Abstract
Background and Aims: Classic risk factors for development of atherosclerosis do not explain all cases of Chronic Heart Disease (CHD). There is a significant evidence that gut microbiota may influence the development of CHD. The widespread prevalence of Helicobacter pylori (HP) infections and the fact that they are frequently asymptomatic may suggest that HP can be a source of antigenic components that stimulate not only local, but also systemic inflammatory response. Considering the mechanism of HP pathogenicity accompanied by massive oxidative stress and gastric epithelial barrier disintegration, it is possible that HP soluble components translocated into circulation may act synergistically with high fat diet in the development of proinflammatory and proatherogenic environment.
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