Abstract
The role of chronic infections in causing coronary artery disease (CAD) has been investigated for the past several years. Among them, the role of Helicobacter pylori has stimulated keen interest. Though initial results were conflicting, there are growing data to support the role of H. pylori in CAD. The main mechanism of endothelial damage is hypothesized to be through molecular mimicry involving heat shock proteins. This study was designed to determine the prevalence of H.pylori and cytotoxin associated gene A (cagA) positive H.pylori infection in patients undergoing coronary artery bypass grafting (CABG) and the potential role of anti-H. pylori specific heat shock protein-60 (Hp-HSP-60) antibody response in these patients, for cardiac events. One hundred patients undergoing CABG and 100 controls were studied. The H.pylori infection and cagA status were determined serologically by enzyme-linked immunosorbent assay (ELISA). Hp-HSP-60 Immunoglobulin G (IgG) antibodies were estimated by using an in house ELISA. Although there was no difference in the prevalence of H.pylori infection in patients and controls (74% vs 70%), 58% of patients were infected with cagA positive H.pylori compared to 36% of controls (P=0.002). Mean systemic levels of Hp-HSP-60 IgG were also higher in patients than in controls (27.9 vs 18.7, P=0.0001). These antibody levels were also significantly higher in H.pylori positive patients (P=0.0001). There was a strong correlation between Hp-HSP-60 antibody levels and occurrence of myocardial infarction (P=0.003). CagA positive H.pylori infection may be associated with the development of CAD. High levels of Hp-HSP-60 antibodies may constitute a marker and/or concomitant pathogenic factor of the disease.
Highlights
Several studies over the past two decades have suggested an association between various microbial infections with atherosclerosis and coronary artery disease (CAD).[1]
Given that H. pylori infection has been shown to result in Immunoglobulin G (IgG) antibodies against heat shock proteins (HSP)-60, it has been stated that this may promote the development of atherosclerosis through interaction of H. pylori immune reactants and host HSP-60.7
The main objectives of the present work were: i) to study the association between virulent H. pylori strains and CAD; ii) to estimate the levels of IgG antibodies against Hp specific HSP-60 (H. pylori specific heat shock protein60) in patients with CAD and healthy subjects; and iii) to compare the prevalence of virulent H. pylori infection and Hp-HSP-60 antibody titers with various risk factors and cardiac events
Summary
Several studies over the past two decades have suggested an association between various microbial infections with atherosclerosis and coronary artery disease (CAD).[1]. There was no difference in the prevao lence of H. pylori infection in patients and conN trols (74% vs 70%), 58% of patients were infectthe form of molecular mimicry.[3] Recently virulent strains of H. pylori that express cytotoxin associated gene A (cagA), have been shown to be significantly associated with CAD.[4,5] heat shock proteins are known to be expressed and secreted by H. pylori and by endogenous cells within atherosclerotic plaques.[6] Given that H. pylori infection has been shown to result in Immunoglobulin G (IgG) antibodies against HSP-60, it has been stated that this may promote the development of atherosclerosis through interaction of H. pylori immune reactants and host HSP-60.7. The main objectives of the present work were: i) to study the association between virulent H. pylori strains and CAD; ii) to estimate the levels of IgG antibodies against Hp specific HSP-60 (H. pylori specific heat shock protein60) in patients with CAD and healthy subjects; and iii) to compare the prevalence of virulent H. pylori infection and Hp-HSP-60 antibody titers with various risk factors and cardiac events
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