title: Aortic stiffness correlates with an increased extracellular matrix turnover in patients with dilated cardiomyopathy.
abstract: BACKGROUND
  An increased extracellular matrix (ECM) turnover has been associated with poor survival in patients with chronic heart failure (CHF) due to dilated cardiomyopathy (DCM). However, the influence of the accelerated collagen turnover on the progressive large artery stiffening process characterizing CHF has not been clarified. This is relevant because aortic stiffening imposes an additional systolic load and impairs exercise tolerance in CHF patients. Therefore, we investigated whether the serum aminoterminal propeptide of type III collagen (PIIINP), an established marker of ECM turnover and tissue fibrosis in DCM, was associated with aortic stiffness in DCM patients.
  
  
  RESULTS
  A total of 89 patients with clinical diagnosis of DCM (age 62 +/- 9 years, 80% men, mean ejection fraction 34% +/- 8%) were selected. Aortic pulse-wave velocity (PWV), a well-established marker of aortic stiffness, was measured by Doppler ultrasonography. Serum concentration of PIIINP was determined by radioimmunoassay. Mean aortic PWV was 5.7 +/- 2.3 m/s, and PIIINP was 5.0 +/- 1.3 microg/L. The variables correlated with aortic PWV were age (r = 0.33, P = .002), PIIINP (r = 0.30, P = .005), heart rate (r = 0.27, P = .02), stroke volume (r = -0.24, P = .03) and New York Heart Association class (r = 0.25, P = .02). In a multivariate analysis, age (P = .02) and PIIINP (P = .01) were independently related with aortic PWV, accounting for 27% of its variance.
  
  
  CONCLUSIONS
  Higher serum PIIINP levels are independently associated with a stiffer aorta in DCM patients. This suggests that abnormalities in the ECM turnover might involve the proximal elastic vasculature and could partially explain the progressive large artery stiffening process characterizing CHF.
authors.affiliation: Divisione Clinicizzata di Cardiologia, Dipartimento di Scienza Biomediche e Chirurgiche, Università di Verona, Verona, Italy.
authors.forename: Stefano
authors.initials: S
authors.lastname: Bonapace
authors.forename: Andrea
authors.initials: A
authors.lastname: Rossi
authors.forename: Mariantonietta
authors.initials: M
authors.lastname: Cicoira
authors.forename: Giorgio
authors.initials: G
authors.lastname: Golia
authors.forename: Luisa
authors.initials: L
authors.lastname: Zanolla
authors.forename: Lorenzo
authors.initials: L
authors.lastname: Franceschini
authors.forename: Luca
authors.initials: L
authors.lastname: Conte
authors.forename: Paolo
authors.initials: P
authors.lastname: Marino
authors.forename: Piero
authors.initials: P
authors.lastname: Zardini
authors.forename: Corrado
authors.initials: C
authors.lastname: Vassanelli
mesh_terms: D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D001011:Aorta / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D001783:Blood Flow Velocity; D002311:Cardiomyopathy, Dilated / Q000097:blood* / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D017023:Coronary Angiography; D015150:Echocardiography, Doppler; D004548:Elasticity; D005109:Extracellular Matrix / Q000378:metabolism*; D005260:Female; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D018377:Neurotransmitter Agents / Q000097:blood; D010446:Peptide Fragments / Q000097:blood*; D011347:Procollagen / Q000097:blood*; D011863:Radioimmunoassay
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D018377:Neurotransmitter Agents; D010446:Peptide Fragments; D011347:Procollagen; C041876:procollagen Type III-N-terminal peptide