CagA-Positive Helicobacter pylori Strains Enhanced Coronary Atherosclerosis by Increasing Serum OxLDL and HsCRP in Patients with Coronary Heart Disease

Background The role of infection in the pathogenesis of atherosclerosis is still a matter of debate. Aims This study aimed to investigate the effect of CagApositive Helicobacter pylori (H. pylori) strains infection on coronary atherosclerosis in patients with coronary heart disease and to elucidate how cytotoxin-associated gene A (CagA)-positive H. pylori strains infections were involved in coronary heart disease by examining the levels of serum lipid, high-sensitivity C-reactive protein (hsCRP) and oxidized low-density protein (oxLDL). Methods Recruited for this study were 159 patients with coronary heart disease. The severity of coronary heart disease was estimated by calculating the Gensini score. Serum oxLDL and hsCRP were examined in all subjects. Current H. pylori infection was determined in all participants by means of a modified (13C) urea breath test ([200 dpm classified as positive). IgG antibodies against CagA protein were analyzed by enzyme immunoassays. Antibody titers against CagA (C8 U/ml) were classified as positive. All subjects were divided into three groups, including an uninfected group (n = 30), an H. pylori?CagA- group (n = 69), and an H. pylori?CagA? group (n = 60). Results Significant differences were found among the three groups in levels of total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, serum hsCRP, oxLDL, and severity of coronary atherosclerosis (p\0.05). The levels of total cholesterol, LDL, apolipoprotein B, serum hsCRP, oxLDL were significantly elevated and the severity of coronary atherosclerosis was significantly increased in H. pylori?CagA? group (p\0.05). Conclusions More serious coronary atherosclerosis was observed in CHD patients with H. pylori?CagA? infection. H. pylori?CagA? infection might be involved in coronary atherosclerosis by modifying serum lipids, enhancing LDL oxidation, and activating the inflammatory responses.