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- W2080996593 abstract "Springer-Verlag 2012 Atrial fibrillation (AF) is the most frequent arrhythmia in the clinical setting and is associated with substantial cardiac morbidity and mortality [19]. Current drug interventions have limited efficacy and are accompanied by significant risk of proarrhythmic events [9]. The generally poor outcome with current antiarrhythmic drugs likely reflects the fact that most of the used agents were developed in the absence of precise understanding of pro- and anti-arrhythmic drug actions and the arrhythmogenic disease-specific cardiac substrate. Conceptually, AF induction requires a vulnerable substrate and a trigger that acts on the substrate to initiate the arrhythmia [25, 35]. Once AF is initiated, the rapid-atrial rate creates progressive AF-related changes in atrial electrical and structural properties (atrial remodeling). Electrical remodeling involves a shortening of the atrial effective refractory period (AERP) and abnormal atrial Ca 2? signaling, whereas increased atrial fibrosis and heterogeneous conduction slowing are typical characteristics of structural remodeling. Atrial remodeling can promote ectopic (triggered) activity and facilitate reentry, thereby contributing to AF perpetuation and the progression from short-lasting (paroxysmal) to" @default.
- W2080996593 created "2016-06-24" @default.
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- W2080996593 date "2012-07-17" @default.
- W2080996593 modified "2023-09-26" @default.
- W2080996593 title "Is altered atrial microRNA-ome a critical contributor to the pathophysiology of atrial fibrillation?" @default.
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- W2080996593 doi "https://doi.org/10.1007/s00395-012-0284-2" @default.
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