Author + information
- Received May 23, 2018
- Revision received August 12, 2018
- Accepted September 22, 2018
- Published online December 17, 2018.
- Anahita Ghorbani, MD, MPHa,
- Vijeta Bhambhani, MS, MPHb,c,
- Robert H. Christenson, PhDd,
- Wouter C. Meijers, MDe,
- Rudolf A. de Boer, MD, PhDe,
- Daniel Levy, MDf,g,
- Martin G. Larson, ScDh,i and
- Jennifer E. Ho, MDb,c,∗ (, )@MassGeneralNews
- aCalhoun Cardiology Center, University of Connecticut Health Center, Farmington, Connecticut
- bCardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts
- cCardiology Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts
- dDepartment of Pathology, University of Maryland School of Medicine, Baltimore, Maryland
- eDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands
- fNational Heart, Lung, and Blood Institute, Boston University's Framingham Heart Study, Framingham, Massachusetts
- gPopulation Sciences Branch, Division of Intramural Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland
- hFramingham Heart Study, Framingham, Massachusetts
- iDepartment of Biostatistics, Boston University School of Public Health, Boston, Massachusetts
- ↵∗Address for correspondence:
Dr. Jennifer E. Ho, Massachusetts General Hospital, 185 Cambridge Street, CPZN #3224, Boston, Massachusetts 02114.
Background Galectin-3 (Gal-3) has been associated with heart failure (HF) and poor cardiovascular outcomes. However, the effect of longitudinal changes in Gal-3 on clinical outcomes remains unclear.
Objectives The authors sought to study clinical determinants of change in Gal-3 among community-dwelling individuals. Further, they sought to examine the role of serial Gal-3 measurements in predicting risk of future HF, cardiovascular disease (CVD), and mortality.
Methods A total of 2,477 participants in the Framingham Heart Study Offspring cohort underwent measurement of plasma Gal-3 levels at 2 examinations (1995 to 1998 and 2005 to 2008). Linear regression models were used to examine clinical correlates of change in Gal-3. Proportional hazards models were used to relate future clinical outcomes with change in Gal-3.
Results The following clinical correlates were associated with greater longitudinal increases in Gal-3 levels: age, female sex, hypertension, diabetes, body mass index, interim development of chronic kidney disease, and HF (p < 0.0001 for all in multivariable model). Change in Gal-3 was associated with future HF (hazard ratio [HR]: 1.39 per 1-SD increase; 95% confidence interval [CI]: 1.13 to 1.71), CVD (HR: 1.29; 95% CI: 1.11 to 1.51), and all-cause mortality (HR: 1.30; 95% CI: 1.17 to 1.46). Change in Gal-3 was associated with both HF with preserved as well as reduced ejection fraction (p < 0.05 for both).
Conclusions Longitudinal changes in Gal-3 are associated with traditional cardiovascular risk factors and renal disease. In turn, change in Gal-3 predicts future HF, CVD, and mortality in the community. Future studies are needed to determine whether serial Gal-3 measures may be useful in disease prevention.
The Galectin-3 assays were provided by BG Medicine. This work was partially supported by the National Heart, Lung, and Blood Institute (Framingham Heart Study, contracts N01-HC25195 and HHSN268201500001I). Dr. Christenson has received honoraria from and served as a consultant for Siemens Diagnostic, Beckman Coulter, PixCell, Quidel, Roche Diagnostics, and Becton Dickinson; and has received research support from Abbott Diagnostics, Fujirebio, BioKit, Siemens Diagnostic, Beckman Coulter, PixCell, Quidel, Roche Diagnostics, Becton Dickinson, and Mitsubishi. Dr. de Boer has served as a consultant for Mandalmed Inc.; has received speaker fees from Servier and Novartis; and has received research grants from AstraZeneca, Bristol-Myers Squibb, and Roche. Dr. Ho is supported by National Institutes of Health grants K23-HL116780, R01-HL134893, and R01-HL130224, and by a Hassenfeld Research Scholar award from Massachusetts General Hospital; and has received research supplies from EcoNugenics, Inc. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Listen to this manuscript's audio summary by Editor-in-Chief Dr. Valentin Fuster on JACC.org.
- Received May 23, 2018.
- Revision received August 12, 2018.
- Accepted September 22, 2018.
- 2018 American College of Cardiology Foundation
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