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. 1998 May;93(5):717-20.
doi: 10.1111/j.1572-0241.1998.212_a.x.

A prospective, controlled study of Helicobacter pylori seroprevalence in coronary artery disease

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A prospective, controlled study of Helicobacter pylori seroprevalence in coronary artery disease

A Khurshid et al. Am J Gastroenterol. 1998 May.

Abstract

Objective: Recent studies have suggested that chronic infections may be a risk factor for coronary artery disease. The aim of this study was to determine whether Helicobacter pylori (H. pylori) infection was an independent risk factor for coronary artery disease.

Methods: A total of 179 patients undergoing coronary angiography for suspected coronary artery disease were prospectively studied. Angiograms were read by experienced invasive cardiologists blinded to the results of H. pylori serology, which was determined by a validated multiwell ELISA assay.

Results: A total of 121 patients (68%) had evidence of coronary artery disease, whereas 58 patients (32%) had normal coronary angiograms. Of the 121 patients with coronary artery disease, 29 had single vessel disease, 39 had double vessel disease, and 53 had triple vessel disease, respectively. There was no significant difference in seroprevalence of H. pylori infection in patients with and without coronary artery disease (p = 0.63). The odds ratio (after adjustment for other known risk factors) for coronary artery disease in H. pylori-infected subjects was 0.45 (95% CI = 0.15, 1.37; p = 0.107). In patients with coronary artery disease, H. pylori infection did not increase the likelihood of severe disease (odds ratio for triple vessel disease = 0.53; 95% CI 0.18, 1.60; p = 0.201).

Conclusion: H. pylori infection rates are similar in patients with normal and abnormal coronary arteries, and infection with H. pylori is not an independent risk factor for coronary artery disease. In patients who have coronary artery disease, H. pylori infection is not a risk factor for more severe disease. These data argue against a causal role for H. pylori in the pathogenesis of coronary artery disease.

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