title: Infectious burden and carotid plaque thickness: the northern Manhattan study.
abstract: OBJECTIVE
  The overall burden of prior infections may contribute to atherosclerosis and stroke risk. We hypothesized that serological evidence of common infections would be associated with carotid plaque thickness in a multiethnic cohort.
  
  
  METHODS
  Antibody titers to 5 common infectious microorganisms (ie, Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpesvirus 1 and 2) were measured among stroke-free community participants and a weighted index of infectious burden was calculated based on Cox models previously derived for the association of each infection with stroke risk. High-resolution carotid duplex Doppler studies were used to assess maximum carotid plaque thickness. Weighted least squares regression was used to measure the association between infectious burden and maximum carotid plaque thickness after adjusting for other risk factors.
  
  
  RESULTS
  Serological results for all 5 infectious organisms were available in 861 participants with maximum carotid plaque thickness measurements available (mean age, 67.2+/-9.6 years). Each individual infection was associated with stroke risk after adjusting for other risk factors. The infectious burden index (n=861) had a mean of 1.00+/-0.35 SD and a median of 1.08. Plaque was present in 52% of participants (mean, 0.90+/-1.04 mm). Infectious burden was associated with maximum carotid plaque thickness (adjusted increase in maximum carotid plaque thickness 0.09 mm; 95% CI, 0.03 to 0.15 mm per SD increase of infectious burden).
  
  
  CONCLUSIONS
  A quantitative weighted index of infectious burden, derived from the magnitude of association of individual infections with stroke, was associated with carotid plaque thickness in this multiethnic cohort. These results lend support to the notion that past or chronic exposure to common infections, perhaps by exacerbating inflammation, contributes to atherosclerosis. Future studies are needed to confirm this hypothesis and to define optimal measures of infectious burden as a vascular risk factor.
authors.affiliation: Neurological Institute, 710 West 168th Street, Box 182, New York, NY 10032, USA. mse13@columbia.edu
authors.forename: Mitchell S V
authors.initials: MS
authors.lastname: Elkind
authors.forename: Jorge M
authors.initials: JM
authors.lastname: Luna
authors.forename: Yeseon Park
authors.initials: YP
authors.lastname: Moon
authors.forename: Bernadette
authors.initials: B
authors.lastname: Boden-Albala
authors.forename: Khin M
authors.initials: KM
authors.lastname: Liu
authors.forename: Steven
authors.initials: S
authors.lastname: Spitalnik
authors.forename: Tanja
authors.initials: T
authors.lastname: Rundek
authors.forename: Ralph L
authors.initials: RL
authors.lastname: Sacco
authors.forename: Myunghee C
authors.initials: MC
authors.lastname: Paik
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000382:microbiology / Q000473:pathology* / Q000821:virology; D001424:Bacterial Infections / Q000150:complications / Q000208:ethnology / Q000473:pathology*; D002339:Carotid Arteries / Q000382:microbiology / Q000473:pathology* / Q000821:virology; D002340:Carotid Artery Diseases / Q000208:ethnology / Q000382:microbiology / Q000473:pathology* / Q000821:virology; D015331:Cohort Studies; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009519:New York City / Q000208:ethnology; D011446:Prospective Studies; D012307:Risk Factors; D020521:Stroke / Q000382:microbiology / Q000473:pathology* / Q000821:virology; D014777:Virus Diseases / Q000150:complications / Q000208:ethnology / Q000473:pathology*