Abstract Body (Do not enter title and authors here): Obscurin is a giant cytoskeletal protein that supports muscle development, tethers intracellular compartments to the sarcolemma, and regulates contraction. In the ObscnΔIg58/59 mouse model, expressing obscurin lacking Immunoglobulin (Ig) domains 58 and 59, aging males exhibit irregular heart rhythm with prominent atrial fibrillation, atrial enlargement, and progressive remodeling of the ventricles. A mechanistic basis for the emergence of arrhythmia at 6-months could not be identified in ObscnΔIg58/59 ventricles, suggesting that the atria are preferentially impacted by deletion of the obscurin Ig58/59 module. We hypothesize that Ig58/59 deletion elicits unique structural, electrical, and functional consequences in the atria preceding ventricular maladaptation. Unlike the ventricles, ObscnΔIg58/59 atria exhibited misalignment of Z-disks in electron micrographs. Spontaneous and stimulated Ca²⁺ cycling behavior were differentially disrupted in atrial cardiomyocytes in 6- and 12-month ObscnΔIg58/59 males. Relatedly, atrial cells showed an age-dependent deterioration in the architecture of the transverse-axial tubules network. Finally, as a function of aging, ObscnΔIg58/59 atria displayed alterations in the expression and phosphorylation of T-cap, a Z-disk associated protein implicated in the integration of t-tubules with the sarcomeric cytoskeleton. The structural and electrical alterations that arise in ObscnΔIg58/59 atria precede ventricular dysfunction and coincide with the emergence of atrial fibrillation. Collectively, our work indicates that the atria are principally affected by Ig58/59 elimination. The ObscnΔIg58/59 mouse model has thus emerged as a proxy for atrial cardiomyopathy.