Association of endothelial dysfunction and cytotoxin-associated gene A-positive Helicobacter pylori in patients with cardiac syndrome X

Rasmi, Y and Rouhrazi, H and Khayati Shal, E and Shirpoor, A and Saboory, E (2016) Association of endothelial dysfunction and cytotoxin-associated gene A-positive Helicobacter pylori in patients with cardiac syndrome X. Biomedical Journal, 39 (5). pp. 339-345.

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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 (CagAþ) infection in CSX patients. Methods: Fifty-six patients with CSX (23 male/33 female; age: 51.25 ± 8.86 years) who were anti-H. pylori IgG-positive [H. pylori(þ)] 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. Results: Endothelial dysfunction biomarkers were higher in H. pylori(þ) than in H. pylori(�) patients (ET-1: 54.60 ± 25.39 vs. 42.59 ± 18.37 pg/ml, p ¼ 0.04; E-selectin: 42.68 ± 14.26 vs. 31.72 ± 8.26 ng/ml, p ¼ 0.001; ICAM-1: 339.68 ± 135.8 vs. 266.51 ± 125.1 ng/ml, p ¼ 0.02). Among H. pylori(þ) subjects, 28 cases were CagA(þ) and 28 cases were CagA(�). There were significant differences in measured levels of E-selectin between CagA(þ) and CagA(�) groups (48.00 ± 16.37 vs. 37.37 ± 9.37 ng/ml, p ¼ 0.004). For ET-1 and ICAM-1 levels, the difference between CagA(þ) and CagA(�) was insignificant (p ¼ 0.174 and p ¼ 0.07, respectively). Conclusion: High levels of endothelial dysfunction biomarkers are found in CSX patients with anti-CagA(þ). These findings suggest the infection with CagA(þ) 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.

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