Research Article Open Access Open Access Research Article Hypertension: Open Access ISSN: 2167-1095 J o u r n a l o f H y p e r t e n s i o n : O p e n A c c e s s Deveci, et al., J Hypertens 2015, 4:1 http://dx.doi.org/10.4172/2167-1095.1000195 Volume 4 • Issue 1 • 1000195 J Hypertens ISSN: 2167-1095 JHOA an open access journal A Novel BioTarget in Treatment of Heart Failure: Changes in Serum Galectin-3 Levels after Spironolactone Therapy Onur Sinan Deveci 1 *, Aziz İnan Çelik 1 , Müslüm Fırat İkikardeş 1 , Çağlar Emre Çağlıyan 1 , Çağlar Özmen 1 , Ali Deniz 1 , Rabia Eker Akıllı 1 , Filiz Kibar 2 , Salih Çetiner 3 , Mesut Demir 1 , Mehmet Kanadaşı 1 and Mustafa Demirtaş 1 1 Department of Cardiology, Çukurova University Faculty of Medicine, Balcalı Hospital, Adana, Turkey 2 Department of Biochemistry, Çukurova University Faculty of Medicine, Balcalı Hospital, Adana, Turkey 3 Department of Microbiology, Çukurova University Faculty of Medicine, Balcalı Hospital, Adana, Turkey Keywords: Galectin 3; Myocardial and vascular ibrosis; Let ventricular ejection; MRAs Introductıon Heart failure (HF) is the leading cause of mortality and morbidity in the western World [1]. Searching for therapeutics to cure HF has led studies to invastigate the mechanisms particularly on neurohumoral activation [2]. During HF, increased levels of catecholamines resulting from activation of sympathetic nervous system lead to chronic stimulation of aldosterone levels causing adverse remodelling of the heart [3]. Aldosterone is a mineralocorticoid hormone hat has been shown to play a pathophysiologic role in cardiovascular remodelling through cardiac hypertrophy, ibrosis and inlmmation [4,5]. Galectin 3 (Gal-3) is a multifunctional protein that participate in various biological events such as angiogenesis and inlammation and an important member of the family of beta-galactoside-binding animal lectins mostly produced by macrophages. he current studies indicate Gal-3 as a novel prognostic marker for cardiac ibrosis associated with high risk for heart failure and mortality. hus, elevated levels of Gal-3 are associated with cardiac ibrosis [6]. It has been demonstrated that GAL-3 expression is stimulated by aldosterone and stimulated GAL-3 plays a critical role in vascular remodelling and inlammation [7]. Use of mineralocorticoid receptor antagonists (MRAs) has provided 35% reductions in hospital admissions due to worsening heart failure by decreasing myocardial and vascular ibrosis [8]. Adding spironolactone to treatment in the patients who use angiotensin converting enzyme inhibitor provided a reduction in morbidity and mortality rates [9,10]. Data substantiating the hypothesis that decreased levels of GAL-3 ater MRAs theraphy may result beneicial outcomes remain unclear. To address this question, it has been aimed to investigate the GAL-3 *Corresponding author: Onur Sinan Deveci, Çukurova University Faculty of Medicine, Department of Cardiology, Balcalı Hospital, Adana, Turkey, Tel: 505 764 7967; E-mail: onurdeveci@yahoo.co.uk Received December 17, 2014; Accepted December 27, 2014; Published January 05, 2015 Citation: Deveci OS, Çelik Aİ, İkikardeş MF, Çağlıyan CE, Özmen C (2015) A Novel BioTarget in Treatment of Heart Failure:Changes in Serum Galectin-3 Levels after Spironolactone Therapy. J Hypertens 4: 195. doi:10.4172/2167-1095.1000195 Copyright: © 2015 Deveci OS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. levels and clinical responses ater addition of spironolactone as a MRA to the current treatment in patients with heart failure with low ejection fraction who received no aldosterone antagonist therapy previously. Methods Study population he study was carried out in the hospital of Çukurova University Faculty of Medicine between April 2013 and March 2014. Our study included 112 patients with heart failure who showed let ventricular ejection fraction (EF) of 35% or below, New York Heart Association (NYHA) Class II-IV symptoms and did not receive MRAs in their current treatment. he patients with creatinine clearance (CrCl) of 60 ml/minute or below (according to Cockrot), advanced stages of liver failure (ALT and AST levels 3-fold higher than upper limit of normal interval), NYHA Class I symptoms, an ejection fraction above 35% and autoimmune and/or collagen tissue disorder were excluded from the study. he study aimed to evaluate serum Gal-3 levels ater the use of spironolactone. herefore, serum Gal-3 levels, serum BNP level, 6-minute walk test and class level of NYHA were examined before Abstract Objectıve: It has been aimed to investigate the Galectin-3 (GAL-3) levels and clinical responses after addition of spironolactone as a mineralocorticoid receptor antagonist (MRA) to the current treatment in patients with heart failure with low ejection fraction who received no aldosterone antagonist therapy previously. Patıents and methods: The study included 112 patients with Heart Failure (HF) who showed left ventricular Ejection Fraction (EF) of 35% or below, New York Heart Association (NYHA) Class II-IV symptoms and did not receive MRAs in their current treatment. Serum Gal-3 levels, serum BNP level, 6-minute walk test and class level of NYHA were examined before and 6 months after treatment of spironolactone in all patients. Results: Mortality developed in 10 of 112 patients. Baseline and 6th month follow-up data obtained from 102 of 112 patients. Mean LVEF (%), BNP levels, Gal-3 levels, NYHA class of functional capacity and mean 6-minute walking test distance of the patients before treatment of spironolactone were 31.3 ± 3.2%, 451,4 ± 50.3 pg/ml, 39 ± 21 ng/ml, 2,8 ± 0.59 and 305 ± 61 m respectively whereas, the same variables were found 32.1 ± 2,8% (p=0.21), 443.6 ± 49 pg/ml (p=0.23), 33 ± 22 ng/ml (p=<0.001), 2,5 ± 0.47 (p=0.037) and 386 ± 87 m (p=<0.001) respectively at 6th follow-up after treatment of spironolactone. Conclusıon: Spironolactone use is associated with regression of Gal-3 along with clinical improvement in HF symptoms. This may suggest that Gal-3 apart from being a biomarker of HF may also be a bio-target in HF management.