Serum levels of large tenascin-C variants, matrix metalloproteinase-9, and tissue inhibitors of matrix metalloproteinases in concentric versus eccentric left ventricular hypertrophy.

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.