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Association of Helicobacter pylori infection with coronary heart disease
P Pieniazek1, E Karczewska, A Duda
1Department of Physiology, Jagiellonian University, Cracow, Poland.
Insights
Helicobacter pylori (HP) infection is linked to a higher risk of coronary artery disease (CAD). Serological evidence of HP and CagA antibodies significantly increases CAD risk, suggesting a role in atherosclerosis.
Area of Science:
- Cardiology
- Infectious Diseases
- Gastroenterology
Background:
- Helicobacter pylori (HP) is a primary cause of gastritis and peptic ulcers.
- HP infection is increasingly associated with cardiovascular diseases, potentially via inflammatory pathways.
- Cytokines like IL-6 and TNF-alpha are implicated in both HP infection and cardiovascular disease.
Purpose of the Study:
- To investigate the seroprevalence of HP infection and antibodies to CagA in patients with coronary artery disease (CAD).
- To assess the correlation between HP infection markers and the presence and severity of CAD.
- To explore the potential role of HP in the pathogenesis of atherosclerosis.
Main Methods:
- Serological IgG antibodies to HP and CagA were measured using ELISA in 76 CAD patients and 81 controls.
- Plasma levels of IL-8, C-reactive protein, fibrinogen, total cholesterol, and lipids were analyzed.
- Coronary angiograms were reviewed to assess CAD status.
Main Results:
- HP seropositivity was significantly higher in CAD patients (81.5%) compared to controls (51%), with an odds ratio of 4.3.
- Anti-CagA antibodies were more prevalent in CAD patients (47.3%) than in controls (28%).
- CAD patients exhibited elevated levels of C-reactive protein, fibrinogen, and total cholesterol.
Conclusions:
- A significant association exists between HP infection and CAD.
- HP infection, particularly with CagA-positive strains, elevates the risk of developing CAD.
- Persistent low-grade inflammation induced by HP may contribute to the atherosclerotic process.
Abstract:
The role of Helicobacter pylori (HP) as the main etiological factor in gastritis and peptic ulcer disease is undisputable. Gastric mucosal damage caused by HP involves various bacterial and host-dependent toxic substances that have been recently associated with an increased risk of coronary artery disease (CAD), possibly through the activation acute phase response and of procoagulant hemostatic factors. Recent studies showed a close and strong correlation between plasma increments of some cytokines such as IL-6 or TNFalpha and cardiovascular diseases. HP infection induces platelet activation and aggregation that could be the pathogenic explanation of the association between HP infection and CAD. The aim of this study was to determine the seroprevalence of HP infection and antibodies to CagA, an antigen that is expressed by the most virulent HP strains inducing an enhanced gastric inflammatory response, in patients undergoing routine coronary artery examination. We studied 76 patients with CAD and 81 healthy controls patients without significant change in coronary circulation. Angiograms were read by two independent experienced cardiologists blinded to the results of HP status. The presence of serum IgG antibodies to HP and to CagA and plasma interleukin-8 (IL-8) levels was measured by ELISA. In addition plasma C-reactive protein fibrinogen, total cholesterol and lipids levels were measured in all studied patients. Seropositivity to HP was found in 81.5 % of cases and in 51% of controls and the difference in prevalence was statistically significant, the odds ratio being 4.3 for Hp patients. Antibody to CagA protein was detected in 47.3% of CAD but only in 28% of healthy controls (OR = 2.3 vs OR = 10). C-reactive protein, plasma fibrinogen and total cholesterol were, respectively higher in patients with CAD than in controls. Present data show that there is significant link between CAD and HP infection. The HP infection significantly increases the risk of CAD, especially when both the anti-HP IgG and anti-CagA IgG are considered. Higher prevalence of cytotoxic HP strains might enhance the atherosclerotic process by inducing a persistent, low grade inflammatory response in arterial wall with enhanced synthesis of acute phase reactants.