IJCS | Volume 32, Nº2, March/April 2019

DOI: 10.5935/2359-4802.20180102 152 ORIGINAL ARTICLE International Journal of Cardiovascular Sciences. 2019;32(2)152-157 Mailing Address: Murillo de Oliveira Antunes Rua Sibipirunas, 100. Postal Code: 12916-425, Bragança Paulista, São Paulo, SP - Brazil. E-mail: dr.murilloantunes@gmail.com , murillo_antunes@terra.com.br Evaluation of Galectin-3 and Myocardial Fibrosis in Patients with Hypertrophic Cardiomyopathy Murillo de Oliveira Antunes, 1 E dmundo Arteaga-Fernández, 1 F abio Fernandes, 1 C arla David Soffiatti, 1 P aula de Cássia Buck, 1 E ster Cerdeira Sabino, 2 C arlos Henrique Valente Moreira, 2 C harles Mady 1 Instituto do Coração (InCor) do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, 1 São Paulo, SP - Brazil Instituto de Medicina Tropical da Faculdade de Medicina da USP (FMUSP), 2 São Paulo, SP - Brazil Manuscript received September 19, 2017; revised manuscript March 23, 2018; accepted July 02, 2018. Abstract Background: Galectin-3 is the designation given to the protein that binds to ß -galactosides, expressed by activated macrophages and described as a cardiac fibrosis mediator. In hypertrophic cardiomyopathy (HCM), myocardial fibrosis is an independent predictor of adverse outcome; however, the association between Galectin-3 and myocardial fibrosis has not been studied in this cardiopathy. Objective: To evaluate the association of Galectin-3 and the presence of myocardial fibrosis in a patient with hypertrophic cardiomyopathy. Methods: Galectin-3 was measured in automated equipment using the Elisa technique in 100 participants divided into two groups: 50 patients with hypertrophic cardiomyopathy and 50 healthy control subjects. All patients with hypertrophic cardiomyopathy underwent magnetic nuclear resonance with the late enhancement technique to investigate myocardial fibrosis. For the statistical analysis, p values < 0.05 were considered statistically significant. Results: Galectin-3 levels were low and did not show significant differences between patients with hypertrophic cardiomyopathy and the control group, 10.3 ± 3.1 ng/dL and 11.3 ± 2.6 ng/dL (p = 0.12) respectively. Myocardial fibrosis was a common finding and was identified in 84% (42/50) of patients with HCM, but no differences were observed between Galectin-3 levels when comparing patients with and without fibrosis, 10.3 ± 2.4 ng/dL and 10.1 ± 2.1 ng/dL (p = 0.59). Conclusion: The results did not show an association between Galectin-3 and myocardial fibrosis in patients with hypertrophic cardiomyopathy, suggesting that non-inflammatory mechanisms of myocardial fibrosis formation and cardiac remodeling are involved in this cardiopathy. (Int J Cardiovasc Sci. 2019;32(2)152-157) Keywords: Cardiomyopathy, Hypertrophic; Endomyocardial Fibrosis; Galectin 3; Diagnostic Imaging; Arrhythmias, Cardiac. Introduction Hypertrophic cardiomyopathy (HCM) is defined by the presence of ventricular hypertrophy in the absence of cardiac or systemic diseases that justify the development of this muscular alteration. 1 It is the most common cardiopathy with a genetic cause, with an estimated prevalence of 0.2% (1:500). 2,3 Histologically, in addition to the hypertrophy and myocyte architecture disarray, varied increase in interstitial collagen and myocardial fibrosis occurs. 4 Recent studies showed that fibrosis presence and extent are an independent predictor for the occurrence of sudden cardiac death (SCD) and progression to heart failure (HF) in these individuals. 5-9 Currently, Galectin-3 (Gal-3), a protein of the lectin family, has emerged as a new biomarker associated with myocardial fibrosis in acute and chronic heart failure (HF). 10,11 In the presence of inflammation, Gal-3 is secreted by activatedmacrophages, having the cardiac fibroblasts as binding sites, resulting in increased