Helicobacter pylori and Atrial Fibrillation: Insights into Their Inter-Relationship

Abstract

Helicobacter pylori (H. pylori) infection and atrial fibrillation (AF) are prevalent global health concerns that significantly impact societal and economic well-being. This study explored the potential associations between H. pylori infection and the incidence and progression of AF. Emerging research suggests that H. pylori may influence AF through various pathways, including systemic inflammation, metabolic disturbances, immune responses, and changes in the gut microbiota. These pathways provide a novel perspective on the etiology of AF, suggesting that chronic H. pylori infection could exacerbate or even initiate the arrhythmic events typical of AF. Current evidence, while preliminary, points to significant correlations, particularly through changes in markers such as C-reactive protein (CRP) and lipid metabolism, which are heightened in individuals with active H. pylori infection. However, the exact mechanisms and causal nature of this relationship remain elusive, with studies showing conflicting results. This inconsistency underscores the need for more comprehensive and rigorously designed clinical and experimental research to elucidate fully the interactions between H. pylori infection and AF. Understanding these connections is crucial for developing innovative treatments and management strategies targeting microbial influences in AF patients. Future research should focus on defining the role of H. pylori eradication in the clinical management of AF assessing its impact on disease progression and patient outcomes.

Keywords: Helicobacter pylori; atrial fibrillation; gut microbiota; inflammation.

Fig. 1.

Possible mechanisms of H. pylori-induced AF. This diagram illustrates the complex interplay between LDL, HCY, and other factors in the context of H. pylori infection, which may culminate in AF. LDL, low density lipoprotein; HCY, homocysteine. The figure is created by Figdraw.

Fig. 2.

Inflammatory mechanism of H. pylori-induced AF. The complex inflammatory pathways implicated in H. pylori-induced AF highlight the roles of Cag A and inflammatory mediators, such as IL-1, IL-6, IL-8, and complement system components. IL, interleukin. The figure is created by Figdraw.

Fig. 3.

Mechanism through which antibodies produced by H. pylori lead to AF. The pathway through which antibodies related to H. pylori infection can lead to atrial fibrillation, emphasizing the role of altered ion handling and ectopic activity in cardiac cells, which contributes to arrhythmogenesis. EADs, early afterdepolarizations; DADs, delayed after-depolarizations; NCX, Na⁺/Ca²⁺ exchanger; TCW, triggered Ca²⁺ waves; SCaEs, SR Ca²⁺-release events; SR, sarcoplasmic reticulum. The figure is created by Figdraw.

Fig. 4.

Mechanism through which H. pylori affects the Th1/Th2 balance that leads to AF. Details of the complex interplay between H. pylori infection and immune cell dynamics within the myocardium highlight how changes in the Th1/Th2 balance due to Vac A may lead to increased fibrosis and subsequent atrial fibrillation. Th1, T helper 1 cell; Th2, T helper 2 cell; Vac A, vacuolating cytotoxin A. The figure is created by Figdraw.