10.6084/m9.figshare.7743587.v1
Murillo de Oliveira Antunes
Murillo de Oliveira
Antunes
Edmundo Arteaga-Fernández
Edmundo
Arteaga-Fernández
Fabio Fernandes
Fabio
Fernandes
Carla David Soffiatti
Carla David
Soffiatti
Paula de Cássia Buck
Paula de Cássia
Buck
Ester Cerdeira Sabino
Ester
Cerdeira Sabino
Carlos Henrique Valente Moreira
Carlos Henrique Valente
Moreira
Charles Mady
Charles
Mady
Evaluation of Galectin-3 and Myocardial Fibrosis in Patients with Hypertrophic Cardiomyopathy
SciELO journals
2019
Cardiomyopathy, Hypertrophic
Endomyocardial Fibrosis
Galectin 3
Diagnostic Imaging
Arrhythmias, Cardiac
2019-02-20 02:52:58
Dataset
https://scielo.figshare.com/articles/dataset/Evaluation_of_Galectin-3_and_Myocardial_Fibrosis_in_Patients_with_Hypertrophic_Cardiomyopathy/7743587
<div><p>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.</p></div>