Association of Helicobacter pylori infection with coronary heart disease. P Pieniazek, E Karczewska, A Duda, W Tracz, M Pasowicz, S J Konturek J Physiol Pharmacol 2000; 50(5):743-751 ICID: 415851
IC™ Value: 5.56
The role of Helicobacter pylori (HP) as the main etiological factor ingastritis and peptic ulcer disease is undisputable. Gastric mucosal damage caused by HP involves variousbacterial and host-dependent toxic substances that have been recently associated with an increased riskof coronary artery disease (CAD), possibly through the activation acute phase response and of procoagulanthemostatic factors. Recent studies showed a close and strong correlation between plasma increments ofsome cytokines such as IL-6 or TNFalpha and cardiovascular diseases. HP infection induces platelet activationand aggregation that could be the pathogenic explanation of the association between HP infection andCAD. 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 inflammatoryresponse, in patients undergoing routine coronary artery examination. We studied 76 patients with CADand 81 healthy controls patients without significant change in coronary circulation. Angiograms wereread by two independent experienced cardiologists blinded to the results of HP status. The presence ofserum 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 inall studied patients. Seropositivity to HP was found in 81.5 % of cases and in 51% of controls and thedifference in prevalence was statistically significant, the odds ratio being 4.3 for Hp patients. Antibodyto 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 withCAD 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-CagAIgG are considered. Higher prevalence of cytotoxic HP strains might enhance the atherosclerotic processby inducing a persistent, low grade inflammatory response in arterial wall with enhanced synthesis ofacute phase reactants.
ICID 415851 PMID 10695556 - click here to show this article in PubMed database
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