Peer-review started: October 20, 2014
First decision: November 27, 2014
Revised: December 14, 2014
Accepted: December 29, 2014
Article in press: January 4, 2015
Published online: January 26, 2015
Processing time: 96 Days and 4.3 Hours
Helicobacter pylori (H. pylori) is a known pathogen implicated in genesis of gastritis, peptic ulcer disease, gastric carcinoma and gastric lymphoma. Beyond the stomach, the organism has also been implicated in the causation of immune thrombocytopenia and iron deficiency anemia. Although an area of active clinical research, the role of this gram negative organism in causation of atherosclerosis and coronary artery disease (CAD) remains enigmatic. CAD is a multifactorial disease which results from the atherosclerosis involving coronary arteries. The major risk factors include age, diabetes mellitus, smoking, hypertension and dyslipidemia. The risk of CAD is believed to increase with chronic inflammation. Various organisms like Chlamydia and Helicobacter have been suspected to have a role in genesis of atherosclerosis via causation of chronic inflammation. This paper focuses on available evidence to ascertain if the role of H. pylori in CAD causation has been proven beyond doubt and if eradication may reduce the risk of CAD or improve outcomes in these patients.
Core tip: Coronary artery disease (CAD) is a multifactorial disease and inflammation plays an important role in Atherogenesis. Helicobacter pylori (H. pylori) is speculated to be one organism which may incite the inflammatory response thereby predisposing infected individuals to CAD. This paper looks at clinical evidence in relation to H. pylori infection and CAD and also examines the evidence of effects of eradication of H. pylori on CAD and its risk factors.