IJCS | Volume 32, Nº2, March/April 2019

155 Table 2 - Comparison between patients with hypertrophic cardiomyopathy with and without myocardial fibrosis With fibrosis (n = 42) Without fibrosis (n = 8) p Age, years, mean ± SD 44 ± 14 42 ± 14 0.85 Gender [M/F], n 33/9 3/5 0.65 Echocardiogram - mm, mean ± sd Septal thickness 21.7 ± 5.4 21.6 ± 4.3 0.91 Posterior wall thickness 11.7 ± 3.0 11.6 ± 2.1 0.94 Left atrial diameter 43. 0 ± 6.5 44.1 ± 6.9 0.70 LV diastolic diameter 43.5 ± 6.1 44.2 ± 2.9 0.82 Ejection fraction,% 66.5 ± 9.0 66.2 ± 3.7 0.94 Gal-3, mean ± SD, ng/dL 10.3 ± 3.4 10.1 ± 2.1 0.59 Minimum - maximum 6.3 - 17.6 8.0 - 12.8 Antunes et al. Galectin-3, myocardial fibrosis and hypertrophic cardiomyopathy Int J Cardiovasc Sci. 2019;32(2)152-157 Original Article synthesis mechanism is known: the reactive pathway, in which fibrosis formation would be secondary to the neurohumoral activationwithout cardiomyocyte necrosis, with the following cellular mediators: angiotensin II, aldosterone and endothelin-1. 17-19 In patients with HCM, cardiac fibrosis is associated with adverse left ventricular remodeling, arrhythmias and worse prognosis. Currently, it is not known what factors decisively contribute to accelerate collagen deposition between the hypertrophiedmyocardial fibers in patients with HCM, and different causal mutations are thought to play an important role, as well as other genetic polymorphisms and environmental factors. 20-22 Kim et al., 23 demonstrated in an experimental study that myocardial fibrosis occurs independently of cell damage and inflammation in this heart disease. When analyzing the hearts of transgenic mice with a cardiac beta-myosin mutation, in which hypertrophy had not yet developed, they reported the early activation of potent fibrosis regulatory pathways and collagen deposition, despite normal cardiac histological findings, demonstrating the existence of a pro-fibrotic environment even before the disease onset. 23 Thus, they corroborate our results, with low serum concentrations of Gal-3 and absence of an association with myocardial fibrosis. The study by Hu et al., 24 aimed to determine the prognosis of myocardial fibrosis associated with Gal-3 levels in patients with non-ischemic cardiomyopathy. The sample consisted of 105 patients with HCM, with an older mean age than that in our study, 52 ± 15 years, and they identified that the association of Gal-3 with fibrosis showed a more significant prognostic value. However, when evaluating serum levels of Gal-3 in patients with HCM with and without fibrosis, they also did not find any significant differences. 24 The findings of the present study contribute to the knowledge of the mechanisms involved in myocardial fibrosis formation in HCM, guiding future lines of research aimed at studying the formation of fibrosis and ventricular remodeling and modifying the natural history of the disease. Conclusion In patientswithHCM, the serumconcentration of Gal-3 is lowand is not associatedwith the presence ofmyocardial fibrosis, suggesting that the reparative pathway of fibrosis formation is little activated in this cardiopathy. Limitations Some limitations should be considered in the study, such as the relatively small number of patients, its cross-sectional design, which did not allow us to establish the prognostic value of the variables, and the evaluation of myocardial fibrosis, which was not quantitatively performed, making it impossible to calculate the correlation of myocardial fibrosis extension with Gal-3 concentrations.