Blood Assay for Galectin-3 Identifies Heart Failure Risk of Patients in the Community Setting

Test may also predict response to therapy
Value-Based Care in Cardiometabolic Health May 2012, Vol 1, No 1
Wayne Kuznar

Chicago, IL—A blood test for galectin-3, a unique protein that binds to carbohydrates known as “beta-galactosides,” appears to be a reliable predictor of incident heart failure (HF) and of the response to treatment for HF, reported Jennifer E. Ho, MD, a practicing cardiologist in San Francisco, CA, using data from the National Heart, Lung, and Blood Institute’s Framingham Heart Study, at the 2012 American College of Cardiology meeting.

Galectin-3 has been implicated in biologic processes important to the development and progression of HF, and is believed to be a primary mediator of progressive cardiac fibrosis.

Data have demonstrated that higher levels of galectin-3 are associated with a more aggressive form of HF, and that ≥33% of patients with mild-tomoderate HF have elevated levels of galectin-3.

In a study presented at the meeting, higher levels of galectin-3 were associated with an increased risk of new-onset HF and all-cause mortality in the community.

The study included 3353 participants (mean age, 59 years) of the Framingham Offspring Cohort whose galectin-3 levels were measured and who were followed for development of HF over 10 years. Of this population, 10% to 25% had an elevated level of galectin-3.

Incident HF was more common as galectin-3 levels increased. In multivariate analyses, each standard deviation (SD) increase in galectin-3 levels was associated with a 23% increase in the hazard ratio (HR) for incident HF, and on sex- and age-adjusted analyses, each SD increase was associated with a 28% increase in HR.

Galectin-3 was also associated with all-cause mortality, with a multivariable-adjusted HR of 1.15.

The study provides further confirmation that elevated levels of galectin-3 in the general population are associated with a markedly increased risk of HF development over the subsequent 10 years, said Dr Ho.

The findings suggest “that cardiovascular injury due to fibrosis may be evident long before the clinical onset of heart failure,” Dr Ho said.

A second analysis found a differential effect of treatment on HF based on patients’ galectin-3 levels. Investigators led by Inder S. Anand, MD, FRCP, FACC, Professor of Medicine at the University of Minnesota, and Director of the Heart Failure Program at the Minneapolis VA Medical Center, looked at treatment response in the Valsartan Heart Failure Trial (Val-HeFT), in which patients with HF were randomized to valsartan (Diovan) or placebo in addition to other therapies for HF.

Plasma samples were available for approximately 30% of the Val-HeFT participants. Compared with placebo, valsartan caused a significant 44% reduction in hospitalizations for HF in a subgroup of patients with galectin- 3 below the median. No effect of valsartan was observed in the subgroup with galectin-3 above the median.

Another subanalysis of a major study, the landmark Multicenter Automatic Defibrillator Implantation Trial with Cardiac Resynchronization Therapy (MADIT-CRT), suggests that galectin-3 may be used to prioritize patients with early-stage HF for cardiac resynchronization therapy (CRT), said Kenneth Stein, MD, Senior Vice President and Chief Medical Officer, Cardiac Rhythm Management at Boston Scientific, Minneapolis.

The data revealed that CRT conveyed an important benefit in patients with low and high galectin-3 levels. However, because of the markedly higher incidence of events in patients with high levels of galectin-3, the absolute benefit of CRT was approximately double that of the benefit in patients with low galectin-3 levels.

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