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Serum levels of large tenascin‐C variants, matrix metalloproteinase‐9, and tissue inhibitors of matrix metalloproteinases in concentric versus eccentric left ventricular hypertrophy
Author(s) -
Franz Marcus,
Berndt Alexander,
AltendorfHofmann Annelore,
Fiedler Nico,
Richter Petra,
Schumm Julia,
Fritzenwanger Michael,
Figulla Hans Reiner,
Brehm Bernhard R.
Publication year - 2009
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1093/eurjhf/hfp128
Subject(s) - left ventricular hypertrophy , matrix metalloproteinase , medicine , eccentric , cardiology , concentric hypertrophy , concentric , muscle hypertrophy , endocrinology , anatomy , blood pressure , geometry , physics , mathematics , quantum mechanics
Aims 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. Methods and 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. Conclusion 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.