Galectin-3 in heart failure with preserved ejection fraction

• Published in: European journal of heart failure Vol. 15; no. 10; pp. 1095 - 1101
• Main Authors: de Boer, Rudolf A., Edelmann, Frank, Cohen-Solal, Alain, Mamas, Mamas A., Maisel, Alan, Pieske, Burkert
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01.10.2013
• Subjects: biomarker; Biomarkers; fibrosis; Fibrosis - metabolism; Galectin 3 - metabolism; galectin-3; heart failure; Heart Failure - metabolism; Heart Failure - pathology; Humans; Myocardium - metabolism; Myocardium - pathology; Stroke Volume; Heart failure; Biomarker; Galectin-3; Fibrosis
• ISSN: 1388-9842; 1879-0844; 1879-0844
• DOI: 10.1093/eurjhf/hft077

In the last decades it has been appreciated that many patients with heart failure (HF) suffer from HF with preserved ejection fraction (HFpEF). The diagnosis and treatment of HFpEF is difficult, as we lack specific markers of the disease and no specific treatments have been identified. Galectin‐3 has a strong relationship to several aspects of the pathophysiology of HF, especially myocardial fibrosis, the transition from compensated to decompensated HF, and co‐morbidities such as renal disease and diabetes. Many of these traits are very commonly observed in patients with HFpEF, and this suggests that galectin‐3 may be particularly important and useful in the study of HFpEF. This review summarizes our knowledge of the role of galectin‐3 in fibrosis, specifically in experimental models of HF and HFpEF. Galectin‐3 may be a marker and also a causal factor, and experimental studies suggested that galectin‐3 may be a target for therapy in HFpEF. The detrimental effects of aldosterone may, in part, be conferred via galectin‐3, and there are data to suggest that aldosterone blockers are of more benefit in patients with high levels of galectin‐3. Furthermore, the relationship of galectin‐3 to clinical correlates of developing HFpEF in human subjects is discussed, and the association between increased levels of galectin‐3 and new‐onset HF and mortality in the general population is highlighted. Additionally, the usefulness of galectin‐3 in patients with established HFpEF is described. We conclude that galectin‐3 may be useful for early detection, phenotyping, risk stratification, and therapeutic targeting of individuals with early or established HFpEF in which fibrosis is a major contributor to the disease. Finally, we propose areas of further research that should validate the role of galectin‐3 in HFpEF.