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Are Plasma ST2 and Galectin-3 Predictors for Clinical Outcomes After Myectomy in Patients With Obstructive Hypertrophic Cardiomyopathy?
Author(s) -
Huang Xiao-hong
Publication year - 2020
Publication title -
journal of human physiology
Language(s) - English
Resource type - Journals
ISSN - 2691-5391
DOI - 10.31829/2691-5391/jhp2020-3(1)-104
Subject(s) - heart failure , ejection fraction , medicine , cardiology , galectin 3 , fibrosis , hypertrophic cardiomyopathy , inflammation , gdf15 , pathological
ST2 is a member of the interleukin-1 receptor family, which is expressed in a trans membrane form (ST2L) as well as in a soluble secreted form [1]. Recently, soluble ST2(sST2) was found to be elevated in patients with chronic heart failure with reduced ejection fraction (HFrEF) and regarded as a promising novel biomarkers that can improve risk stratification [2, 3]. In 2012, Broch K et al. showed that baseline sST2 was associated with death due to worsening heart failure (HF), hospitalization due to worsening HF, and all cardiovascular hospitalization in older patients with ischemic HF[4]. In a multicenter study enrolled 447 patients with acutely decompensated heart failure, sST2 was an independent predictor of mortality for 1 year follow-up, regardless of the left ventricular ejection fraction[5]. As a β-galactoside-binding lectin secreted by activated macrophages, galectin-3 (Gal-3) exists in the cytoplasm and in a secreted form, and is involved in several physiological and pathological processes that contribute to HF, including myocardial fibrosis, inflammation and cardiac remodeling [6-8]. Sub study of RELAX trial suggested that Gal-3 levels were associated with severity of renal dysfunction. De Boer et al. found that Gal-3 is an independent marker for composite end of all-cause mortality and HF hospitalization in HF and appears to be more powerful in patients with heart failure with preserved ejection fraction (HFpEF)[9]. According to results from the Aldo-DHF trial, plasma Gal-3 in HFpEF was associated with adverse outcome, independent of treatment or NT-proBNP [10].

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