Abstract
It is well accepted that calcium handling abnormalities can precipitate atrial fibrillation (AF). Both ionic and ultrastructural remodeling have been associated with deranged calcium signaling and AF through altered channel and transporter expression and function, reduced density and regularity of the transverse-axial tubule system (TATS), and subcellular re-distribution of calcium-handling proteins. However, it remains unclear whether ionic and ultrastructural remodeling interact to affect arrhythmogenic propensity.
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