IJCS | Volume 32, Nº2, March/April 2019

154 Table 1 - Comparison between the hypertrophic cardiomyopathy and controls groups HCM (n = 50) Controls (n = 50) p Age, years, mean ± SD 43 ± 14 39 ± 10 0.09 Gender [M/F], n 36/14 35/15 0.41 Gal-3, mean ± SDP, ng/dL 10.3 ± 3.1 11.3 ± 2.6 0.42 Minimum - maximum 6.3 - 17.6 5.2 - 15.9 Percentile 25 8.7 9.3 50 10.4 11.4 75 12.8 13.2 HCM: hypertrophic cardiomyopathy. Figure 1 - Distribution of serum Gal-3 levels in patients with HCM and control subjects. The chart shows the medians (horizontal bars), the 25 th and 75 th percentiles (lower and upper limits of the boxes) and the lower and upper absolute values (error bars) Galectin-3 (ng/dL) HCM Controls Antunes et al. Galectin-3, myocardial fibrosis and hypertrophic cardiomyopathy Int J Cardiovasc Sci. 2019;32(2)152-157 Original Article gender (Table 1). The values found for serum Gal-3 measurements were low and showed no statistical differences between the two groups, HCM versus control, 10.3 ± 3.1 and 11.3 ± 2.6, p = 0.12 (Figure 1 ). The patients with HCM were 72% males, with a mean age of 44 ± 12 years. All of them had preserved LVEF, mean septal thickness of 21.7 ± 5.2 mm and 29% had left ventricular outflow gradient > 30 mmHg at rest. Myocardial fibrosis was identified in 84% of these patients, and Gal-3 levels did not show any differences between the groups with present and absent myocardial fibrosis, 10.3 ± 3.4 and 10.1 ± 2.1, p = 0.59 (Table 2). Discussion In the present study, serum Gal-3 levels were low and did not show any differences between patients with HCM and the control group. Myocardial fibrosis was a common finding, present in 84% of HCM patients, but Gal-3 values ​also showed no differences between patients with and without fibrosis. Therefore, our findings suggest that other non-inflammatory mechanisms of myocardial structural remodeling are involved in the pathophysiology of fibrosis in this cardiopathy. Galectin-3 is expressed by activated monocytes/ macrophages and is involved in the regulation of inflammatory processes and pro-fibrotic pathways, acting as myocardial fibrosis mediator under conditions where necrosis and/or cellular apoptosis and consequent inflammatory reactions occur, described as a pathway of reparative fibrosis. 12,16 However, another collagen