ABC | Volume 114, Nº4, April 2020

Original Article Galectin-3 Levels in Patients with Chronic Constrictive Pericarditis Fábio Fernandes, 1, 2 Dirceu Thiago Pessoa de Melo, 1 Felix José Alvarez Ramires, 1,2 Ester Cerdeira Sabino, 3 Carlos Henrique Valente Moreira, 4 L uiz Alberto Benvenutti, 1,2 Viviane Tiemi Hotta, 1, 2 A na Luiza Carrari Sayegh, 2 F rancis Ribeiro de Souza, 2 Ricardo Ribeiro Dias, 1,2 Charles Mady 1,2 Instituto do Coração HC-FMUSP - Unidade Clínica de Miocardiopatias e Doenças da Aorta, 1 São Paulo, SP – Brazil Universidade de São Paulo Faculdade de Medicina Hospital das Clínicas Instituto do Coração, 2 São Paulo, SP – Brazil Universidade de São Paulo - Instituto de Medicina Tropical de São Paulo São Paulo, 3 São Paulo, SP – Brazil Emilio Ribas Institute for Infectious Diseases, 4 São Paulo, SP – Brazil Mailing Address: Dirceu Thiago Pessoa de Melo • Universidade de São Paulo Faculdade de Medicina Hospital das Clínicas Instituto do Coração - Dr. Eneas de Carvalho Aguiar, 44. Postal Code 05403‑000, São Paulo, SP – Brazil E-mail: dirceumelo@yahoo.com.br Manuscript received March 01, 2019, revised manuscript June 11, 2019, accepted June 23, 2019 DOI: https://doi.org/10.36660/abc.20190152 Abstract Background: Galectin-3 (Gal-3) is a proinflammatory, profibrotic molecule implicated in the pathogenesis of heart failure. The role of Gal-3 in patients with chronic constrictive pericarditis (CCP) is not clear. Objective: The aim of this study was to assess plasma Gal-3 in patients with CCP and correlate it with clinical, functional and histologic parameters. Methods: We prospectively evaluated 25 symptomatic patients with CCP referred for pericardiectomy and 21 healthy controls. Patients underwent clinical assessment, Gal-3 and B-type natriuretic peptide (BNP) measurements, echocardiography, cardiac magnetic resonance imaging and cardiopulmonary exercise test (CPET) at baseline. Six months after pericardiectomy CPET was repeated. An alpha error < 5% was considered statistically significant, with a confidence interval of 95%. Results: Twenty-five patients with a median age of 45 years were included. Etiology was mainly idiopathic (n = 19, 76%); and 14 (56%) patients had NYHA functional class III/IV. Median BNP and Gal-3 were 143 (89-209) pg/dL and 14.8 (9.7‑17.2) ng/mL, respectively. Gal-3 levels were not significantly higher in CCP patients than in control (p = 0.22). There were no significant correlations of Gal-3 with BNP, echocardiographic and cardiac magnetic resonance measures and histological findings. After pericardiectomy, it was found a statistically significant correlation between Gal-3 and the CPTE measures test duration (r = –0.79; p < 0.001) and exercise time (r = –0.79; p < 0.001). Conclusions: Patients with CCP had normal levels of Gal-3 as compared to the controls. Gal-3 did not correlate with morphological and functional measures before pericardiectomy. However, the associations between Gal-3 and exercise intolerance after pericardiectomy may suggest a role of Gal-3 in prognosis prediction after pericardiectomy. (Arq Bras Cardiol. 2020; 114(4):683-689) Keywords: Pericardite Constrictive/surgery; Galectin 3; Cell Diferentiation; Pericardiectomy/methods; Fibrosis. Introduction Patients with chronic constrictive pericarditis (CCP) have pericardial thickness that leads to restriction of diastolic filling of the ventricles. Clinical presentation of CCP is usually indolent and nonspecific in the early stages. Symptoms are attributable to biventricular diastolic dysfunction and include fatigue and decreased exercise tolerance. 1 The progression of pericardial inflammation is a continuous event. Pericardial constriction after acute pericarditis seems to be related to fibroblast proliferation and fibrinous exudate, resulting in a thickened and inelastic pericardium. 2 However, the mechanisms underlying pericardial fibrosis and calcification in CCP remain poorly understood. Galectin-3 (Gal-3), a beta-galactosidase binding lectin, is secreted by activated macrophages and is involved in the fibrogenesis process. Gal-3 is also a strong proinflammatory mediator. 3,4 Limited data are available on galectin levels in patients with pericardial disease. In a pilot study, Ntsekhe et al. 5 studied patients with normal pericardium and patients with tuberculous pericarditis to define the levels of endogenous Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline) and Gal‑3 in normal pericardial fluid. They found that AcSDKP, a tetrapeptide with antifibrotic properties, and Gal-3 are detectable in normal pericardial fluid, and that tuberculous pericarditis was associated with low levels of pericardial AcSDKP and normal Gal-3 levels. Nevertheless, the role of Gal-3 in patients with CPP is not clear. Given the role of pericardial inflammation and fibrosis in the pathogenesis of CCP, we hypothesized that Gal-3 may 683