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The utility of galectin-3 for predicting cause-specific death in hospitalized patients with heart failure
Yuhui Zhang1, Rongcheng Zhang1, Tao An1
1State Key Laboratory of Cardiovascular Disease, Heart Failure Center Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Insights
This study found that higher galectin-3 levels predict death in heart failure (HF) patients. While not predicting in-hospital death alone, galectin-3 improves risk prediction for all-cause and cardiovascular death when combined with other markers.
Area of Science:
- Cardiology
- Biomarkers
- Heart Failure Research
Background:
- Galectin-3 is implicated in cardiac fibrosis and adverse events in heart failure (HF).
- The prognostic value of galectin-3 for cause-specific mortality in HF remains unclear.
- Understanding galectin-3's role is crucial for improving HF patient outcomes.
Purpose of the Study:
- To evaluate baseline galectin-3 as a predictor of all-cause, cardiovascular (CV), and in-hospital death in hospitalized HF patients.
- To assess the added prognostic value of galectin-3 beyond established risk factors.
- To explore the combined predictive utility of galectin-3 with N-terminal pro-B-type natriuretic peptide.
Main Methods:
- A cohort of 1,440 hospitalized HF patients had galectin-3 measured.
- Cox regression, discrimination, and reclassification analyses were employed.
- Median follow-up was 582 days, with 283 total deaths recorded.
Main Results:
- Elevated galectin-3 (highest 2 tertiles) significantly predicted all-cause, CV, and progressive HF death.
- Galectin-3 did not significantly predict sudden or in-hospital death alone.
- Combining elevated galectin-3 and N-terminal pro-B-type natriuretic peptide identified the highest risk for death.
Conclusions:
- Galectin-3 serves as an independent predictor of death in hospitalized HF patients.
- Galectin-3 enhances prognostic models for all-cause and CV death.
- Galectin-3's predictive power for sudden or in-hospital death is limited when used in isolation.
Objectives:
Galectin-3 has been shown to be involved in the process of cardiac fibrosis and to predict adverse events in heart failure (HF), but the association of galectin-3 with cause-specific death has not been well established. The purpose of this study was to investigate the prognostic value of baseline galectin-3 for all-cause, cardiovascular (CV), and in-hospital death in patients with HF.
Methods And Results:
From March 2009 to April 2013, we consecutively measured galectin-3 in a large cohort of 1,440 hospitalized patients with HF. Cox proportional hazards regression, discrimination, and reclassification analyses were used to evaluate the association between galectin-3 and death. During a median follow-up of 582 days, 283 deaths were identified, of which 64 were patients who died during hospitalization. Compared with the lowest galectin-3 tertile, the highest 2 tertiles were significantly associated with all-cause, CV, and progressive HF death, but not significant for sudden and in-hospital death when analyzed by multivariable Cox regression. The utility of combining galectin-3 and N-terminal pro-B-type natriuretic peptide was assessed by dichotomizing these 2 biomarkers according to their median values. The highest risk of death due to all-cause, CV, and progressive HF was observed when both biomarkers were elevated after adjustment for established risk factors. Addition of galectin-3 to the prediction model for all-cause and CV death significantly improved discrimination and reclassification.
Conclusions:
Galectin-3 independently predicted death and added additional prognostic value beyond established risk factors in hospitalized patients with HF. The utility of galectin-3 alone as a risk predictor was not strong enough to assess sudden or in-hospital death.
