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Galectin-3 and cardiac function in survivors of acute myocardial infarction
Robin A P Weir1, Colin J Petrie, C Aengus Murphy
1Cardiology Department, Hairmyres Hospital, Lanarkshire, United Kingdom. robinweir75@hotmail.com
Insights
Galectin-3, a biomarker for inflammation and fibrosis, showed a link to extracellular matrix turnover but not definitively to left ventricular remodeling after heart attack. Further research is needed to clarify its role in cardiac remodeling.
Area of Science:
- Cardiology
- Biomarker Research
- Cardiac Remodeling
Background:
- Galectin-3 is a known biomarker for inflammation and fibrosis.
- It predicts adverse outcomes in heart failure patients with preserved ejection fraction.
- Its role in left ventricular (LV) remodeling post-myocardial infarction is not well understood.
Purpose of the Study:
- To investigate the relationship between galectin-3 and LV remodeling after acute myocardial infarction.
- To explore associations between galectin-3, extracellular matrix biomarkers, and LV remodeling.
Main Methods:
- Measured circulating galectin-3 and extracellular matrix biomarkers in 100 acute myocardial infarction patients.
- Assessed LV remodeling using cardiac MRI at baseline and 24 weeks.
- Analyzed relationships across the cohort and stratified by baseline LV ejection fraction.
Main Results:
- Galectin-3 levels increased significantly over 24 weeks (P=0.007).
- Baseline galectin-3 did not correlate with LV parameters or remodeling.
- A positive association between galectin-3 and remodeling was observed in patients with higher baseline LV ejection fraction (>49.2%).
- Galectin-3 correlated with matrix metalloproteinase-3 and monocyte chemoattractant protein-1.
Conclusions:
- Galectin-3 correlated with specific extracellular matrix biomarkers.
- A definitive relationship between galectin-3 and LV remodeling was not established.
- The pathological role of galectin-3 in cardiac remodeling requires further investigation.
Background:
Galectin-3 is a biomarker associated with inflammation and fibrosis that predicts adverse outcome and relates to biomarkers of extracellular matrix turnover in patients with heart failure, particularly when left ventricular (LV) systolic function is preserved. Whether galectin-3 is related to LV remodeling after acute myocardial infarction is unknown.
Methods And Results:
Circulating galectin-3 and various extracellular matrix biomarkers were measured in 100 patients (age, 58.9±12.0 years; 77% men) admitted with acute myocardial infarction and LV dysfunction, at baseline (mean 46 hours) and at 24 weeks, with cardiac MRI at each time-point. LV remodeling was defined as change in LV end-systolic volume index. Relationships among galectin-3, biomarkers, and LV remodeling were analyzed across the entire cohort, then according to median baseline LV ejection fraction. Galectin-3 levels were elevated in 22 patients (22%) at baseline and increased significantly over time from 14.7±5.5 to 16.3±6.6 ng/mL (P=0.007). Baseline galectin-3 did not correlate with any LV parameters at baseline or change in any parameter over time. Galectin-3 was positively associated with remodeling in patients with supramedian baseline LV ejection fraction (ie, >49.2%; r=0.40; P=0.01) but not when LV ejection fraction was ≤49.2%. Galectin-3 correlated significantly with matrix metalloproteinase-3 and monocyte chemoattractant protein-1 at baseline, biomarkers that have been shown to relate to LV remodeling in this cohort.
Conclusions:
Galectin-3 correlated significantly with certain biomarkers involved in extracellular matrix turnover, although no definite relationship was identified with LV remodeling. Whether galectin-3 plays a pathological role in remodeling remains unclear but merits further study.
Clinical Trial Registration:
URL: http://www.clinicaltrials.gov. Unique identifier: NCT00132093.
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