Abstract

Abstract Funding Acknowledgements Type of funding sources: None. Background In systemic sclerosis (SSc) myocardial fibrosis contributes to the impairment of the myocardial function resulting in manifest diastolic and subclinical systolic dysfunction of the left ventricle (LV) and impaired left atrial (LA) function. The pathophysiology of this connective tissue disease is still not fully elucidated. Recently, however, elevated serum levels of galectin-3 and soluble suppression of tumorigenicity 2 (sST2) have been reported in SSc patients suggesting that these fibrotic markers may participate in the fibrotic process in this disease. Thus we aimed to investigate the potential associations between galectin-3 and sST2 levels and the echocardiographic markers of the LV and LA function in SSc patients. Methods Forty patients (57.3 ± 13.7 years, 36 female) were enrolled into the study. In addition to the conventional echocardiography, tissue Doppler and speckle-tracking-derived strain techniques were used to estimate the LV systolic and diastolic function as well as the LA size and function. To assess the correlations between galectin-3 and sST2 levels and the echocardiographic variables, partial correlation method was used with age as correcting factor. Results In age adjusted analysis galectin-3 level showed significant correlation with LV global longitudinal strain (r = 0.460, p = 0.005); grade of LV diastolic dysfunction (r = 0.394, p = 0.013); septal e’ (r=-0.369, p = 0.021); septal E/e’ (r = 0.380, p = 0.017) and with the grade of mitral regurgitation (r = 0.323, p = 0.048) (Figure 1). No significant correlation was found between sST2 levels and the echocardiographic variables. Conclusions Galectin-3 levels, but not sST2 levels show significant correlation with the parameters of the LV diastolic function and with LV global longitudinal strain, a parameter reflecting the subclinical impairment of the LV systolic function. Galectin-3 may be a useful biomarker for identifying SSc patients with high risk for cardiac involvement. Abstract Figure 1

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