In patients with chronic HF with or without a reduced LVEF, increasing IVC diameter identifies patients with an adverse outcome.

This article presents findings and a commentary on late‐breaking trials presented during the meeting of the Heart Failure Society of America in September 2009. Unpublished reports should be considered as preliminary, since analyses may change in the final publication. The FAST trial showed somewhat better performance of intrathoracic impedance for prediction of deterioration in patients with heart failure (HF) when compared with daily weighing. The IMPROVE‐HF study reported the benefits of education on the management of patients with systolic HF. Galectin‐3 appeared a useful method for improving risk stratification of patients with chronic HF in a substudy of the COACH trial. A nuclear substudy of the HF‐ACTION trial failed to demonstrate that resting myocardial perfusion imaging, a measure of myocardial scar and viability, was clinically useful. A small randomized controlled trial (DAD‐HF) suggested that the use of low‐dose dopamine in patients with acutely decompensated HF was associated with less deterioration in renal function and less hypokalaemia. The MARVEL‐1 trial raises further concerns about the safety of myoblast transplantation in ischaemic HF.

Heart failure is a leading cause of death and disability. Galectin-3 expression is associated with myocardial fibrosis; recombinant galectin-3 can induce myocardial fibrosis in experimental animals. However, the fact that endogenous galectin-3 is causative of myocardial fibrosis is yet to be firmly established. Nevertheless, the important discovery that N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a naturally occurring anti-inflammatory and antifibrotic peptide, inhibits galectin-3 expression, which prevents cardiac remodeling and dysfunction, provides impetus for translational research into anti-galectin therapy. The lack of a close relationship between galectin-3 and brain natriuretic peptide creates the possibility of a complimentary role. Thus, whilst brain natriuretic peptide is a useful biomarker for diagnosing heart failure, galectin-3 appears to be a culprit biomarker that mediates the development of heart failure, raising the possibility that specific anti-galectin therapy may halt the development of heart failure. Furthermore, data are beginning to emerge supporting the hypothesis that galectin-3 is crucial in the angiotensin-aldosterone pathway leading to salt and water retention, a key mechanism which can result in the development of heart failure. Thus, one might expect patients with heart failure and raised levels of galectin-3 to benefit from aldosterone antagonist therapy. Numerous clinical trials have already established the role of galectin-3 in predicting response to heart failure management, in particular how high levels of galectin-3 predicts mortality. A recent post hoc analysis of the Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA) suggested that patients with relatively low galectin-3 levels (<19 ng/ml) are most likely to benefit from statin therapy. This generated an important hypothesis that deserves further study.