Key result
Chronic atrioventricular block-induced remodeling enhances intracellular calcium load and activates the Ca2+-calmodulin-CaMKII system, contributing to arrhythmogenic afterdepolarizations.
Population
Rabbit model with chronic atrioventricular block (CAVB) and isolated ventricular cardiomyocytes
Comparison
Chronic atrioventricular block remodeling and… vs Control (non-CAVB) rabbits/cells
Design
Preclinical
Follow-up
up to 2 weeks
Authors
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May heighten TdP risk via Ca2+ dysregulation in bradycardia; leaves open human mechanistic and therapeutic translation.
In a rabbit model of chronic AV block, activation of the Ca2+-calmodulin-CaMKII system contributes significantly to arrhythmogenic early afterdepolarizations, suggesting a potential therapeutic target for bradycardia-related long-QT syndrome.
Qi et al. (2009) studied Bradycardia-Related Acquired Long-QT Syndrome. Chronic atrioventricular block (CAVB) vs. Baseline/unexposed state was evaluated on Ca2+ handling abnormalities and early afterdepolarizations (EADs). Chronic atrioventricular block-induced remodeling enhances intracellular calcium load and activates the Ca2+-calmodulin-CaMKII system, contributing to arrhythmogenic afterdepolarizations.
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