Abstract 14384: Plasma Levels of Galectin-3 in the Community: Galectin-3 is Associated with Pre-Clinical Ventricular Dysfunction and Subsequent Incident Heart Failure and Mortality

Abstract

Background: Galectin-3 (Gal3) is implicated in the pathogenesis of cardiac fibrosis. We hypothesized that Gal3 levels are associated with fibrosis-related LV remodeling and dysfunction, incident heart failure (HF) and death in in the general population.

Methods: A random sample of Olmsted County, MN residents aged ≥ 45 yrs and free from clinical HF were studied (clinical, lab, and echo data and stored plasma) between 1997 and 2000. Gal3 levels and echo at study entry and follow up for incident HF and all-cause death were obtained through 2011. The associations between Gal3 levels and echo indices at study entry and with subsequent outcomes were assessed adjusting for pertinent covariates.

Results: Of 1825 subjects enrolled, 725 were normal (no cardiovascular disease, normal EF and diastolic function). In normals, Gal3 levels were higher in females, increased with age and renal dysfunction (p<0.0003 for all) but were not associated with BMI. In the entire cohort, adjusting for age, sex and renal function, Gal3 was inversely associated with EF and LV size and directly associated with markers of diastolic dysfunction (E/e’, and RVSP) (Table 1). 190 subjects developed HF and 289 died. After adjusting for clinical factors, Gal3 was associated with both incident HF and death (Table 2).

Conclusions: In the community, Gal3 is associated with systolic and diastolic dysfunction prior to the onset of clinical HF and with subsequent HF and death. These data suggests that Gal3 activation contributes to the development of systolic and diastolic dysfunction, subsequent HF and death and supports testing therapies targeting the Gal3-mediated pro-fibrotic pathway as a strategy to prevent HF.