Abstract
Calcium handling abnormalities can precipitate atrial fibrillation (AF). In recent years, both ionic remodeling (i.e., changes in expression and function of channels and transporters) and ultrastructural remodeling (i.e., decreased density and regularity of the transverse-axial tubule system, TATS, and disrupted channel and transporter distribution) have been associated with deranged calcium signaling and excitation-contraction coupling. Here, we used a three-dimensional computational model of the human atrial myocyte, in which electrophysiology and subcellular calcium signaling are coupled with a spatially-detailed description of TATS structure, to predict the effect of variation in cell structure on atrial myocyte calcium signaling and electrophysiology.Our simulations predict that atrial myocytes with sparse and irregular tubules exhibit greater vulnerability to arrhythmia (e.g., shorter latency and higher amplitude of delayed afterdepolarizations, DADs, and lower pacing threshold for alternans).
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call