Relationships among Helicobacter pylori seropositivity, the triglyceride-glucose index, and cardiovascular disease: a cohort study using the NHANES database

BACKGROUND: Helicobacter pylori (H. pylori), a widely prevalent pathogen that can be cured through relatively simple medical methods, is thought to be potentially associated with the risk of cardiovascular diseases (CVD), although controversy remains. Currently, it is unclear whether the triglyceride-glucose index (TGI), a classic indicator of insulin resistance, influences the relationship between H. pylori infection and CVD. The present work explored the relationships between H. pylori seropositivity, the TGI and CVD, and the potential effect of TGI in this association. METHODS: In this cross-sectional and cohort study, data from the National Health and Nutrition Examination Survey (NHANES) III (1988-1994) and NHANES (1999-2000) were used. The effects of the TGI, H. pylori seropositivity, and their interaction on the risk of CVD were assessed using logistic regression models. The hazard ratios (HRs) and 95% confidence intervals (CI) for all-cause mortality (ACM) were calculated using the Cox proportional hazards model. Restricted cubic spline (RCS) curves were employed to investigate potential non-linear or linear relationships among the TGI, H. pylori seropositivity, occurrence of CVD, and ACM. Mediation analyses were employed to assess the potential effects of H. pylori seropositivity and TGI on the risk of CVD and mortality. RESULTS: Of the 9,399 participants, 4,488 (47.75%) were H. pylori-immunoglobulin G (IgG)-positive, and 3,934 (41.86%) were diagnosed with CVD. In the general population, participants with a TGI ≥ 75th percentile who were positive for H. pylori-IgG antibody had the highest risk of developing CVD (odds ratio = 1.487; 95% CI: 1.088-2.033). Among patients with CVD, those with a TGI ≥ 75th percentile & positive for H. pylori-IgG antibody were at a higher ACM risk (HR = 1.227; 95% CI: 1.009-1.491). H. pylori exhibited a significant mediating effect on CVD occurrence (Pindir = 0.004) and mortality (Pindir = 0.004) via the TGI. CONCLUSIONS: H. pylori seropositivity may indirectly elevate the risk of CVD and mortality via the TGI. Combining the patient's H. pylori serological status with their TGI could enhance the predictive ability for CVD occurrence and related mortality. Therefore, the clinical practice of screening for and eradicating H. pylori in CVD patients may be anticipated.