title: CagA-positive Helicobacter pylori strains enhanced coronary atherosclerosis by increasing serum OxLDL and HsCRP in patients with coronary heart disease.
abstract: BACKGROUND
  The role of infection in the pathogenesis of atherosclerosis is still a matter of debate.
  
  
  OBJECTIVE
  This study aimed to investigate the effect of CagA-positive 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 (≥8 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.
authors.affiliation: Department of Cardiology, The He Xian Memorial Hospital of Panyu District, Guangzhou, People's Republic of China. hbs8311@163.com
authors.forename: Bingsheng
authors.initials: B
authors.lastname: Huang
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xie
authors.forename: Guixiong
authors.initials: G
authors.lastname: Lin
authors.forename: Yuyan
authors.initials: Y
authors.lastname: Wu
authors.forename: Yanlin
authors.initials: Y
authors.lastname: Feng
authors.forename: Jingcao
authors.initials: J
authors.lastname: Li
authors.forename: Yufeng
authors.initials: Y
authors.lastname: Zhuo
authors.forename: Peng
authors.initials: P
authors.lastname: Zhang
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000942:Antigens, Bacterial / Q000378:metabolism*; D001426:Bacterial Proteins / Q000378:metabolism*; D002097:C-Reactive Protein / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000097:blood / Q000382:microbiology* / Q000503:physiopathology; D003327:Coronary Disease / Q000097:blood* / Q000503:physiopathology; D005260:Female; D016481:Helicobacter Infections / Q000150:complications; D016480:Helicobacter pylori / Q000145:classification* / Q000378:metabolism*; D006801:Humans; D008055:Lipids / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D008055:Lipids; D008077:Lipoproteins, LDL; C080866:cagA protein, Helicobacter pylori; C099252:oxidized low density lipoprotein; D002097:C-Reactive Protein