Elsevier, Clinica Chimica Acta, 1-2(409), p. 96-99
DOI: 10.1016/j.cca.2009.09.001
Full text: Unavailable
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)