Helicobacter pylori and Early Vascular Aging: Endothelial Dysfunction, Arterial Stiffness, and Conditional Cardiovascular Vulnerability

Helicobacter pylori (H. pylori) infection has been investigated as a potential contributor to extra-gastric vascular injury, although its cardiovascular relevance remains uncertain and context-dependent. This state-of-the-art narrative review synthesizes clinical, translational, and experimental evidence linking H. pylori infection to endothelial dysfunction and arterial stiffness, two complementary phenotypes of early vascular aging. Evidence is strongest for endothelial dysfunction, particularly in the presence of active or cytotoxin-associated gene A (CagA)-positive infection, extracellular-vesicle-mediated signaling, oxidative stress, impaired endothelial repair, selective attenuation of endothelium-dependent vasodilation, and short-term improvement after eradication. Associations with arterial stiffness are less consistent and appear more evident in selected settings characterized by younger age, inflammatory or metabolic vulnerability, and severe gastric injury. Conversely, serology-based studies and studies using late structural vascular endpoints frequently report null or discordant findings. Overall, H. pylori should not be considered a universal cardiovascular risk factor, but it may amplify early vascular injury in susceptible subgroups. Prospective studies using active-infection testing, virulence profiling, gastric histology, and prespecified vascular endpoints are needed to determine whether eradication produces sustained vascular benefit.