JACC: Basic to Translational Science (Apr 2016)

Galectin-3 Regulates Atrial Fibrillation Remodeling and Predicts Catheter Ablation Outcomes

  • 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,
  • José Jalife, MD

DOI
https://doi.org/10.1016/j.jacbts.2016.03.003
Journal volume & issue
Vol. 1, no. 3
pp. 143 – 154

Abstract

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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.

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