Helicobacter pylori-seropositivity along with pro-inflammatory interleukin-1 polymorphisms correlated with myocardial infarction

Host genetic factors of interleukin (IL)-1 polymorphisms influence Helicobacter pylori infection pathogenic activity. We examined whether H. pylori-infected patients with IL-1 polymorphisms are associated with myocardial infarction (MI). We recruited 594 consecutive coronary artery disease patients and excluded those who met exclusion criteria. After matching age and sex, 82 cases with MI and 82 controls were enrolled. Immunoglobulin G antibodies against H. pylori and IL-1 polymorphisms (IL-1 beta-511 base pairs and IL-1 receptor antagonist) were analyzed. We assessed high sensitivity C-reactive protein (hs-CRP) level and reactive hyperemia-peripheral arterial tonometry (RH-PAT) index (RHI) using the EndoPAT2000 system. The simultaneous prevalence of H. pylori-seropositivity and IL-1 polymorphisms was 45.1% and 19.5% in the cases and controls, respectively (P = 0.001). H. pylori-positive patients with IL-1 polymorphisms showed significantly higher serum levels of natural logarithm of hs-CRP in the cases and controls (− 2.8 ± 1.0 vs. − 3.4 ± 0.6, respectively; P = 0.003 and − 2.8 ± 0.9 vs. − 3.2 ± 0.6, respectively; P = 0.02) and significantly lower levels of natural logarithm of RHI in the cases and controls (0.51 ± 0.13 vs. 0.61 ± 0.23, respectively; P = 0.039 and 0.47 ± 0.13 vs. 0.69 ± 0.23, respectively; P = 0.005). H. pylori-seropositivity with IL-1 polymorphisms was significantly associated with MI by logistic regression analysis (odds ratio, 4.83; 95% confidence interval, 1.99–11.7; P < 0.001). H. pylori-positive patients with IL-1 polymorphisms showed higher levels of hs-CRP and lower levels of RHI, and were significantly correlated with the MI.