title: Impact of viral and bacterial infectious burden on long-term prognosis in patients with coronary artery disease.
abstract: BACKGROUND
  The number of infectious pathogens to which an individual has been exposed (infectious burden) may correlate with coronary artery disease (CAD). In a prospective study, we evaluated the effect of 8 pathogens and the aggregate pathogen burden on the risk for future fatal cardiac events among patients with angiographically documented CAD. Methods and Results-In 1018 patients, IgG or IgA antibodies to herpes simplex virus types 1 and 2, cytomegalovirus, Epstein-Barr virus, Haemophilus influenzae, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Helicobacter pylori were determined. Moreover, highly sensitive C-reactive protein was measured. Follow-up information on cardiovascular events was obtained (mean 3.1 years, maximum 4.3 years). Seropositivities to Epstein-Barr virus (P=0.001), H pylori (P=0.002), and herpes simplex virus type 2 (P=0.045) were independently associated with the future risk of cardiovascular death. An increasing number for pathogen burden was significantly predictive of the long-term prognosis (P<0.0001). Infectious burden divided into 0 to 3, 4 or 5, and 6 to 8 seropositivities was associated with an increasing mortality of 3.7%, 7.2%, and 12.6%, respectively. Patients seropositive to >5 pathogens compared with those seropositive to <4 pathogens had a 5.1 (1.4 to 18.3) higher risk of future cardiac death. This result was mainly driven by the pathogen burden of seropositivities to Herpesviridae (P<0.0001). The prognostic impact of total or viral pathogen burden was independent of the C-reactive protein level.
  
  
  CONCLUSIONS
  These results support the hypothesis that the number of infectious pathogens to which an individual has been exposed independently contributes to the long-term prognosis in patients with documented CAD.
authors: Department of Medicine II , Johannes Gutenberg University Mainz, Mainz, Germany.rupprecht@2-med.klinik.uni-mainz.de
authors: H J
authors: HJ
authors: Rupprecht
authors: S
authors: S
authors: Blankenberg
authors: C
authors: C
authors: Bickel
authors: G
authors: G
authors: Rippin
authors: G
authors: G
authors: Hafner
authors: W
authors: W
authors: Prellwitz
authors: W
authors: W
authors: Schlumberger
authors: J
authors: J
authors: Meyer
mesh_terms: D000907:Antibodies, Bacterial / Q000097:blood; D000914:Antibodies, Viral / Q000097:blood; D001424:Bacterial Infections / Q000175:diagnosis* / Q000453:epidemiology / Q000276:immunology; D002097:C-Reactive Protein / Q000378:metabolism; D016993:Chlamydophila pneumoniae / Q000276:immunology; D015897:Comorbidity; D003327:Coronary Disease / Q000175:diagnosis / Q000453:epidemiology / Q000276:immunology / Q000382:microbiology*; D003587:Cytomegalovirus / Q000276:immunology; D005260:Female; D005500:Follow-Up Studies; D006193:Haemophilus influenzae / Q000276:immunology; D016480:Helicobacter pylori / Q000276:immunology; D018259:Herpesvirus 1, Human / Q000276:immunology; D018258:Herpesvirus 2, Human / Q000276:immunology; D004854:Herpesvirus 4, Human / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D008297:Male; D008875:Middle Aged; D009177:Mycoplasma pneumoniae / Q000276:immunology; D016017:Odds Ratio; D011379:Prognosis; D018570:Risk Assessment; D016036:Seroepidemiologic Studies; D014777:Virus Diseases / Q000175:diagnosis* / Q000453:epidemiology / Q000276:immunology
chemical_list: D000907:Antibodies, Bacterial; D000914:Antibodies, Viral; D007074:Immunoglobulin G; D002097:C-Reactive Protein