Helicobacter pylori and cardiovascular biomarkers in acute myocardial infarction

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Abstract Background Helicobacter pylori (H. pylori) infection, particularly involving strains with virulence factor Cytotoxin-associated gene A (CagA), has been associated with myocardial infarction (MI). However, the mechanism underlying this association is uncertain. Purpose We aimed to test the hypothesis that H. pylori infection was associated with pre-specified inflammatory and vascular biomarkers in patients with acute MI and to explore whether a broader panel of biomarkers could predict infection status. Furthermore, we evaluated if H. pylori status and biomarker predictors were associated with adverse outcomes post-MI. Methods H. pylori and CagA serology was analysed in 1061 MI patients admitted 2008-2014. 175 cardiovascular biomarkers were analysed using Proximity Extension Assay and Multiple Reaction Monitoring mass spectrometry. First, the association between H. pylori infection and seven pre-selected biomarkers reflecting inflammation and vascular calcification were evaluated using multiple linear regression. Second, an exploratory analysis including all biomarkers and clinical data was performed. Using receiver operating characteristics, a random forest and a Lasso regression model were trained to predict H. pylori serology status, and the five most important biomarkers for each model were identified and further evaluated. H. pylori status and the most important biomarker predictors were used to study associations with major adverse cardiovascular events (MACE) and all-cause death. Results Median age was 65 years and 78% of patients were male. H. pylori and CagA seroprevalence was 45% and 18%, respectively. Among the pre-selected biomarkers, C-reactive protein (CRP) was elevated in CagA-positive H. pylori-positive patients specifically (beta coefficient 0.35, 95% CI 0.01-0.69). The predictive performance for H. pylori status using all biomarkers was moderate (Area under the curve [AUC] 0.68 for Lasso regression, AUC 0.63 for random forest). Further analysis of top five predictors for each model revealed that C-C motif chemokine ligand 20 (CCL20) and Immunoglobulin Heavy Constant Gamma 3 (IGHG3) concentrations were significantly higher, while TNF-related apoptosis-inducing ligand (TRAIL) levels were lower in H. pylori positive patients, after adjusting for multiple testing. Higher concentrations of CCL20, but not H. pylori status, was associated with MACE when comparing the highest and the lowest quartile (hazard ratio 2.15, 95% CI 1.41-3.29). Conclusions In acute MI, we confirmed our hypothesis that CagA-positive H. pylori serology was associated with inflammation reflected by higher CRP concentrations. The association with inflammation was further supported by the exploratory analyses where CCL20, IGHG3 and TRAIL, all involved in inflammation and immune response, were identified as the most important predictors. Higher CCL20 concentrations were associated with increased risk of MACE on follow-up.

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