Published Online
on October 22, 2009

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Original Article

Episodes of Acute Heart Failure Syndrome are Associated with Increased Levels of Troponin and Extracellular Matrix Markers

Andreia Biolo; Mark Fisch; Joshua Balog; Tania Chao; P. Christian Schulze; Henry Ooi; Deborah Siwik and Wilson S. Colucci¹

Boston University Medical Center, Boston, MA

^* Corresponding author; email: wilson.colucci{at}bmc.org

Background—Increased myocyte loss and extracellular matrix (ECM) turnover are central mechanisms that contribute to pathologic myocardial remodeling in chronic heart failure (HF). We tested the hypothesis that episodes of acute heart failure syndrome (AHFS) are associated with transient increases in markers of myocyte injury and ECM turnover beyond those observed in chronic stable HF.

Methods and Results—Markers of myocyte injury and ECM turnover were assessed in 80 patients prospectively divided into 3 groups: AHFS (n = 39); chronic stable systolic HF (n = 21); and control subjects without HF (n = 20). Myocyte injury was assessed by measuring plasma troponin I. ECM turnover was assessed by measuring plasma matrix metalloproteinases (MMPs), tissue inhibitors of MMPs (TIMPs), and pro-collagen N-terminal types I (PINP) and III (PIIINP). In the AHFS group, biomarkers were obtained a) at the time of hospital admission for an episode of HF decompensation, b) at the time of hospital discharge, and c) several weeks after discharge in patients who had returned to a chronic stable compensated state. In patients with stable HF (vs. non-HF controls), there was a small increase in troponin I, and little or no difference in any marker of ECM turnover. In patients with AHFS, troponin I and three markers of ECM turnover (MMP-2, TIMP-1 and PIIINP) were elevated (vs. chronic stable HF), and all fell toward chronic HF levels in patients who returned to a compensated state.

Conclusion—Episodes of AHFS are associated with transient increases in markers of myocyte injury and ECM turnover that may reflect an acceleration of pathologic myocardial remodeling during AHFS.

Key Words: matrix metalloproteinase • tissue inhibitor of metalloproteinase • troponin