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Galectin-3: A Link between Myocardial and Arterial Stiffening in Patients with Acute Decompensated Heart Failure?
Radu Ioan Lala1, Dan Darabantiu1, Luminita Pilat1
1Vasile Goldis West University Arad, Romania.
Insights
High galectin-3 levels in heart failure patients did not correlate with arterial stiffness but predicted impaired ventricular-arterial coupling and poorer outcomes. This biomarker may indicate increased pulmonary artery pressures.
Area of Science:
- Cardiology
- Biomarkers
- Vascular Physiology
Background:
- Heart failure is linked to abnormal ventricular-vascular interaction, increased myocardial and arterial stiffness.
- Galectin-3, a biomarker, is implicated in myocardial and vascular fibrosis, contributing to heart failure progression.
Purpose of the Study:
- To investigate the correlation between galectin-3 levels and arterial stiffening markers.
- To assess the relationship between galectin-3 and impaired ventricular-arterial coupling in decompensated heart failure.
Main Methods:
- Evaluated 79 inpatients with acute decompensated heart failure.
- Measured serum galectin-3, performed echocardiography, and Doppler ultrasonography for vascular indices.
Main Results:
- No correlation found between galectin-3 and arterial stiffening markers (pulse wave velocity, carotid distensibility, Young's modulus).
- Elevated galectin-3 correlated with impaired ventricular-arterial coupling (Ea/Elv ratio) and lower rates of left ventricular pressure rise.
- High galectin-3 and pulmonary artery pressure were independent risk factors for mortality and readmissions.
Conclusions:
- Serum galectin-3 levels do not correlate with arterial stiffening in heart failure.
- High galectin-3 levels predict impaired ventricular-arterial coupling and may indicate elevated pulmonary artery pressures.
- Elevated galectin-3, along with pulmonary hypertension, are independent predictors of adverse outcomes in heart failure.
Background:
Heart failure is accompanied by abnormalities in ventricular-vascular interaction due to increased myocardial and arterial stiffness. Galectin-3 is a recently discovered biomarker that plays an important role in myocardial and vascular fibrosis and heart failure progression.
Objectives:
The aim of this study was to determine whether galectin-3 is correlated with arterial stiffening markers and impaired ventricular-arterial coupling in decompensated heart failure patients.
Methods:
A total of 79 inpatients with acute decompensated heart failure were evaluated. Serum galectin-3 was determined at baseline, and during admission, transthoracic echocardiography and measurements of vascular indices by Doppler ultrasonography were performed.
Results:
Elevated pulse wave velocity and low arterial carotid distensibility are associated with heart failure in patients with preserved ejection fraction (p = 0.04, p = 0.009). Pulse wave velocity, carotid distensibility and Young's modulus did not correlate with serum galectin-3 levels. Conversely, raised galectin-3 levels correlated with an increased ventricular-arterial coupling ratio (Ea/Elv) p = 0.047, OR = 1.9, 95% CI (1.0‑3.6). Increased galectin-3 levels were associated with lower rates of left ventricular pressure rise in early systole (dp/dt) (p=0.018) and raised pulmonary artery pressure (p = 0.046). High galectin-3 levels (p = 0.038, HR = 3.07) and arterial pulmonary pressure (p = 0.007, HR = 1.06) were found to be independent risk factors for all-cause mortality and readmissions.
Conclusions:
This study showed no significant correlation between serum galectin-3 levels and arterial stiffening markers. Instead, high galectin-3 levels predicted impaired ventricular-arterial coupling. Galectin-3 may be predictive of raised pulmonary artery pressures. Elevated galectin-3 levels correlate with severe systolic dysfunction and together with pulmonary hypertension are independent markers of outcome.
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