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Galectin-3 and the development of heart failure after acute coronary syndrome: pilot experience from PROVE IT-TIMI 22
E Wilson Grandin1, Petr Jarolim, Sabina A Murphy
1TIMI Study Group, Department of Mediicne, Brigham and Women's Hospital, Boston, MA 02115, USA. wgrandin1@partners.org
Insights
Elevated galectin-3 levels after acute coronary syndrome (ACS) predict the development of heart failure (HF). This biomarker is associated with adverse cardiac remodeling and may represent a therapeutic target for post-ACS HF.
Area of Science:
- Cardiology
- Biomarker Research
- Translational Medicine
Background:
- Galectin-3 is a lectin implicated in cardiac fibrosis and remodeling.
- Elevated galectin-3 is observed in heart failure (HF) and has prognostic value.
- The role of galectin-3 in HF development post-acute coronary syndrome (ACS) is not well understood.
Purpose of the Study:
- To investigate the association between baseline serum galectin-3 levels and the incidence of new or worsening HF after ACS.
- To determine if galectin-3 can serve as a predictive biomarker for HF development in ACS patients.
Main Methods:
- A nested case-control study was conducted using data from the PROVE IT-TIMI 22 trial.
- 100 ACS patients who were hospitalized for HF (cases) were matched with controls.
- Serum galectin-3 was measured at baseline (within 7 days post-ACS).
Main Results:
- Patients who developed HF had significantly higher baseline galectin-3 levels compared to controls.
- Higher galectin-3 levels were associated with an increased odds ratio for developing HF post-ACS.
- A graded relationship was observed between galectin-3 levels and HF risk, which remained significant after adjusting for clinical factors.
Conclusions:
- Baseline galectin-3 is associated with an increased risk of developing HF following ACS.
- These findings support galectin-3 as a biomarker for adverse cardiac remodeling and a potential therapeutic target in the context of post-ACS HF.
Background:
Galectin-3 is a β-galactoside-binding lectin that has been implicated in cardiac fibrosis and remodeling, is increased in models of failure-prone hearts, and has prognostic value in patients with heart failure (HF). The relationship between galectin-3 and the development of HF after acute coronary syndrome (ACS) is unknown.
Methods:
In a nested case-control study among patients with ACS in PROVE IT-TIMI 22, we identified 100 cases with a hospitalization for new or worsening HF. Controls were matched (1:1) for age, sex, ACS type, and randomized treatment. Serum galectin-3 was measured at baseline (within 7 days post-ACS).
Results:
Patients who developed HF had higher baseline galectin-3 [median 16.7 μg/L (25th, 75th percentile 14.0, 20.6) vs 14.6 μg/L (12.0, 17.6), P=0.004]. Patients with baseline galectin-3 above the median had an odds ratio of 2.1 (95% CI 1.2-3.6) for developing HF, P=0.010. Galectin-3 showed a graded relationship with risk of HF. Cases were more likely to have hypertension, diabetes, prior MI, and prior HF; after adjustment for these factors, this graded relationship with galectin-3 quartile and HF remained significant [adjusted OR 1.4 (95% CI 1.1-1.9), P=0.020]. When BNP was added to the model, the relationship between galectin-3 and HF was attenuated [adjusted OR 1.3 (95% CI: 0.96-1.9), P=0.08].
Conclusions:
The finding that galectin-3 is associated with the risk of developing HF following ACS adds to emerging evidence supporting galectin-3 as a biomarker of adverse remodeling contributing to HF as well as a potential therapeutic target.
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