title: Clinical factors, but not C-reactive protein, predict progression of calcific aortic-valve disease: the Cardiovascular Health Study.
abstract: OBJECTIVE
  The purpose of this study was to examine the relationship between C-reactive protein (CRP) and calcific aortic valve disease in a large, randomly selected, population-based cohort.
  
  
  BACKGROUND
  The pathobiology of calcific aortic stenosis involves an active inflammatory, atheromatous, osteogenic process. Elevations in CRP, a measure of systemic inflammation, have been associated with aortic stenosis.
  
  
  METHODS
  Two-dimensional and Doppler echocardiography and CRP measurement were performed at baseline in 5,621 participants in the Cardiovascular Health Study. Multivariable analysis was used to identify CRP as a predictor of baseline and incident aortic stenosis.
  
  
  RESULTS
  At a mean echocardiographic follow-up of 5 years, 9% of subjects with aortic sclerosis progressed to some degree of aortic stenosis. Increasing age (odds ratio [OR] 1.13, 95% confidence interval [CI] 1.09 to 1.16; p < 0.001) and male gender (OR 3.05, 95% CI 1.76 to 5.27; p < 0.001) were related to risk of incident aortic stenosis, whereas increasing height (OR 0.96, 95% CI 0.94 to 0.99; p = 0.013) and African-American ethnicity conveyed a lower risk (OR 0.49, 95% CI 0.25 to 0.95; p = 0.035). C-reactive protein, treated as a continuous variable, was not associated with baseline aortic stenosis, progression to aortic sclerosis (adjusted OR 0.93, 95% CI 0.85 to 1.02; p = 0.107), or progression to aortic stenosis (adjusted OR 0.85, 95% CI 0.70 to 1.03; p = 0.092).
  
  
  CONCLUSIONS
  In this large population-based cohort, approximately 9% of subjects with aortic sclerosis progressed to aortic stenosis over a 5-year follow-up period. There was no association between CRP levels and the presence of calcific aortic-valve disease or incident aortic stenosis. C-reactive protein appears to be a poor predictor of subclinical calcific aortic-valve disease.
authors.affiliation: Department of Cardiology, Cleveland Clinic Florida, Weston, Florida 33331, USA. novarog@ccf.org
authors.forename: Gian M
authors.initials: GM
authors.lastname: Novaro
authors.forename: Ronit
authors.initials: R
authors.lastname: Katz
authors.forename: Ronnier J
authors.initials: RJ
authors.lastname: Aviles
authors.forename: John S
authors.initials: JS
authors.lastname: Gottdiener
authors.forename: Mary
authors.initials: M
authors.lastname: Cushman
authors.forename: Bruce M
authors.initials: BM
authors.lastname: Psaty
authors.forename: Catherine M
authors.initials: CM
authors.lastname: Otto
authors.forename: Brian P
authors.initials: BP
authors.lastname: Griffin
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001021:Aortic Valve / Q000473:pathology*; D001024:Aortic Valve Stenosis / Q000097:blood / Q000473:pathology; D002097:C-Reactive Protein / Q000378:metabolism*; D002114:Calcinosis / Q000097:blood* / Q000473:pathology*; D002318:Cardiovascular Diseases / Q000097:blood / Q000473:pathology; D015331:Cohort Studies; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006349:Heart Valve Diseases / Q000097:blood* / Q000473:pathology*; D006801:Humans; D008297:Male; D012307:Risk Factors
chemical_list: D002097:C-Reactive Protein