**8. Conclusions**

*H. pylori* infection significantly increases the risk for CVDs including atherosclerosis, HTN, CHD, cerebrovascular disease, and peripheral arterial diseases especially in younger patients (< 65 years old). *H. pylori* infection significantly impairs vascular endothelial function through multiple mechanisms including increased ROS production and oxidative stress, inflammation, decreased NO formation, modification of the expression of cytokines and miRNAs, interruption of lipid and glucose metabolisms, and exosomes-mediated pathways as shown in **Figure 4**. Endothelial dysfunction associated with *H. pylori* infection is reversible in both animal model and human subjects if the infection could be eliminated in a timely fashion (within one year of infection for human subjects and 6 months for mice). Accumulating data suggests that *H. pylori* infection is an additional risk factor for endothelial dysfunction and CVDs. Screening young male population for *H. pylori* infection once a year and treating accordingly could be an effective approach for early prevention of CVDs especially premature atherosclerosis associated with *H. pylori* infection.

#### **Figure 4.**

*Schematic illustration of the mechanism on endothelial dysfunction and atherosclerosis associated with*  H. pylori *infection. It is proposed that* H. pylori *infection could impair endothelial function through exosomemediated mechanisms. CagA protein is only from CagA+* H. pylori*, and could serve as an ideal tracking molecule for exosome trafficking in vivo. CagA<sup>+</sup>* H. pylori *translocate CagA protein into gastric epithelial cells (GES-1). CagA-containing exosomes are released into circulation from GES-1, then enter into endothelial cells, leading to endothelial dysfunction.* H. pylori *Infection could also decrease endothelial function through increased production of reactive oxygen species, oxidative stress, and inflammation, decreased cellular nitric oxide formation, modification of the expression of cytokines and miRNAs, and interruption of lipid and glucose metabolisms. [adopted and modified from (47) with permission].*

Helicobacter pylori *Infection and Endothelial Dysfunction DOI: http://dx.doi.org/10.5772/intechopen.97260*
