title: Extracellular matrix alterations in patients with paroxysmal and persistent atrial fibrillation: biochemical assessment of collagen type-I turnover.
abstract: OBJECTIVE
  We investigated whether the serum markers of collagen turnover differed in various forms of atrial fibrillation (AF) and in sinus rhythm (SR) in humans.
  
  
  BACKGROUND
  Structural alterations and fibrosis have been implicated in the generation and perpetuation of AF.
  
  
  METHODS
  Serum C-terminal propeptide of collagen type-I (CICP), C-terminal telopeptide of collagen type-I (CITP), matrix metalloproteinase-1, and tissue inhibitor of matrix metalloproteinases-1 were measured as markers of collagen synthesis and degradation in 70 patients with AF and 20 healthy control subjects in SR.
  
  
  RESULTS
  C-terminal propeptide of collagen type-I and CITP were significantly higher in AF patients than in control subjects (91 +/- 27 ng/ml vs. 67 +/- 11 ng/ml, p < 0.001 and 0.38 +/- 0.20 ng/ml vs. 0.25 +/- 0.08 ng/ml, p < 0.001, respectively). Persistent AF patients had higher levels of CICP (105 +/- 28 ng/ml vs. 80 +/- 21 ng/ml, p < 0.001), but not CITP, compared with those with paroxysmal AF. Patients with persistent AF had lower levels of matrix metalloproteinase-1 but increased levels of tissue inhibitor of matrix metalloproteinases-1 compared with patients with paroxysmal AF (11.90 +/- 4.79 ng/ml vs. 14.98 +/- 6.28 ng/ml, p = 0.03 and 155 +/- 45 ng/ml vs. 130 +/- 38 ng/ml, p < 0.001, respectively). Tissue inhibitor of matrix metalloproteinases-1 levels were significantly lower in control subjects compared with those in both paroxysmal and persistent AF patients (102 +/- 15 ng/ml vs. 130 +/- 38 ng/ml vs. 155 +/- 45 ng/ml, respectively, p < 0.001).
  
  
  CONCLUSIONS
  Serum markers of collagen type-I turnover differed significantly between patients with AF and SR. Furthermore, these markers also differed significantly between paroxysmal and persistent AF patients, suggesting that the intensity of the extracellular synthesis and degradation of collagen type-I may be related to the burden or type of AF.
authors.affiliation: Department of Cardiology, University Hospital of Heraklion, Crete, Greece.
authors.forename: Eleftherios M
authors.initials: EM
authors.lastname: Kallergis
authors.forename: Emmanuel G
authors.initials: EG
authors.lastname: Manios
authors.forename: Emmanuel M
authors.initials: EM
authors.lastname: Kanoupakis
authors.forename: Hercules E
authors.initials: HE
authors.lastname: Mavrakis
authors.forename: Dimitris A
authors.initials: DA
authors.lastname: Arfanakis
authors.forename: Niki E
authors.initials: NE
authors.lastname: Maliaraki
authors.forename: Chrisovalantis E
authors.initials: CE
authors.lastname: Lathourakis
authors.forename: Gregory I
authors.initials: GI
authors.lastname: Chlouverakis
authors.forename: Panos E
authors.initials: PE
authors.lastname: Vardas
mesh_terms: D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000097:blood / Q000201:enzymology / Q000378:metabolism* / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D024042:Collagen Type I / Q000097:blood / Q000378:metabolism*; D005109:Extracellular Matrix / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005355:Fibrosis / Q000378:metabolism; D006801:Humans; D008297:Male; D020781:Matrix Metalloproteinase 1 / Q000378:metabolism; D008875:Middle Aged; D013997:Time Factors; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000378:metabolism
chemical_list: D015415:Biomarkers; D024042:Collagen Type I; D019715:Tissue Inhibitor of Metalloproteinase-1; D020781:Matrix Metalloproteinase 1