title: Contribution of selected serum inflammatory mediators to the progression of chronic rheumatic valve disease, subsequent valve calcification and NYHA functional class.
abstract: OBJECTIVE
  The mechanism of the underlying principle of the progression of chronic rheumatic valve disease (RVD) and subsequent valve calcification are yet not clearly understood. The study aim was to determine whether serum markers of inflammation impact on the severity of chronic RVD, subsequent valve calcification and NYHA functional class.
  
  
  METHODS
  The study group comprised 92 patients (27 males, 65 females; mean age 40 +/- 14 years) with RVD; the control group included 50 age- and gender-matched subjects without echocardiographic signs of RVD. All patients underwent echocardiographic of rheumatic valve severity, valve calcification and NYHA functional class. Levels of cytokines (interleukin-6 (IL-6), interleukin-2 receptor (IL-2R), interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha)) and serum inflammatory markers (fibrinogen, high-sensitive C-reactive protein (hs-CRP)) were measured in all subjects.
  
  
  RESULTS
  Plasma levels of IL-6, IL-8, IL-2R, TNF-alpha and hs-CRP were significantly higher in patients with RVD than in controls (p < 0.001). Significant correlations were identified between mitral score and fibrinogen (p = 0.002), IL-6 (p = 0.007), TNF-alpha (p < 0.001) and hs-CRP levels (p < 0.001). Fibrinogen, hs-CRP, IL-6, TNF-alpha and IL-2R levels correlated with functional class severity, while IL-6 and TNF-a levels correlated strongly with valve calcification (p < 0.001).
  
  
  CONCLUSIONS
  The chronic phase of RVD is associated with ongoing serum inflammatory mediators which correlate strongly with the severity of valve involvement, valve scarring, subsequent valve calcification and decreasing functional status. Future research in this area should focus on whether anti-inflammatory drugs might reduce progression, morbidity and mortality in patients with chronic RVD.
authors.affiliation: Department of Cardiology, Gaziantep University, School of Medicine, Gaziantep, Turkey. davutoglu@gantep.edu.tr
authors.forename: Vedat
authors.initials: V
authors.lastname: Davutoglu
authors.forename: Ahmet
authors.initials: A
authors.lastname: Celik
authors.forename: Mehmet
authors.initials: M
authors.lastname: Aksoy
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D002114:Calcinosis / Q000209:etiology* / Q000503:physiopathology*; D002908:Chronic Disease; D018450:Disease Progression; D005260:Female; D006349:Heart Valve Diseases / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood / Q000502:physiology*; D008297:Male; D012214:Rheumatic Heart Disease / Q000097:blood / Q000150:complications* / Q000503:physiopathology*; D012720:Severity of Illness Index
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators