Background: A growing body of evidence links macrophage activation and fibrosis to the pathogenesis of heart failure (HF). Galectin-3 is one of the most likely mediators between macrophage activation and myocardial fibrosis. However, the exact relationship is unknown in humans. We assessed the impact of galectin-3 on serum markers of cardiac extracellular matrix (ECM) turnover in HF patients.
Methods: Patients with HF manifestations and a left ventricular ejection fraction (LVEF) <or=50% were enrolled in this study. Gender, age, medications, serum biochemical data, and outcomes of heart failure were recorded. Serum galectin-3, extracellular matrix including type I and III aminoterminal propeptide of procollagen (PINP and PIIINP), matrix metalloproteinase-2 (MMP-2), and tissue inhibitor of metalloproteinase-1 (TIMP-1) were analyzed.
Results: A total of 106 (83 males and 23 females) patients were enrolled. The age was 61+/-16 y and LVEF was 35+/-9%. Their mean NYHA functional class was 2.2. Log galectin-3 was significantly correlated with log PIIINP (p=0.006), log TIMP-1 (p=0.025), log MMP-2 (p=0.016), and NYHA functional class (p=0.034); but not age, sex or LVEF. After adjusting for age, sex, smoking status and LVEF, the relationship between galectin-3 and ECM turnover biomarkers (including PIIINP, TIMP, and MMP-2) remained significant. After adjusting for age, sex, smoking status and NYHA functional class, the relationship between galectin-3 and PIIINP or MMP-2 remained significant.
Conclusions: Galectin-3 is significantly correlated with serum markers of cardiac ECM turnover in HF patients. This implies a relationship between macrophage activation and ECM turnover in patients with HF.