In:
European Journal of Heart Failure, Wiley, Vol. 11, No. 11 ( 2009-11), p. 1057-1062
Abstract:
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.
Type of Medium:
Online Resource
ISSN:
1388-9842
,
1879-0844
DOI:
10.1093/eurjhf/hfp128
Language:
English
Publisher:
Wiley
Publication Date:
2009
detail.hit.zdb_id:
1500332-2
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