Helicobacter pylori infection, in patients with classic risk factors of coronary heart disease, can present with typical clinical manifestations of ischemic heart disease without characteristic electrocardiographic changes or elevation of serum cardiac biomarkers. H. pylori does not participate in the initiation of inflammatory process of coronary atherosclerotic plaque. Instead, a commensal bacterium increases the coronary blood flow even in presence of classic risk factors of coronary heart disease. Under certain circumstances, Helicobacter pylori may aggravate an already existing inflammatory atherosclerotic process of coronary vasculature with consequent rupture and development of ischemic heart disease. This is in analogy with the physiologic role of platelet in primary haemostatic plug versus its undesired role in formation of vascular thrombosis. The factors that lead to shifting of Helicobacter pylori from a commensal promoter of coronary blood flow to a pathogenic organism activating the inflammatory response of atherosclerotic plaque remain to be elucidated.