1. Galectin-3 Regulates Atrial Fibrillation Remodeling and Predicts Catheter Ablation Outcomes
- Author
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Yoshio Takemoto, MD, PhD, Rafael J. Ramirez, PhD, Miki Yokokawa, MD, Kuljeet Kaur, PhD, Daniela Ponce-Balbuena, PhD, Mohamad C. Sinno, MD, B. Cicero Willis, MD, Hamid Ghanbari, MD, Steven R. Ennis, PhD, Guadalupe Guerrero-Serna, PhD, Bettina C. Henzi, MD, Rakesh Latchamsetty, MD, Roberto Ramos-Mondragon, PhD, Hassan Musa, PhD, Raphael P. Martins, MD, Sandeep V. Pandit, PhD, Sami F. Noujaim, PhD, Thomas Crawford, MD, Krit Jongnarangsin, MD, Frank Pelosi, MD, Frank Bogun, MD, Aman Chugh, MD, Omer Berenfeld, PhD, Fred Morady, MD, Hakan Oral, MD, and José Jalife, MD
- Subjects
atrial fibrillation ,catheter ablation ,fibrosis ,galectin-3 ,upstream therapy ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
Atrial fibrillation (AF) usually starts as paroxysmal but can evolve relentlessly to the persistent and permanent forms. However, the mechanisms governing such a transition are unknown. The authors show that intracardiac serum levels of galectin (Gal)-3 are greater in patients with persistent than paroxysmal AF and that Gal-3 independently predicts atrial tachyarrhythmia recurrences after a single ablation procedure. Using a sheep model of persistent AF the authors further demonstrate that upstream therapy targeting Gal-3 diminishes both electrical remodeling and fibrosis by impairing transforming growth factor beta–mediated signaling and reducing myofibroblast activation. Accordingly, Gal-3 inhibition therapy increases the probability of AF termination and reduces the overall burden of AF. Therefore the authors postulate that Gal-3 inhibition is a potential new upstream therapy to prevent AF progression.
- Published
- 2016
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