title: Helicobacter pylori infection is related to atheroma in patients undergoing coronary angiography.
abstract: OBJECTIVE
  Helicobacter pylori infection has been related to an increased risk of ischaemic heart disease (IHD) possibly by raising plasma fibrinogen. The evidence for this association is conflicting. Furthermore, no attempt has been made to distinguish between an effect on atheroma and thrombosis. We have determined the association of H. pylori status with IHD assessed by coronary angiography. We have also evaluated the influence of H. pylori infection on haemostatic factors.
  
  
  METHODS
  Caucasian patients undergoing coronary angiography for suspected IHD were recruited. H. pylori status was determined by serology (Helico G). Plasma fibrinogen was measured by the Clauss assay. Coronary angiograms were assessed and significant atheroma defined as > or = 50% stenosis. A history of myocardial infarction was ascertained by WHO criteria.
  
  
  RESULTS
  292 patients were recruited (median age 59, 95 female); 204 (70%) patients had IHD and 185 (64%) of all patients were H. pylori-positive; 68% patients with IHD were H. pylori-positive compared with 50% without IHD (P = 0.003). When adjusted for other risk factors by logistic regression, H. pylori remained significantly associated with IHD (odds ratio = 2.4, 95% CI = 1.2-5.1, P = 0.02). H. pylori status was not related to a history of myocardial infarction. Circulating levels of PAI-1, vWF, Factor VII and fibrinogen were not related to H. pylori status.
  
  
  CONCLUSIONS
  This study suggests that infection with H. pylori is associated with coronary atheroma, but that this relationship is unlikely to be mediated through raised plasma fibrinogen.
authors.affiliation: Unit of Molecular Vascular Medicine, Leeds General Infirmary, UK.
authors.forename: N
authors.initials: N
authors.lastname: Ossei-Gerning
authors.forename: P
authors.initials: P
authors.lastname: Moayyedi
authors.forename: S
authors.initials: S
authors.lastname: Smith
authors.forename: D
authors.initials: D
authors.lastname: Braunholtz
authors.forename: J I
authors.initials: JI
authors.lastname: Wilson
authors.forename: A T
authors.initials: AT
authors.lastname: Axon
authors.forename: P J
authors.initials: PJ
authors.lastname: Grant
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001161:Arteriosclerosis / Q000097:blood / Q000382:microbiology / Q000473:pathology; D017023:Coronary Angiography; D003327:Coronary Disease / Q000097:blood / Q000382:microbiology* / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology; D005167:Factor VII / Q000032:analysis; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D016481:Helicobacter Infections / Q000097:blood / Q000150:complications* / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D014841:von Willebrand Factor; D005167:Factor VII; D005340:Fibrinogen