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Relationships between plasma levels of matrix metalloproteinases and neurohormonal profile in patients with heart failure
Author(s) -
Yan Andrew T.,
Yan Raymond T.,
Spinale Francis G.,
Afzal Rizwan,
Gunasinghe Himali R.,
Stroud Robert E.,
McKelvie Robert S.,
Liu Peter P.
Publication year - 2008
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2007.12.002
Subject(s) - matrix metalloproteinase , medicine , heart failure , cardiology
Background: Both neurohormonal derangements and alterations in the myocardial extracellular matrix are thought to contribute to adverse ventricular remodelling that results in worsening heart failure (HF). There is also emerging preclinical information to suggest that these signalling pathways mutually regulate in HF. Aim: To assess the relationships between plasma levels of matrix metalloproteinases (MMPs), tissue inhibitor of metalloproteinase (TIMP), and neurohormonal profiles in chronic HF. Methods and results: In this substudy of 184 HF patients enrolled in the Randomized Evaluation of Strategies for Left Ventricular Dysfunction (RESOLVD) trial, plasma norepinephrine and epinephrine were measured with HPLC; atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), angiotensin II, aldosterone, and endothelin‐1 were measured with immunoassays; MMP‐2, MMP‐9, and TIMP‐1 were measured with 2‐site sandwich ELISA assays. We used Spearman's rank correlation to examine the relationships between plasma MMP and neurohormone levels. Circulating ANP, BNP, and endothelin‐1 levels were positively correlated with MMP‐2 and TIMP‐1 levels. Plasma level of aldosterone showed a weak positive correlation with MMP‐9, but there was no significant correlation between angiotensin II, epinephrine or norepinephrine and MMP‐2, MMP‐9, or TIMP‐1. Conclusions: These findings suggest that specific neurohormones and extracellular matrix modulators may play a coordinated role in the pathogenesis of HF.