title: Increased myocardial collagen turnover in patients with progressive cardiac conduction disease.
abstract: BACKGROUND
  Histopathologically, progressive cardiac conduction disease (PCCD) is characterized by progressive fibrosis and sclerodegenerative changes in the proximal and distal conduction system of the heart. Therefore, we sought to determine the serum levels of myocardial collagen turnover markers, extracellular matrix components, transforming growth factor beta(1) (TGFbeta(1)), and bone morphogenic protein-7 (BMP-7) in this population.
  
  
  METHODS
  Study population included 20 patients (6 M/14 F, mean age 76 +/- 8 years) with acquired, permanent 2:1, or complete atrioventricular block and compared with age- and sex-matched, asymptomatic, healthy control subjects (n = 18, 6 M/12 F, mean age 75 +/- 7 years). Serum myocardial collagen turnover markers:matrix metalloproteinases (MMP-1, 2, 9), tissue inhibitor of matrix metalloproteinase (TIMP-1), amino-terminal propeptide of procollagen type I (PINP) and type III (PIIINP), carboxy-terminal telopeptide of collagen type I (CITP), and carboxy-terminal propeptide of procollagen type I (PICP), serum extracellular matrix components (laminin and fibronectin), TGFbeta(1), and BMP-7 levels were measured in both groups.
  
  
  RESULTS
  Serum PICP (849 +/- 396 vs 631 +/- 294 ng/mL, P = 0.04), PIIINP (3.7 +/- 1.3 vs 3 +/- 1 mug/L, P = 0.03), CITP (0.68 +/- 0.35 vs 0.48 +/- 0.25 ng/mL, P = 0.037), and plasma MMP-9 (58.8 +/- 56 vs 25.9 +/- 17.3 ng/mL, P = 0.006) levels were higher in patient population compared to control subjects. Serum MMP-1 (24.1 +/- 20.5 vs 13.6 +/- 7.5 ng/mL, P = 0.045) and MMP-2 (1310 +/- 139 vs 1186 +/- 163 ng/mL, P = 0.01) levels were higher in control subjects compared to patient population. There was no difference in serum TIMP-1, PINP, laminin, fibronectin, TGFbeta(1), and BMP-7 levels between two groups.
  
  
  CONCLUSIONS
  Our findings demonstrate the presence of increased myocardial collagen turnover and active fibrotic process in patients with PCCD compared to control subjects.
authors.affiliation: Department of Cardiology, Ege University School of Medicine, Izmir, Turkey.
authors.forename: Yasemin T
authors.initials: YT
authors.lastname: Bozkaya
authors.forename: Hikmet H
authors.initials: HH
authors.lastname: Aydin
authors.forename: Handan A
authors.initials: HA
authors.lastname: Celik
authors.forename: Meral
authors.initials: M
authors.lastname: Kayikcioglu
authors.forename: Serdar
authors.initials: S
authors.lastname: Payzin
authors.forename: Hakan
authors.initials: H
authors.lastname: Kultursay
authors.forename: Mehmet
authors.initials: M
authors.lastname: Aydin
authors.forename: Murat
authors.initials: M
authors.lastname: Yesil
authors.forename: Levent H
authors.initials: LH
authors.lastname: Can
authors.forename: Can
authors.initials: C
authors.lastname: Hasdemir
mesh_terms: D000368:Aged; D003094:Collagen / Q000097:blood*; D004719:Endomyocardial Fibrosis / Q000097:blood*; D016326:Extracellular Matrix Proteins / Q000097:blood*; D005260:Female; D006801:Humans; D008297:Male; D011226:Pre-Excitation Syndromes / Q000097:blood*
chemical_list: D016326:Extracellular Matrix Proteins; D003094:Collagen