study:
- To evaluate the evidence supporting a correlation between HP infection and CHD.
- To assess the reliability of studies examining the HP-CHD association.
Main Methods:
- Review of 35 studies investigating HP seropositivity and CHD occurrence.
- Analysis of 8 publications with definitive CHD diagnosis via coronary angiography.
- Inclusion of a meta-analysis of 18 studies with 10,000 patients.
Main Results:
- Only 2 of 8 angiographically verified studies showed a significant association between HP positivity and CHD.
- A meta-analysis of 18 studies found no correlation between HP seropositivity and acute phase proteins.
- The overall evidence for a positive correlation between HP and CHD is not conclusive.
Conclusions:
- A definitive link between gastric HP colonization and CHD has not been established.
- Further research is needed to confirm proposed mechanisms like hyperhomocysteinemia or autoimmune responses.
- The association between HP infection and cardiovascular health requires more robust scientific validation.
Abstract:
In 1994 Mendall et al. (9) have suggested that there might be a correlation between Helicobacter pylori (HP) infection and coronary heart disease (CHD), mediated by a chronic low-grade acute phase reaction with mildly raised serum or plasma concentrations of C-reactive protein and fibrinogen. According to this hypothesis, a gastric HP colonization might be an additional risk factor for CHD. In the meantime, 35 studies have examined whether HP seropositivity is associated with CHD occurrence. However, in 8 publications only CHD was definitively proven (in CHD+ patients) or excluded (in the corresponding control groups) by coronary artery angiography, and in only 2 of them (1 abstract, 1 full-length publication) a significant association between HP positivity (serologically proven) and CHD was ascertained. Additionally, a metaanalysis of 18 studies including 10,000 patients could not demonstrate any correlations between HP seropositivity and different acute phase proteins (66). Thus, a positive correlation between gastric HP colonization and CHD is far from being proven. Further proposed links between HP infection and CHD such as hyperhomocysteinemia (67) or autoimmune mechanisms (71) due to cross-reacting antibodies to HP HSP60/65 (heat shock protein) with human endothel-derived HSP60/65 need further confirmation.