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Galectin-3 level and the severity of cardiac diastolic dysfunction using cellular and animal models and clinical
Cho-Kai Wu1,2, Mao-Yuan Su3, Jen-Kuang Lee1
1Division of Cardiology, Department of Internal Medicine, National Taiwan University College of Medicine and Hospital, Taipei, Taiwan.
Insights
Plasma and myocardial Galectin-3 levels correlate with the severity of diastolic dysfunction in heart failure with preserved ejection fraction (HFPEF). This finding highlights Galectin-3 as a potential biomarker for HFPEF progression.
Area of Science:
- Cardiology
- Biomarkers
- Pathophysiology
Background:
- Heart failure with preserved ejection fraction (HFPEF) is a complex condition characterized by myocardial interstitial fibrosis and diastolic dysfunction.
- Current diagnostic and prognostic markers for HFPEF are limited, necessitating the identification of novel biomarkers.
Purpose of the Study:
- To investigate the association between Galectin-3 levels and the severity of diastolic dysfunction in patients with HFPEF.
- To explore the role of Galectin-3 in a canine model of HFPEF and in a cellular model of mechanical stretch.
Main Methods:
- Recruited 146 patients with HFPEF, assessing severity using Doppler imaging (E/Em) and cardiac magnetic resonance imaging (CMRI).
- Induced HFPEF in canine models via aortic banding, collecting hemodynamic and echocardiographic data.
- Utilized cultured cardiomyocytes subjected to mechanical stretch as a cellular model.
- Measured plasma and myocardial Galectin-3 levels and correlated them with diastolic dysfunction parameters and fibrosis.
Main Results:
- Patients with severe HFPEF exhibited significantly higher plasma Galectin-3 levels.
- A significant correlation was observed between plasma Galectin-3 and E/Em in advanced HFPEF patients.
- In canine models, myocardial Galectin-3 expression increased with pressure overload and correlated with diastolic dysfunction severity and fibrosis.
- Mechanical stretch of cardiomyocytes increased Galectin-3 secretion, and Galectin-3 levels remained associated with diastolic parameters in humans and canines after adjusting for confounders.
Conclusions:
- Both plasma and myocardial Galectin-3 levels are significantly correlated with the severity of cardiac diastolic dysfunction in HFPEF.
- Galectin-3 emerges as a potential biomarker for assessing diastolic dysfunction and disease severity in HFPEF.
- These findings support the role of Galectin-3 in the pathophysiology of HFPEF-related diastolic dysfunction.
Abstract:
Heart failure with preserved ejection fraction (HFPEF) is characterized by myocardial interstitial fibrosis. A total of 146 patients with HFPEF, were recruited. HFPEF severity was determined using Doppler imaging (E/Em) and also cardiac magnetic resonance imaging (CMRI). Canine modeling of HFPEF was induced by aortic banding. Hemodynamic and echocardiographic data were obtained before and after pressure loading and myocardial Galectin-3 was determined. Mechanical stretch of cultured cardiomyocytes served as the cellular model of HFPEF. Patients with severe HFPEF had significantly higher plasma Galectin-3 levels. Significant correlation between plasma Galectin-3 and E/Em in advanced HFPEF patients was noted. After 2 weeks of pressure overload in canine models, the protein expression of Galectin-3 from LV myocardial tissue was significantly increased (p < 0.01) compared with controls. Galectin-3 expression paralleled the severity of LV diastolic dysfunction by evaluation of CMRI (r = -0.58, p = 0.003) and tissue fibrosis (r = 0.59, p = 0.002). After adjusting for confounders for diastolic dysfunction, Galectin-3 levels were still associated with diastolic parameters both in humans (p < 0.001) and canine model (p = 0.041). Mechanical stretch increased Galectin-3 secretion in cultured cardiomyocytes. Both plasma and myocardial Galectin-3 levels correlated with severity of cardiac diastolic dysfunction.
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