Helicobacter pylori relation to acute myocardial infarction in an Iranian sample

Known risk factors for coronary heart diseases do not explain all of clinical and epidemiological features of the disease and additional environmental factors probably contribute to clinical atherothrombotic events. This study examined the association of Helicobacter pylori (H. pylori) infection with acute and chronic coronary syndromes assessed by coronary angiography as well as the influence of H. pylori on fibrinogen level. Paired sera from 52 patients with acute myocardial infarction (AMI) according to WHO criteria, 51 patients with positive coronary angiography and 55 patients with negative coronary angiography reports were investigated for antibodies to H. pylori and fibrinogen levels. H. pylori antibodies were determined by ELISA method. Plasma fibrinogen was measured by the Clauss assay. Coronary angiograms were reviewed by two cardiologists independently (weighted κ=0.64) and significant lesion was defined as ≥50% stenosis of at least one coronary vessel. There was significant relationship between H. pylori infection and acute myocardial infarction (Odds ratio=13.2, 95% CI=5.1–34.3, P=0.00), however, no significant difference between patients with positive or negative coronary angiography (Odds ratio=2.0, 95% CI=0.76–5.35, P=0.24) was seen. The crude prevalence of H. Pylori was not related significantly to the childhood socioeconomic class (P>0.05) while showing significant inverse relationship with current socioeconomic class (P<0.05). Fibrinogen levels were significantly higher among H. pylori positive than H. pylori negative patients (331.7±78.2 vs 304.6±66.4 mg/dl) (P=0.04). While the Odds ratios for positivity of H. pylori antibodies in relation to smoking status, current socioeconomic classes were significant (P<0.05), sex and childhood socioeconomic classes showed no significant association with H. pylori infection (P>0.05). These results may support the hypothesis that H. pylori may influence acute myocardial infarction through enhancing thrombosis possibly mediated by raised fibrinogen level.