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Objective: Keshan disease (KD) is a fatal endemic dilated cardiomyopathy with unclear etiology and pathogenesis, and a high mortality in China. Pathologic studies confirmed that different degree of myocardial fibrosis existed in various types of KD. Myocardial fibrosis is an important contributor to the pathophysiology of left ventricular remodeling. Recently, galectin-3 (Gal-3) as a marker of cardiac fibrosis and heart failure was approved by the US FDA. The aim of this study was to evaluate the changes of serum level of Gal-3 in chronic KD (CKD) and their clinical implications. Methods: The levels of serum Gal-3 were measured by using enzyme-linked immunosorbent assay (ELISA) in 37 CKD patients and 32 healthy controls. Echocardiography was used to determine parameter of left ventricular ejection fraction (LVEF) and left ventricular end-diastolic dimension (LVEDD). Results: The serum concentration of Gal-3 ([95.81±18.99] ng/ml versus [48.16±11.09] ng/ml, t=6.906, P<0.001) and LVEDD ([60.46±7.63] mm versus (42.69±10.66) mm, t=3.61, P<0.01) were significantly higher, while LVEF ([42.69±10.66]% versus [62.16±6.38]%, t=4.679, P<0.01) were significantly lower in CKD patients compared with healthy controls. A negative correlation was found between elevated Gal-3 and lower LVEF (r=-0.882, P<0.001) and a positive correlation was found between elevated Gal-3 levels and enlarged LVEDD (r=0.834, P<0.001) or higher NYHA class (r=0.854, P<0.01) in CKD patients. Conclusion: Serum concentration of Gal-3 is strongly correlated with poorer left ventricular systolic function, enlarged LVEDD and higher New York Heart Association (NYHA) class, which may provide indirectly diagnostic information on myocardial fibrosis and heart function in CKD patients.
Objective: Keshan disease (KD) is a fatal endemic dilated cardiomyopathy with unclear etiology and pathogenesis, and a high mortality in China. Pathologic studies that different degree of myocardial fibrosis existed in various types of KD. Myocardial fibrosis is an important contributor to the pathophysiology of left ventricular remodeling. Recently, galectin-3 (Gal-3) as a marker of cardiac fibrosis and heart failure was approved by the US FDA. The aim of this study was to evaluate the changes of serum level of Gal-3 in Methods: The levels of serum Gal-3 were measured by using enzyme-linked immunosorbent assay (ELISA) in 37 CKD patients and 32 healthy controls. Echocardiography was used to determine parameter of left ventricular ejection fraction (LVEF) and left ventricular end-diastolic dimension (LVEDD). Results: The serum concentration of Gal-3 ([95.81 ± 18.99] ng / ml versus [48.16 ± 11.09] ) and LVEDD ([42.69 ± 10.66]% versus [62.16 ± 6.38]%, t = 4.679, P <0.01) 0.01) were significantly lower in CKD patients compared with healthy controls. A negative correlation was found between elevated Gal-3 and lower LVEF (r = -0.882, P <0.001) and a positive correlation was found between elevated Gal-3 levels and enlarged LVEDD (r = 0.834, P <0.001) or higher NYHA class (r = 0.854, P <0.01) in CKD patients. Conclusion: Serum concentration of Gal-3 is strongly correlated with poorer left ventricular systolic function, York Heart Association (NYHA) class, which may provide indirectly diagnostic information on myocardial fibrosis and heart function in CKD patients.