Role of Helicobacter pylori Specific Heat Shock Protein-60 Antibodies in the Aetiology of Coronary Artery Disease

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.