Serum levels of large tenascin-C variants, matrix metalloproteinase-9, and tissue inhibitors of matrix metalloproteinases in concentric versus eccentric left ventricular hypertrophy.
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.
Franz
Marcus
M
Department of Internal Medicine I/Cardiology, University Hospital of Jena, Erlanger Allee 101, 07740 Jena, Germany. marcus.franz@med.uni-jena.de
Berndt
Alexander
A
Altendorf-Hofmann
Annelore
A
Fiedler
Nico
N
Richter
Petra
P
Schumm
Julia
J
Fritzenwanger
Michael
M
Figulla
Hans Reiner
HR
Brehm
Bernhard R
BR
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
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