title: Association of endothelial dysfunction and cytotoxin-associated gene A-positive Helicobacter pylori in patients with cardiac syndrome X.
abstract: Existence of coronary endothelial dysfunction has been demonstrated in patients with cardiac syndrome X (CSX). In addition, Helicobacter pylorus (H. pylori) has been associated with CSX. We aimed to assess the possible association of endothelial dysfunction and cytotoxin-associated gene A-positive H. pylori (CagA+) infection in CSX patients.
  
  
  
  Fifty-six patients with CSX (23 male/33 female; age: 51.25 ± 8.86 years) who were anti-H. pylori IgG-positive [H. pylori(+)] and 24 CSX patients (7 male/17 female; age: 52.79 ± 9.88 years) who were H. pylori(-) were included. Also, anti-H. pylori IgG-positive patients were determined by the presence of IgG antibody to CagA. Levels of endothelin-1 (ET-1), E-selectin and intercellular adhesion molecule-1 (ICAM-1) were measured.
  
  
  
  Endothelial dysfunction biomarkers were higher in H. pylori(+) than in H. pylori(-) patients (ET-1: 54.60 ± 25.39 vs. 42.59 ± 18.37 pg/ml, p = 0.04; E-selectin: 42.68 ± 14.26 vs. 31.72 ± 8.26 ng/ml, p = 0.001; ICAM-1: 339.68 ± 135.8 vs. 266.51 ± 125.1 ng/ml, p = 0.02). Among H. pylori(+) subjects, 28 cases were CagA(+) and 28 cases were CagA(-). There were significant differences in measured levels of E-selectin between CagA(+) and CagA(-) groups (48.00 ± 16.37 vs. 37.37 ± 9.37 ng/ml, p = 0.004). For ET-1 and ICAM-1 levels, the difference between CagA(+) and CagA(-) was insignificant (p = 0.174 and p = 0.07, respectively).
  
  
  
  High levels of endothelial dysfunction biomarkers are found in CSX patients with anti-CagA(+). These findings suggest the infection with CagA(+) H. pylori strain may play a role as a risk factor in development of CSX through provocation of endothelial dysfunction. Therefore, a long term follow up to investigate the outcomes of these patients is proposed.
authors.affiliation: Cellular and Molecular Research Center, Urmia University of Medical Sciences, Urmia, Iran; Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran. Electronic address: rasmiy@umsu.ac.ir.
authors.forename: Yousef
authors.initials: Y
authors.lastname: Rasmi
authors.affiliation: Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
authors.forename: Hadi
authors.initials: H
authors.lastname: Rouhrazi
authors.affiliation: Department of Cardiology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
authors.forename: Ebrahim
authors.initials: E
authors.lastname: Khayati-Shal
authors.affiliation: Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
authors.forename: Alireza
authors.initials: A
authors.lastname: Shirpoor
authors.affiliation: Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
authors.forename: Ehsan
authors.initials: E
authors.lastname: Saboory
mesh_terms: D000942:Antigens, Bacterial / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics; D003603:Cytotoxins; D016481:Helicobacter Infections / Q000276:immunology; D016480:Helicobacter pylori / Q000235:genetics*; D006801:Humans; D007074:Immunoglobulin G; D017566:Microvascular Angina
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D003603:Cytotoxins; D007074:Immunoglobulin G
keywords: Cardiac syndrome X; Cytotoxin-associated gene A; Endothelial dysfunction; Helicobacter pylori