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Electrical and structural remodeling in atrial tissue refers to a series of adaptive and maladaptive changes at the cellular and tissue level, often triggered by cardiovascular disease, inflammation, or sustained arrhythmia[1][2][3]. Electrical remodeling involves changes in ion channel expression, most notably a reduction in L-type calcium current and altered potassium channel function, which shortens atrial action potential duration and increases susceptibility to arrhythmias such as atrial fibrillation[1][2][3][4]. Structural remodeling encompasses atrial fibrosis, altered cellular ultrastructure, and changes in intercellular connectivity (e.g., connexins), leading to slowed or heterogeneous conduction and an increased propensity for reentry and sustained arrhythmias[1][2][3]. These pathways may be assessed with imaging (echocardiography, MRI), genetic or protein markers, and ECG analysis but are not captured by a single molecular entity or receptor, making them unsuitable for classification as discrete therapeutic targets.
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