title: Role of inflammation in nonrheumatic, regurgitant heart valve disease. A comparative, descriptive study regarding apolipoproteins and inflammatory cells in nonrheumatic heart valve disease.
abstract: BACKGROUND
  Nonrheumatic aortic stenosis is the predominant cause of heart valve surgery in the Western world. Aortic and mitral regurgitation account for a lesser amount of the heart valve surgery. During the 1990s, inflammatory cell infiltrates have been demonstrated in nonrheumatic stenotic aortic valves. These findings suggest an inflammatory component in the pathogenesis of nonrheumatic aortic valve stenosis. However, nonrheumatic regurgitant aortic and mitral valves have not been investigated in this respect. The aim of this study was to compare nonrheumatic regurgitant aortic and mitral valves with stenotic aortic valves regarding the presence of T lymphocytes, macrophages, apolipoprotein B, and apolipoprotein A-I.
  
  
  METHODS
  Valve specimens were obtained from 42 patients referred to hospital for surgery because of significant heart valve disease. From these patients, 29 aortic stenotic valves, 9 aortic regurgitant, and 6 mitral regurgitant valves, all nonrheumatic, were obtained for the study. Fourteen valves collected from subjects undergoing clinical/medicolegal autopsy were used as control. In order to identify mononuclear inflammatory cells and apolipoproteins, sections were investigated with immunohistochemical analyses and then categorized semiquantitatively.
  
  
  RESULTS
  Regurgitant and control valves showed a significantly lower degree of inflammatory cell infiltrate and a lower degree of apolipoprotein deposition as compared to stenotic aortic valves.
  
  
  CONCLUSIONS
  The signs of inflammation seen in nonrheumatic aortic stenosis are not prominent features in the nonrheumatic, regurgitant valves. This is consistent with the multi-factorial pathogenesis of these conditions.
authors.affiliation: Department of Cardiology, University Hospital, Linköping, Sweden. lars.wallby@lio.se
authors.forename: Lars
authors.initials: L
authors.lastname: Wallby
authors.forename: Wallby
authors.initials: W
authors.lastname: Lars
authors.forename: Thora
authors.initials: T
authors.lastname: Steffensen
authors.forename: Steffensen
authors.initials: S
authors.lastname: Thora
authors.forename: Mats
authors.initials: M
authors.lastname: Broqvist
authors.forename: Broqvist
authors.initials: B
authors.lastname: Mats
mesh_terms: D000328:Adult; D000368:Aged; D001022:Aortic Valve Insufficiency / Q000378:metabolism / Q000473:pathology*; D001024:Aortic Valve Stenosis / Q000378:metabolism / Q000473:pathology*; D016632:Apolipoprotein A-I / Q000378:metabolism; D001055:Apolipoproteins B / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D005260:Female; D006349:Heart Valve Diseases / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000378:metabolism / Q000473:pathology*; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D013601:T-Lymphocytes / Q000378:metabolism / Q000473:pathology
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D002118:Calcium