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High-Resolution Endocardial and Epicardial Optical Mapping in a Sheep Model of Stretch-Induced Atrial Fibrillation
Published on: July 29, 2011
Atrial Fibrillation Increases Proarrhythmic Mechanisms in the Ventricle
Paul Spangler1, Thea Bommer1, Laura Stengel2
1Department of Internal Medicine II, University Medical Center Regensburg, Germany.
JACC. Basic to Translational Science
|May 9, 2026
Summary
Atrial fibrillation (AF) significantly increases the risk of ventricular arrhythmias. This study reveals that AF promotes these dangerous heart rhythms by altering cellular electrical activity and calcium handling in the heart.
Area of Science:
- Cardiology
- Electrophysiology
- Molecular Biology
Background:
- Ventricular arrhythmias and sudden cardiac death are major concerns for patients with atrial fibrillation (AF).
- Understanding the mechanisms by which AF triggers ventricular arrhythmias is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the cellular and molecular mechanisms by which atrial fibrillation (AF) promotes ventricular arrhythmias.
- To characterize electrophysiological changes in the left ventricle (LV) of AF patients.
Main Methods:
- Human LV samples from patients with sinus rhythm and rate-controlled AF were analyzed for cellular electrophysiology.
- In vitro AF simulation in murine LV cardiomyocytes was performed.
- Oxidative activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) was assessed.
- Genetic ablation of CaMKII oxidation was studied in MMVV knock-in mice.
Main Results:
- LV cardiomyocytes from AF patients exhibited significantly more delayed afterdepolarizations and Ca2+ waves compared to sinus rhythm patients.
- AF simulation in murine LV cardiomyocytes increased ventricular proarrhythmic activity.
- Oxidative CaMKII activation was elevated in murine LV cardiomyocytes following AF simulation.
- MMVV knock-in mice lacking CaMKII oxidation did not show ventricular proarrhythmic activity after AF simulation.
Conclusions:
- Atrial fibrillation promotes ventricular arrhythmogenesis through specific cellular electrophysiological changes.
- Oxidative activation of CaMKII plays a critical role in mediating AF-induced ventricular arrhythmias.
- These findings provide novel mechanistic insights into the interplay between AF and ventricular arrhythmias.
Keywords:
Ca(2+) homeostasisatrial fibrillationexcitation-contraction couplingtranslational studiesventricular arrhythmiasMore Related Videos
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