title: Prevalence of Helicobacter pylori positivity in patients undergoing percutaneous coronary intervention.
abstract: BACKGROUND
  The adverse effect of haemorrhagic complications after percutaneous coronary intervention (PCI) on outcome is well established with Helicobacter pylori infection known to be an important precipitant of peptic ulcer disease in patients receiving non-steroidal anti-inflammatory drug therapy. The prevalence of H. pylori positivity in patients undergoing PCI and receiving subsequent antiplatelet therapy is unknown.
  
  
  OBJECTIVE
  We sought to determine the prevalence and features associated with H. pylori positivity in patients undergoing PCI.
  
  
  METHODS
  All patients undergoing PCI between August 2008 and April 2009 were identified and assessed for H. pylori positivity with serological status determined by using a commercially supplied enzyme-linked immunosorbent assay.
  
  
  RESULTS
  A total of 245 patients undergoing PCI during the study period had samples obtained for H. pylori serology. Of these, 91 were positive for H. pylori serology (37%) and 148 were negative (60%) with six samples being equivocal (3%). Of those patients positive for H. pylori, 75% were on agents at admission known to promote or precipitate gastrointestinal haemorrhage. Patients positive for H. pylori tended to be older, with increased creatinine and more likely to be receiving proton pump inhibitor therapy.
  
  
  CONCLUSIONS
  In an unselected cohort of patients undergoing PCI in a single centre, we detected a prevalence of H. pylori positivity in 37% of patients; this denotes a potentially treatable precipitant of haemorrhage in a considerable portion of patients receiving dual antiplatelet therapy after PCI. Further prospective study is required to determine if the presence of H. pylori positivity is associated with adverse events in terms of gastrointestinal and cardiac outcomes.
authors.affiliation: Cardiovascular Unit, John Hunter Hospital, University of Newcastle, Newcastle, New South Wales, Australia.
authors.forename: C
authors.initials: C
authors.lastname: Hiew
authors.forename: A
authors.initials: A
authors.lastname: Duggan
authors.forename: T
authors.initials: T
authors.lastname: de Malmanche
authors.forename: R
authors.initials: R
authors.lastname: Hatton
authors.forename: F
authors.initials: F
authors.lastname: Baker
authors.forename: J
authors.initials: J
authors.lastname: Attia
authors.forename: N
authors.initials: N
authors.lastname: Collins
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000627:therapeutic use; D000907:Antibodies, Bacterial / Q000097:blood*; D015331:Cohort Studies; D015897:Comorbidity; D003404:Creatinine / Q000097:blood; D004198:Disease Susceptibility; D005260:Female; D006471:Gastrointestinal Hemorrhage / Q000139:chemically induced* / Q000382:microbiology; D016481:Helicobacter Infections / Q000150:complications / Q000188:drug therapy / Q000453:epidemiology*; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009517:New South Wales / Q000453:epidemiology; D010437:Peptic Ulcer / Q000453:epidemiology / Q000209:etiology / Q000382:microbiology; D010438:Peptic Ulcer Hemorrhage / Q000139:chemically induced / Q000209:etiology / Q000382:microbiology; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects* / Q000627:therapeutic use; D011241:Prednisone / Q000009:adverse effects / Q000627:therapeutic use; D054328:Proton Pump Inhibitors / Q000627:therapeutic use; D012307:Risk Factors; D016036:Seroepidemiologic Studies; D015607:Stents
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000907:Antibodies, Bacterial; D010975:Platelet Aggregation Inhibitors; D054328:Proton Pump Inhibitors; D003404:Creatinine; D011241:Prednisone