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European Journal of Heart Failure 2004 6(1):41-45; doi:10.1016/j.ejheart.2003.05.002
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© 2004 European Society of Cardiology

Circulating matrix metalloproteinase-2 is elevated in patients with congestive heart failure

Taketoshi Yamazaki, Jong-Dae Lee*, Hiromasa Shimizu, Hiroyasu Uzui and Takanori Ueda

First Department of Internal Medicine Fukui Medical University, 23-3 Shimoaizuki, Matsuoka, Fukui, 910-1193, Japan

* Corresponding author. Tel.: +81-776-613111; fax: +81-776-618109. E-mail address: jdlee{at}fmsrsa.fukui-med.ac.jp


   Abstract

Background and aims: It has been reported that matrix metalloproteinase (MMP) protein concentration and activity are upregulated in the failing human heart. However, there are few reports describing the role of elevated level of circulating MMPs in congestive heart failure (CHF) patients. This study examined whether circulating matrix metalloproteinases (MMPs) are also related to the pathogenesis of CHF.

Methods: We measured circulating levels of matrix metalloproteinase-2 (MMP-2) in 52 patients with CHF (left ventricular ejection fraction (LVEF) <50%). The patients were also subdivided into two groups according to NYHA functional class; mild CHF (class II, n=43) and severe CHF (class III, n=9). Results: The serum level of MMP-2 and MMP-2/TIMP-2 ratio were significantly higher in CHF than in controls (P<0.01). Among patient groups, serum levels of MMP-2 were significantly higher in patients with severe CHF than in patients with mild CHF (P<0.01). Plasma levels of BNP had a significant positive correlation with circulating levels of MMP-2 (r=0.78; P<0.01) and MMP-2/TIMP-2 ratio (r=0.60; P<0.01).

Conclusions: Our data showed that the circulating MMP-2 concentration was increased in CHF patients and that the levels were related to the plasma levels of BNP in CHF, suggesting that the elevated levels are related to developing heart failure syndrome.

Key Words: Matrix metalloproteinases • Congestive heart failure • Brain natriuretic peptide

Received November 12, 2002; Revised April 14, 2003; Accepted May 7, 2003


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