title: Inflammation, infection, and aortic valve sclerosis; Insights from the Olmsted County (Minnesota) population.
abstract: Atherosclerosis-related mechanisms, including inflammation and possibly infection, are likely to be involved in the pathogenesis of calcific aortic valve disease. The purpose of this study was to examine whether systemic inflammatory markers and Chlamydia pneumoniae seropositivity are associated with aortic valve sclerosis (AVS) in a sample of the general population. Transesophageal echocardiography was performed in 381 subjects (median age: 67 years, range: 51-101; 52% men), a sample of the adult population in Olmsted County, Minnesota. The associations between systemic inflammatory markers (blood counts, including white blood cells differential counts, fibrinogen, and high-sensitivity C-reactive protein [hs-CRP]), C. pneumoniae immunoglobulin G (IgG) antibody titers, and AVS were examined. AVS was present in 140 subjects (37% of the population). After adjustment for age, sex, and smoking status: (1). hs-CRP was associated with AVS (odds ratio: 1.20 per two-fold increase in hs-CRP; 95% confidence interval: 1.01-1.43; P = 0.04) but this association was not significant after adjustment for additional risk factors for AVS, including body mass index (P = 0.52). (2). Blood counts and fibrinogen were not associated with AVS (P-values >0.30). (3). C. pneumoniae IgG antibody titers (low [1:16-1:32], intermediate [1:64-1:128], or high [>or=1:256] titers, compared with titers <1:16) were not associated with AVS (P = 0.21). In conclusion, hs-CRP is weakly associated with AVS, an association that is not independent of other AVS risk factors. Blood counts, fibrinogen, and C. pneumoniae seropositivity are not associated with AVS. These findings suggest that other non-inflammatory non-infectious mechanisms are likely to have a role in the pathogenesis of calcific aortic valve disease.
authors.affiliation: Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Mayo Foundation, 200 First Street SW, Rochester, MN 55905, USA.
authors.forename: Yoram
authors.initials: Y
authors.lastname: Agmon
authors.forename: Bijoy K
authors.initials: BK
authors.lastname: Khandheria
authors.forename: A
authors.initials: A
authors.lastname: Jamil Tajik
authors.forename: James B
authors.initials: JB
authors.lastname: Seward
authors.forename: JoRean D
authors.initials: JD
authors.lastname: Sicks
authors.forename: Angela J
authors.initials: AJ
authors.lastname: Fought
authors.forename: W Michael
authors.initials: WM
authors.lastname: O'Fallon
authors.forename: Thomas F
authors.initials: TF
authors.lastname: Smith
authors.forename: David O
authors.initials: DO
authors.lastname: Wiebers
authors.forename: Irene
authors.initials: I
authors.lastname: Meissner
mesh_terms: D017677:Age Distribution; D000368:Aged; D000369:Aged, 80 and over; D001024:Aortic Valve Stenosis / Q000175:diagnosis / Q000000981:diagnostic imaging* / Q000453:epidemiology*; D002690:Chlamydia Infections / Q000175:diagnosis* / Q000453:epidemiology; D015331:Cohort Studies; D015897:Comorbidity; D017548:Echocardiography, Transesophageal; D005260:Female; D006801:Humans; D015994:Incidence; D018836:Inflammation Mediators / Q000032:analysis*; D016015:Logistic Models; D008297:Male; D008403:Mass Screening / Q000379:methods; D008875:Middle Aged; D008910:Minnesota / Q000453:epidemiology; D011336:Probability; D018570:Risk Assessment; D012424:Rural Population; D017678:Sex Distribution; D018709:Statistics, Nonparametric
chemical_list: D018836:Inflammation Mediators