Contribution of plasma matrix metalloproteinases to development of left ventricular hypertrophy and diastolic dysfunction in hypertensive subjects
Tohoku Journal of Experimental Medicine, cilt.208, sa.2, ss.117-122, 2006 (Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 208 Sayı: 2
- Basım Tarihi: 2006
- Doi Numarası: 10.1620/tjem.208.117
- Dergi Adı: Tohoku Journal of Experimental Medicine
- Derginin Tarandığı İndeksler: Scopus
- Sayfa Sayıları: ss.117-122
- Anahtar Kelimeler: matrix metalloproteinases, left ventricular hypertrophy, diastolic dysfunction
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Matrix metalloproteinases (MMPs) are involved in the regulation of the extracellular matrix (ECM) of the myocardium and thus the pathogenesis of vascular and cardiac hypertrophy. In this study, we investigated contribution of plasma matrix metalloproteinases to development of left ventricular hypertrophy (LVH) and diastolic dysfunction in hypertensive subjects. Hypertensive patients with (n = 27) and without LVH (n = 23) were included. All participants underwent a complete transthoracic echocardiographic examination, including recordings of the mitral annular early, late, systolic and diastolic velocities by Doppler imaging. Plasma concentrations of MMP-3 and MMP-9 were determined by the one-step sandwich enzyme immunoassay method. Plasma MMP-3 and MMP-9 concentrations were significantly higher in patients with LUH than those without LVH (2.4 ± 1.2 vs 1.5 ± 0.7 ng/ml, p = 0.006 and 5.2 ± 2.8 vs 3.3 ± 1.7 ng/ml, p = 0.003, respectively). MMP-3 and MMP-9 levels were also correlated with left ventricular posterior wall thickness and Doppler indices of diastolic dysfunction. Our findings have suggested that increased MMP levels may contribute to LVH and left ventricular diastolic dysfunction. Therefore, treatment of hypertension with MMP lowering drugs, such as angiotensin converting enzyme inhibitors and angiotensin receptor blockers, may have favorable effects on LVH and left ventricular diastolic dysfunction. © 2006 Tohoku University Medical Press.