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Atrial Fibrillation Increases Proarrhythmic Mechanisms in the Ventricle
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DOI：10.1016/j.jacbts.2026.101558.png)
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Abstract
En 中文
• AF is associated with ventricular arrhythmic triggers: ventricular cardiomyocytes from patients with AF exhibited increased diastolic Ca2+ waves and delayed afterdepolarizations compared with sinus rhythm controls. • Irregular ventricular activation alone induces proarrhythmic mechanisms: in murine ventricular cardiomyocytes, AF simulation with irregular pacing induced arrhythmic events. • Oxidative CaMKII activation and NCX mediate AF-induced arrhythmogenesis: AF simulation increased CaMKII oxidation and phosphorylation of Ca2+-handling proteins, promoted diastolic Ca2+-release, and increased NCX activity, facilitating NCX-mediated triggered activity. • Genetic ablation of CaMKII oxidation prevents AF-induced ventricular arrhythmogenesis: cardiomyocytes lacking regulatory CaMKII oxidation sites were protected from AF-induced arrhythmogenic Ca2+-release events. • These findings identify a mechanistic link between AF and ventricular arrhythmias.
Keywords:
atrial fibrillation
Ca2+ homeostasis
excitation-contraction coupling
ventricular arrhythmias
translational studies
AF
atrial fibrillation
AS
aortic stenosis
CaMKII
Ca2+/calmodulin-dependent protein kinase II
DAD
delayed afterdepolarization
EF
ejection fraction
HF
heart failure
LV
left ventricular
NCX
sodium–calcium exchanger
PLB
phospholamban
RyR2
ryanodine receptor type 2
SCD
sudden cardiac death
SERCA
sarcoplasmic/endoplasmic reticulum Ca2+–adenosine triphosphatase
SR
sinus rhythm
TSAD
tissue slicing-assisted digestion
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