Clinical Information

Heart failure is a complex cardiovascular disorder with a variety of etiologies and heterogeneity with respect to the clinical presentation of the patient. Heart failure is significantly increasing in prevalence with an aging population and is associated with high short- and long-term mortality rate. Over 80% of patients diagnosed and treated for acute heart failure syndromes in the emergency department are readmitted within the forthcoming year, incurring costly treatments and therapies.(1)

The development and progression of heart failure is a clinically silent process until manifestation of the disorder, which typically occurs late and irreversibly into its progression. Mechanistically, heart failure, whether due to systolic or diastolic dysfunction, is thought to progress primarily through adverse cardiac remodeling and fibrosis in response to cardiac injury and/or stress. Galectin-3 is a biomarker that appears to be actively involved in both the inflammatory and fibrotic pathways that are thought to be involved.

Galectin-3 is a carbohydrate-binding lectin whose expression is associated with inflammatory cells including macrophages, neutrophils, and mast cells. Galectin-3 has been linked to cardiovascular physiological processes including myofibroblast proliferation, tissue repair, and cardiac remodeling in the setting of heart failure. Concentrations of galectin-3 have been used to predict adverse remodeling after a variety of cardiac insults.