title: Serum levels of large tenascin-C variants, matrix metalloproteinase-9, and tissue inhibitors of matrix metalloproteinases in concentric versus eccentric left ventricular hypertrophy.
abstract: OBJECTIVE
  Chronic hypertension may cause left ventricular hypertrophy (LVH). The role of matrix metalloproteinases (MMPs), tissue inhibitors of matrix metalloproteinases (TIMPs), and tenascin-C (Tn-C) splice variants in concentric vs. eccentric left ventricular remodelling has not been investigated.
  
  
  RESULTS
  Serum levels of B or C domain containing Tn-C, MMP-9, TIMP-1, -2, and -4 were determined in concentric (left ventricular posterior wall thickness >13 mm and intraventricular septum >13 mm, n = 61) and eccentric (end-diastolic left ventricular diameter >55 mm or end-systolic left ventricular diameter >40 mm, n = 34) LVH by enzyme-linked immunoassays. Levels of B domain containing Tn-C were higher in patients with LVH than in normal volunteers (P = 0.020) and higher in eccentric LVH (EH) compared with concentric LVH (CH) (P = 0.003). A cut-off value of 900 ng/mL might discriminate between these different forms of LVH. Matrix metalloproteinase-9 was higher in patients with LVH than in normal volunteers (P = 0.042), and levels were decreased in EH compared with CH (P = 0.028). Patients with LVH had higher levels of TIMP-1 (P = 0.059), TIMP-2 (P = 0.043), and TIMP-4 (P = 0.163) than normal volunteers, but there were no differences between the LVH groups.
  
  
  CONCLUSIONS
  Our data suggest that myocardial remodelling in LVH is associated with changes in serum levels of MMP-9, TIMP-1, -2, -4, and Tn-C splice variants. In addition, B domain containing Tn-C discriminated EH from CH and might be suggested as a potential diagnostic marker.
authors.affiliation: Department of Internal Medicine I/Cardiology, University Hospital of Jena, Erlanger Allee 101, 07740 Jena, Germany. marcus.franz@med.uni-jena.de
authors.forename: Marcus
authors.initials: M
authors.lastname: Franz
authors.forename: Alexander
authors.initials: A
authors.lastname: Berndt
authors.forename: Annelore
authors.initials: A
authors.lastname: Altendorf-Hofmann
authors.forename: Nico
authors.initials: N
authors.lastname: Fiedler
authors.forename: Petra
authors.initials: P
authors.lastname: Richter
authors.forename: Julia
authors.initials: J
authors.lastname: Schumm
authors.forename: Michael
authors.initials: M
authors.lastname: Fritzenwanger
authors.forename: Hans Reiner
authors.initials: HR
authors.lastname: Figulla
authors.forename: Bernhard R
authors.initials: BR
authors.lastname: Brehm
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D005260:Female; D015870:Gene Expression; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood* / Q000473:pathology*; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000097:blood*; D061965:Matrix Metalloproteinase Inhibitors; D008875:Middle Aged; D012680:Sensitivity and Specificity; D019063:Tenascin / Q000097:blood* / Q000235:genetics; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000097:blood; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000097:blood; D019714:Tissue Inhibitor of Metalloproteinases / Q000097:blood*; D020257:Ventricular Remodeling; D000097792:Tissue Inhibitor of Metalloproteinase-4
chemical_list: D015415:Biomarkers; D020780:Matrix Metalloproteinase 9; D061965:Matrix Metalloproteinase Inhibitors; D019063:Tenascin; D019715:Tissue Inhibitor of Metalloproteinase-1; D019716:Tissue Inhibitor of Metalloproteinase-2; D019714:Tissue Inhibitor of Metalloproteinases; D000097792:Tissue Inhibitor of Metalloproteinase-4