Abstract 12204: Obesity and Weight Reduction: Impact on the Substrate for Atrial Fibrillation
Introduction: Whether the substrate for AF due to obesity can be reversed by weight loss is unknown.
Methods: 20 sheep with induced obesity and 10 lean controls were studied. Of the obese sheep, 10 underwent weight loss while 10 were maintained as obese controls. Each underwent: bi-atrial endocardial electroanatomic mapping, hemodynamic assessment, and imaging. Electrophysiological evaluation included: ERP (7 sites), conduction velocity (CV), voltage mapping and AF inducibility. Fatty infiltration, atrial fibrosis, TGFβ1 and Connexin43 expression were analysed.
Results: See table. Obesity resulted in structural and hemodynamic remodelling which reversed with weight loss. In contrast, the electrophysiological changes with obesity partially reversed. Epicardial fat infiltrated the posterior LA in obese group (vs controls) and did not regress upon weight loss. Fibrosis and atrial TGFβ1 protein increased and Connexin43 expression decreased in obese group (vs controls) and all reversed with weight loss.
Conclusion: The increase in TGFβ1 and concurrently fibrosis with reduced Connexin43 expression in obesity and their reversal upon weight loss support their role in mechanistic link between obesity and AF. This study also demonstrates that epicardial fat infiltrates underlying atrial muscle in obesity. This could potentially alter conduction by forming areas of electrical silence promoting re-entry and provide another novel mechanism by which obesity predisposes to AF. It could explain maintained AF vulnerability despite weight loss in our model. Importantly, weight reduction resulted in partial AF substrate reversal underling its role for AF management in obesity.
- © 2012 by American Heart Association, Inc.