Basic/Translational Science -> Whole Animal Electrophysiology and Pharmacology (includes Neurohumoral Modulation)
D-PO06 - Poster Session VI (ID 26)
Poster
D-PO06-018 - Influence Of Obesity And Epicardial Fat On The Progression Of Electrical And Structural Remodeling In A Canine Atrial Fibrillation Obesity Model (ID 1513)
Abstract
Background: Obesity and epicardial fat (EF), a manifestation of obesity, are important risk factors for atrial fibrillation (AF). The underlying mechanisms of obesity linking EF to AF progression have not been fully examined.
Objective: To investigate the impact of obesity linked to EF on electrophysiologic and anatomical AF substrates.
Methods: Twenty dogs were divided into four groups (n=5 per each): normal diet without rapid atrial pacing (RAP) (control group [median body weight: 12.0kg]), RAP for 4-8 weeks with a normal diet (AF group [12.0kg]), high-fat diet (HFD) without RAP (MetS group [16.0kg]), and HFD and RAP for 4-8 weeks (Mets-AF group [17.0kg]). The effective refractory period (ERP) and AF inducibility were determined. Hearts were excised for histopathological and gene expression analyses.
Results: The left atrial (LA) pressure was more significantly increased in MetS than the MetS-AF, AF, and control groups. The LA/pulmonary vein ERP at a basic cycle length of 400ms was shorter in the Mets-AF and AF than MetS and control groups. Short duration AF was more induced in the Mets and MetS-AF than AF and control groups (Figure). Histological examinations showed the fatty infiltration extending from EF increased more in the Mets and Mets-AF than AF and control groups (Figure). The Fibronectin 1 and collagen I/III mRNA levels increased more in the MetS-AF and AF than MetS and control groups.
Conclusion: AF vulnerability was associated with increased LA pressures and EF in the MetS group, and with fibrofatty infiltration from EF with subtle fibrosis in the MetS-AF group. This suggested that EF plays an important role in AF pathogenesis in obese patients.
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Objective: To investigate the impact of obesity linked to EF on electrophysiologic and anatomical AF substrates.
Methods: Twenty dogs were divided into four groups (n=5 per each): normal diet without rapid atrial pacing (RAP) (control group [median body weight: 12.0kg]), RAP for 4-8 weeks with a normal diet (AF group [12.0kg]), high-fat diet (HFD) without RAP (MetS group [16.0kg]), and HFD and RAP for 4-8 weeks (Mets-AF group [17.0kg]). The effective refractory period (ERP) and AF inducibility were determined. Hearts were excised for histopathological and gene expression analyses.
Results: The left atrial (LA) pressure was more significantly increased in MetS than the MetS-AF, AF, and control groups. The LA/pulmonary vein ERP at a basic cycle length of 400ms was shorter in the Mets-AF and AF than MetS and control groups. Short duration AF was more induced in the Mets and MetS-AF than AF and control groups (Figure). Histological examinations showed the fatty infiltration extending from EF increased more in the Mets and Mets-AF than AF and control groups (Figure). The Fibronectin 1 and collagen I/III mRNA levels increased more in the MetS-AF and AF than MetS and control groups.
Conclusion: AF vulnerability was associated with increased LA pressures and EF in the MetS group, and with fibrofatty infiltration from EF with subtle fibrosis in the MetS-AF group. This suggested that EF plays an important role in AF pathogenesis in obese patients.
