title: Are morphological or functional changes in the carotid artery wall associated with Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, or herpes simplex virus infection?
abstract: OBJECTIVE
  Chronic infection with Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus (CMV), and herpes simplex virus (HSV) has been implicated in the pathogenesis of atherosclerosis. The carotid intima-media thickness (IMT) can be taken to indicate early atherosclerosis, the presence of a carotid stenosis is a marker of a manifest carotid atherosclerosis, and an increase in arterial stiffness is used as marker of structural and functional changes in an atherosclerotic vessel wall.
  
  
  METHODS
  In 504 patients (75% men; mean age 62.9 [SD 10] years), we measured the IMT and the elastic pressure modulus (EP; n=445) of the common carotid artery and the prevalence of a internal or external carotid artery stenosis. Blood samples were taken, and antibodies against C pneumoniae, H pylori, CMV, and HSV types 1 and 2 were evaluated. Statistical evaluation was performed with regression procedures and multivariate logistic regression analyses.
  
  
  RESULTS
  Seropositivity for C pneumoniae was an independent predictor for a combined end point of highest category of IMT and carotid artery stenosis (OR 1.8, 95% CI 1.1 to 3.1; adjusted) for IgG titers. Independently, CMV increased the risk for the combined end point (OR 1.7, 95% CI 1.1 to 2.8; adjusted) for IgG titers and for IgA titers (OR 2.3, 95% CI 1.1 to 4. 9; adjusted). We found a significant correlation between IgG antibodies against CMV and EP; HSV type 2 IgG titers were associated with IMT and carotid stenosis, but the latter results were no longer significant after adjustment. There was no association with H pylori or HSV type 1.
  
  
  CONCLUSIONS
  We found a significant association of IgG antibodies against C pneumoniae and CMV with early and advanced carotid atherosclerosis. CMV was also correlated to functional changes of the carotid artery, but this could not be confirmed after adjustment.
authors.affiliation: 2nd Department of Medicine, Johannes-Gutenberg University, Mainz, Germany. espinola@mail.uni-mainz.de
authors.forename: C
authors.initials: C
authors.lastname: Espinola-Klein
authors.forename: H J
authors.initials: HJ
authors.lastname: Rupprecht
authors.forename: S
authors.initials: S
authors.lastname: Blankenberg
authors.forename: C
authors.initials: C
authors.lastname: Bickel
authors.forename: H
authors.initials: H
authors.lastname: Kopp
authors.forename: G
authors.initials: G
authors.lastname: Rippin
authors.forename: G
authors.initials: G
authors.lastname: Hafner
authors.forename: U
authors.initials: U
authors.lastname: Pfeifer
authors.forename: J
authors.initials: J
authors.lastname: Meyer
mesh_terms: D001161:Arteriosclerosis / Q000382:microbiology* / Q000821:virology; D002339:Carotid Arteries / Q000382:microbiology* / Q000473:pathology / Q000821:virology; D016893:Carotid Stenosis / Q000209:etiology*; D002690:Chlamydia Infections / Q000150:complications; D016993:Chlamydophila pneumoniae; D003587:Cytomegalovirus; D003586:Cytomegalovirus Infections / Q000150:complications; D016481:Helicobacter Infections / Q000150:complications; D016480:Helicobacter pylori; D006561:Herpes Simplex / Q000150:complications; D006801:Humans; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D018139:Simplexvirus