Association of Helicobacter pylori infection with coronary heart disease

The role of Helicobacter pylori (HP) as the main etiological factor in gast ritis and peptic ulcer disease is undisputable. Gastric mucosal damage caus ed by HP involves various bacterial and host-dependent toxic substances tha t have been recently associated with an increased risk of coronary artery d isease (CAD), possibly through the activation acute phase response and of p rocoagulant hemostatic factors. Recent studies showed a close and strong co rrelation between plasma increments of some cytokines such as IL-6 or TNF a lpha 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 s eroprevalence of HP infection and antibodies to CagA, an antigen that is ex pressed by the most virulent HP strains inducing an enhanced gastric inflam matory 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 ind ependent 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 protei n fibrynogen, total cholesterol and lipids levels were measured in all stud ied patients. Seropositivity to HP was found in 81.5% of cases and in 51% o f controls and the difference in prevalence was statistically significant, the odds ratio being 4.3 for Hp patients. Antibody to CagA protein was dete cted 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, resp ectively higher in patients with CAD than in controls. Present data show th at 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 str ains might enhance the atherosclerotic process by inducing a persistent, lo w grade inflammatory response in arterial wall with enhanced synthesis of a cute phase reactants.