Helicobacter pylori infection and atherosclerosis: is there a causal relationship?

For many years, the coexistence of Helicobacter pylori (H. pylori) infection and atherosclerotic diseases in a disproportional number of patients has inspired the presumption that a causal relationship exists between the conditions. This presumption was evidenced by the simultaneously declining epidemics of duodenal ulcer and coronary artery diseases in the United States in the past 40 years, and was further evidenced by the detection of H. pylori and their DNA in atherosclerotic plaques. Suggested mechanisms underlying this possible causality include intensified inflammatory stress, dyslipidemia, abnormal glucose metabolism, arterial stiffness, increased blood pressure and malnutrition. However, a causal relationship was disproved by results from other studies, which indicated that common risk factors shared by H. pylori infection and atherosclerosis, such as aging, cigarette smoking, disadvantageous socioeconomic status and high salt intake, may predestine their coexistence. Understanding the nature of the relationship between H. pylori infection and atherosclerosis is of vital importance, because a causality may indicate a possible strategy for preventing and treating atherosclerosis by eradicating H. pylori infection in selected individuals. This review assessed current evidence for and against a causal relationship between H. pylori infection and atherosclerosis.