Galectin‐3 and Risk of Heart Failure and Death in Blacks and Whites

Author:

McEvoy John W.12,Chen Yuan1,Halushka Marc K.3,Christenson Eric4,Ballantyne Christie M.5,Blumenthal Roger S.2,Christenson Robert H.6,Selvin Elizabeth1

Affiliation:

1. Department of Epidemiology and the Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD

2. Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins University School of Medicine, Baltimore, MD

3. Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD

4. Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD

5. Section of Cardiovascular Research, Department of Medicine, Baylor College of Medicine and Houston Methodist DeBakey Heart and Vascular Center, Houston, TX

6. Department of Pathology, University of Maryland School of Medicine, Baltimore, MD

Abstract

Background The association between galectin‐3 and heart failure ( HF ) or death is well established for white, but not for black, adults. Methods and Results Galectin‐3 was measured in 1809 participants (1375 white, 434 black), enrolled in a substudy of the Atherosclerosis Risk in Communities ( ARIC ) observational cohort during 2004–2005. We used Cox proportional hazard models to estimate the adjusted association between galectin‐3 and outcomes. Analyses were conducted overall and by race category. Median (interquartile range) galectin‐3 levels were 13.4 (11.2–16.4) and 14.8 (12–17.6) ng/mL, in white and black participants, respectively. In the sample overall, galectin‐3 was not independently associated with HF or death over a maximum of 7.9 years. However, in race‐stratified analyses, galectin‐3 was independently associated with a composite of HF or death among whites (eg, hazard ratio 2.2, 95% CI 1.2–3.9, comparing Q4 versus Q1); but not among blacks (hazard ratio of 0.8 [0.4–1.8] for Q4 versus Q1, race interaction P =0.03). Associations between galectin‐3 and both outcomes analyzed individually also demonstrated similar racial differences. Furthermore, results were qualitatively similar with galectin‐3 modeled as a continuous exposure. In addition, galectin‐3 improved discrimination for the composite of HF or death among whites (increase in Harrell's C statistic from 0.729 to 0.735 [difference of +0.006], P =0.049), but not among blacks (0.696 to 0.695 [difference of −0.001], P =0.814). Conclusions In contrast to whites, galectin‐3 may have limited prognostic utility for predicting HF and death in blacks. While our results require replication, they could reflect racial differences in the processes by which galectin‐3 mediates disease.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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