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Galectin-3 may serve as predictor of HF
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High levels of the protein galectin-3 appeared to increase the risks for HF and all-cause mortality, according to data published in the Journal of the American College of Cardiology.
Researchers evaluated 3,353 participants in the Framingham offspring cohort (mean age, 59 years; 53% women) to assess the link between galectin-3 — a marker of cardiac fibrosis — and incident HF. They measured concentrations of galectin-3 in blood samples collected from the participants during routine examinations from 1996 to 1998.
During a mean follow-up of 8.1 years, 166 participants developed incident HF and 468 died. Analyses revealed an association between galectin-3 and incident HF (HR=1.28 per 1 standard deviation increase in log galectin-3; 95% CI, 1.14-1.43) — a relationship that remained significant after adjustment for clinical variables and B-type natriuretic peptide (HR=1.23; 95% CI, 1.04-1.47). The researchers also found an association between galectin-3 and all-cause mortality, with a multivariable-adjusted HR of 1.15 (95% CI, 1.04-1.28).
Age- and sex-adjusted analyses also revealed an association between galectin-3 and left ventricular mass (P=.001), although this relationship was attenuated in multivariate analyses (P=.06).
“Future potential clinical uses of [galectin-3] measurement might include the identification of asymptomatic subjects with early evidence of cardiac fibrosis, in whom targeted therapies may be useful to delay the onset of HF,” the researchers concluded.
In an editorial comment, David A. Morrow, MD, MPH, and Michelle L. O’Donoghue, MD, MPH, both of Brigham and Women’s Hospital in Boston and members of the TIMI Study Group, said the findings raise questions and highlight opportunities for research into treating HF.
“Because [galectin-3] did not add convincingly to improve discrimination or reclassification of risk, appropriately, the investigators do not argue a role for routine screening,” they wrote. “However, their findings lend support to the notion of [galectin-3] as a causal factor in human cardiac disease. Further investigation of [galectin-3] may lead to advances in our understanding of cardiac fibrosis and remodeling, as well as shine a light toward new therapies for a challenging and increasingly prevalent disease.”
For more information:
Ho JE. J Am Coll Cardiol. 2012;doi:10.1016/j.jacc.2012.04.053.
Morrow DA. J Am Coll Cardiol. 2012;doi:10.1016/j.jacc.2012.05.032.
Disclosure: This study was supported by the NHLBI’s Framingham Heart Study, and Dr. Ho is supported by an American Heart Association Clinical Research Program award. Galectin-3 assays were provided by BG Medicine. See the invited editorial for a full list of Drs. Morrow and O’Donoghue’s disclosures.